Academic literature on the topic 'Myocardial infarction. Fibrin. Stem cells'
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Journal articles on the topic "Myocardial infarction. Fibrin. Stem cells"
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Venugopal, Jayarama Reddy, Molamma P. Prabhakaran, Shayanti Mukherjee, Rajeswari Ravichandran, Kai Dan, and Seeram Ramakrishna. "Biomaterial strategies for alleviation of myocardial infarction." Journal of The Royal Society Interface 9, no. 66 (April 13, 2011): 1–19. http://dx.doi.org/10.1098/rsif.2011.0301.
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World Health Organization estimated that heart failure initiated by coronary artery disease and myocardial infarction (MI) leads to 29 per cent of deaths worldwide. Heart failure is one of the leading causes of death in industrialized countries and is expected to become a global epidemic within the twenty-first century. MI, the main cause of heart failure, leads to a loss of cardiac tissue impairment of left ventricular function. The damaged left ventricle undergoes progressive ‘remodelling’ and chamber dilation, with myocyte slippage and fibroblast proliferation. Repair of diseased myocardium with in vitro -engineered cardiac muscle patch/injectable biopolymers with cells may become a viable option for heart failure patients. These events reflect an apparent lack of effective intrinsic mechanism for myocardial repair and regeneration. Motivated by the desire to develop minimally invasive procedures, the last 10 years observed growing efforts to develop injectable biomaterials with and without cells to treat cardiac failure. Biomaterials evaluated include alginate, fibrin, collagen, chitosan, self-assembling peptides, biopolymers and a range of synthetic hydrogels. The ultimate goal in therapeutic cardiac tissue engineering is to generate biocompatible, non-immunogenic heart muscle with morphological and functional properties similar to natural myocardium to repair MI. This review summarizes the properties of biomaterial substrates having sufficient mechanical stability, which stimulates the native collagen fibril structure for differentiating pluripotent stem cells and mesenchymal stem cells into cardiomyocytes for cardiac tissue engineering.
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Guo, Hai-Dong, Hai-Jie Wang, Yu-Zhen Tan, and Jin-Hong Wu. "Transplantation of Marrow-Derived Cardiac Stem Cells Carried in Fibrin Improves Cardiac Function After Myocardial Infarction." Tissue Engineering Part A 17, no. 1-2 (January 2011): 45–58. http://dx.doi.org/10.1089/ten.tea.2010.0124.
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Dyr, Jan E., Tomas Riedel, Jana Stikarova, Jiri Suttnar, Jaroslav Cermak, Roman Kotlin, Martin Hajsl, Petr Tousek, Viktor Kocka, and Martin Maly. "Spatially Organized Structure of Coronary Thrombus in Acute Myocardial Infarction." Blood 128, no. 22 (December 2, 2016): 716. http://dx.doi.org/10.1182/blood.v128.22.716.716.
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Abstract Introduction The use of thromboaspiration in primary percutaneous intervention (PCI) for ST-segment elevation myocardial infarction (STEMI) has offered a unique opportunity to study thrombus composition, its dynamic formation, and architecture in vivo. There has been, however, several limitations, not least the fact that the technique has not yet allowed a precise transversal analysis from one side of the artery to the other, as is done in histological analysis. The dynamic process of intracoronary thrombus formation in STEMI patients is thus still not well understood. Ischemic time was hypothesized to be among the strongest independent correlates of thrombus architecture. In time the platelets are decreasing its proportion and fibrin proportion is increasing (J Silvain, J-P Collet, JW Weisel et al, J Am Coll Cardiol 2011; 57:1359). However, no real report on the internal structures of the in vivo formed thrombi has been shown so far. Therefore, we investigated both the surface and the composition of longitudinally freeze-fractured thrombi. Methods Thrombi were collected by PCI from 119 STEMI patients. Out of the patients there were "early comers " (˃12 h from symptom onset; 23 patients) and "late comers" (more than 720 min; 29 patients). The mean age of all patients was 64 years, 70% of patients were males, 51% were smokers, 50% had arterial hypertension, 20% were diabetics and 23% had chronic renal insufficiency. Scanning electron microscopy; collected thrombi obtained by PCI were thoroughly washed in saline solution and stored in 4% formaldehyde prior dehydration. To reveal the internal structures of the thrombi selected samples were longitudinally freeze fractured in liquid nitrogen and coated with platinum. Samples were examined in SEM Vega Plus TS 5135 (Tescan s.r.o., Brno, Czech Republic). Whole areas of the freeze-fractured thrombi were scanned. Results and discussion The thrombus composition of longitudinally freeze-fractured thrombi was compared between groups of "early-comers" and "late-comers. The distribution of the components in the "early comers" thrombi freeze-fracture seemed to be uniform. Platelets were far the main component (about 75 % in proportion) of the "early comers" thrombus, followed by fibrin and other compounds. The amount of red blood cells was negligible (about 2 - 8 %). We did not observe any significant differences between the thrombi in the group of early comers. Thrombi of the "late-comers" group were composed mainly of red blood cells; platelets and fibrin formed only minority of the thrombi. In contrast to the "early comers" the distribution of the main thrombus components in the "late comers" thrombi was dramatically different between individual parts of the thrombus. The number of platelets and red blood cells varied from 0% to almost 99% and vice versa. It was possible to estimate the initiating place of the thrombus as well as the direction of the growth. Each thrombus could be divided into parts formed mainly either by platelets or by red blood cells. It seems that thrombus develops a regional architecture defined by the extent of platelet activation and packing density. It has been reported that in contracted clots and thrombi, erythrocytes are compressed to close-packed polyhedral structures with platelets and fibrin on the surface demonstrating how contracted clots form an impermeable barrier important for hemostasis and wound healing (D Cines, T Lebedeva, J Weisel et al, Blood 2014; 123:1596). Our investigation of the composition of the in vivo formed thrombi supports these results and helps to explain how fibrinolysis is greatly retarded as clots grow and contract. We have found that on the surfaces of late-comers thrombi fibrin thick fibrils were present. It has been shown that the association of soluble fibrinogen with the fibrin clot results in the reduced adhesiveness of such fibrinogen/fibrin matrices toward leukocytes and platelets (VK Lishko, T Burke, T Ugarova, Blood 2007; 109:1541). Fibrinopeptides A are less accessible for thrombin in surface bound fibrinogen which thus provides additional level of protection of thrombi from premature dissolution (T Riedel, L Medved, JE Dyr, Blood 2011; 117:1700). These findings may have great impact on our knowledge of pathophysiology of the thrombus growth and possible therapeutic consequences related to the time of symptom onset. Disclosures No relevant conflicts of interest to declare.
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Sun, Cheuk-Kwan, Yen-Yi Zhen, Steve Leu, Tzu-Hsien Tsai, Li-Teh Chang, Jiunn-Jye Sheu, Yung-Lung Chen, et al. "Direct implantation versus platelet-rich fibrin-embedded adipose-derived mesenchymal stem cells in treating rat acute myocardial infarction." International Journal of Cardiology 173, no. 3 (May 2014): 410–23. http://dx.doi.org/10.1016/j.ijcard.2014.03.015.
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Mattapally, Saidulu, Wuqiang Zhu, Vladimir G. Fast, Ling Gao, Chelsea Worley, Ramaswamy Kannappan, Anton V. Borovjagin, and Jianyi Zhang. "Spheroids of cardiomyocytes derived from human-induced pluripotent stem cells improve recovery from myocardial injury in mice." American Journal of Physiology-Heart and Circulatory Physiology 315, no. 2 (August 1, 2018): H327—H339. http://dx.doi.org/10.1152/ajpheart.00688.2017.
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The microenvironment of native heart tissue may be better replicated when cardiomyocytes are cultured in three-dimensional clusters (i.e., spheroids) than in monolayers or as individual cells. Thus, we differentiated human cardiac lineage-induced pluripotent stem cells in cardiomyocytes (hiPSC-CMs) and allowed them to form spheroids and spheroid fusions that were characterized in vitro and evaluated in mice after experimentally induced myocardial infarction (MI). Synchronized contractions were observed within 24 h of spheroid formation, and optical mapping experiments confirmed the presence of both Ca2+ transients and propagating action potentials. In spheroid fusions, the intraspheroid conduction velocity was 7.0 ± 3.8 cm/s on days 1– 2 after formation, whereas the conduction velocity between spheroids increased significantly ( P = 0.003) from 0.8 ± 1.1 cm/s on days 1– 2 to 3.3 ± 1.4 cm/s on day 7. For the murine MI model, five-spheroid fusions (200,000 hiPSC-CMs/spheroid) were embedded in a fibrin patch and the patch was transplanted over the site of infarction. Later (4 wk), echocardiographic measurements of left ventricular ejection fraction and fractional shortening were significantly greater in patch-treated animals than in animals that recovered without the patch, and the engraftment rate was 25.6% or 30% when evaluated histologically or via bioluminescence imaging, respectively. The exosomes released from the spheroid patch seemed to increase cardiac function. In conclusion, our results established the feasibility of using hiPSC-CM spheroids and spheroid fusions for cardiac tissue engineering, and, when fibrin patches containing hiPSC-CM spheroid fusions were evaluated in a murine MI model, the engraftment rate was much higher than the rates we have achieved via the direct intramyocardial injection. NEW & NOTEWORTHY Spheroids fuse in culture to produce structures with uniformly distributed cells. Furthermore, human cardiac lineage-induced pluripotent stem cells in cardiomyocytes in adjacent fused spheroids became electromechanically coupled as the fusions matured in vitro, and when the spheroids were combined with a biological matrix and administered as a patch over the infarcted region of mouse hearts, the engraftment rate exceeded 25%, and the treatment was associated with significant improvements in cardiac function via a paracrine mechanism, where exosomes released from the spheroid patch.
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Zou, Lili, Hui Liang, LI Hou, Tao Li, Yan Zhang, Baorong LI, Yingmiao LIU, et al. "Neutrophil Extracellular Traps Promote Hypercoagulability in ST-Elevated Myocardial Infarction Following Fibrinolytic Administration." Blood 132, Supplement 1 (November 29, 2018): 3797. http://dx.doi.org/10.1182/blood-2018-99-116105.
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Abstract Introduction:Fibrinolysis plays an important role in the treatment of ST-elevated myocardial infarction (STEMI) when percutaneous coronary intervention is not readily available. Early and successful myocardial reperfusion with thrombolytic therapy effectively reduces the infarct size and improves the clinical outcome. However, the process of restoring blood flow to the ischemic myocardium can induce injury and reduce the beneficial effects of myocardial reperfusion. Previous studies had shown that platelets, leukocytes and TF play important role in thrombotic complications after fibrinolysis in AMI. However, there are still 10-15% patients who have risk for re-occlusion after antiplatelet and anticoagulant therapies. Thus, we speculate that there may be other mechanisms involved in the hypercoagulability after STEMI fibrinolysis. Neutrophil extracellular traps (NETs) are double-edge swords that could ensnare and kill microbial pathogens but also contribute to thrombosis. However, the role of NETs during STEMI fibrinolysis-induced re-occlusion is largely unknown. Our aims were to determine the procoagulant role of NETs after successful thrombolysis, and to elucidate its interaction with endothelial cells (ECs). Methods:31 STEMI patients with successfully fibrinolysis and 12 healthy controls were enrolled. Patient blood samples were collected at 0 h, 2 h, 6 h, 12 h and 24 h after fibrinolysis. Cell-free DNA (cf-DNA) was quantified using the Quant-iT PicoGreen dsDNA Assay Kit. ELISA was used to detect MPO-DNA complexes and TAT (thrombin-antithrombin) complexes. Wright-Giemsa and immunofluorescence confocal microscope were used to analyze and quantify NETs formation in neutrophil cells. ECs were incubated in growth media containing 20% pooled serum obtained from healthy donors in the presence or absence of 20-fold concentrated neutrophil extracellular chromatin. The procoagulant activity (PCA) of neutrophils and ECs was measured by clotting time and purified coagulation complex assays. DNase I or anti-TF were included in the inhibition assays. Results: We found that cf-DNA, MPO-DNA and TAT are significantly reduced at 2 hours in STEMI patients with successful fibrinolysis. Their levels then increased and peaked at 6 hours (Figure 1A, B, E). Interestingly, the level of cf-DNA at 6 hours in STEMI thrombotic patients was positively correlated with TAT (r=0.959; p<0.01; Figure 1G). Wright-Giemsa and immunofluorescence staining showed that NETs were released by STEMI reperfusion neutrophils or by control neutrophils treated with plasma obtained from STEMI patients with fibrinolysis (Figure 1D,F), and the percentage of NETs-releasing PMNs was about 30% (Figure 1C). Isolated neutrophils from fibrinolytic patients in vitro demonstrated significantly shortened coagulation time and increased fibrin formation after 2 hours fibrinolysis, and peaked at 6 hours. DNase I but not anti-tissue factor antibody could inhibit these effects. Co-incubation assays revealed that NETs triggered PS exposure on ECs, converting them to a procoagulant phenotype. Confocal imaging of NETs-treated ECs illustrated that bound FVa and FXa colocalized within PS-enriched areas of ECs to form prothrombinase, and further supported fibrin formation. Moreover, patients with recurrent ischemia showed significantly higher NETs release and thrombin generation than non-recurrent ischemia. Conclusions: Our study reveals that the PCA of STEMI following fibrinolytic administration decrease after 2 hours, then increase and peak at 6 hours, which is at least partly due to the release of NETs induced by activated PMNs. Additionally, NETs partly contribute to ECs injury after myocardial reperfusion. DNase I can disconnect NETs and may therefore serve as a promising therapeutic target in STEMI reinfarction and recurrent ischemia. Disclosures No relevant conflicts of interest to declare.
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Chen, Jiangwei, Yingfei Zhan, Yabin Wang, Dong Han, Bo Tao, Zhenli Luo, Sai Ma, et al. "Chitosan/silk fibroin modified nanofibrous patches with mesenchymal stem cells prevent heart remodeling post-myocardial infarction in rats." Acta Biomaterialia 80 (October 2018): 154–68. http://dx.doi.org/10.1016/j.actbio.2018.09.013.
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Chi, Nai-Hsin, Ming-Chia Yang, Tze-Wen Chung, Jia-Yu Chen, Nai-Kuan Chou, and Shoei-Shen Wang. "Cardiac repair achieved by bone marrow mesenchymal stem cells/silk fibroin/hyaluronic acid patches in a rat of myocardial infarction model." Biomaterials 33, no. 22 (August 2012): 5541–51. http://dx.doi.org/10.1016/j.biomaterials.2012.04.030.
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Wang, Lei, Jixian Deng, Weichen Tian, Bo Xiang, Tonghua Yang, Gang Li, Jian Wang, et al. "Adipose-derived stem cells are an effective cell candidate for treatment of heart failure: an MR imaging study of rat hearts." American Journal of Physiology-Heart and Circulatory Physiology 297, no. 3 (September 2009): H1020—H1031. http://dx.doi.org/10.1152/ajpheart.01082.2008.
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This study assessed the potential therapeutic efficacy of adipose-derived stem cells (ASCs) on infarcted hearts. Myocardial infarction was induced in rat hearts by occlusion of the left anterior descending artery (LAD). One week after LAD occlusion, the rats were divided into three groups and subjected to transplantation of ASCs or transplantation of cell culture medium (CCM) or remained untreated. During a 1-mo recovery period, magnetic resonance imaging showed that the ASC-treated hearts had a significantly greater left ventricular (LV) ejection fraction and LV wall thickening than did the CCM-treated and untreated hearts. The capillary density in infarct border zone was significantly higher in the ASC-treated hearts than in the CCM-treated and untreated hearts. However, only 0.5% of the ASCs recovered from the ASC-treated hearts were stained positive for cardiac-specific fibril proteins. It was also found that ASCs under a normal culture condition secreted three cardiac protective growth factors: vascular endothelial growth factor, hepatocyte growth factor, and insulin-like growth factor-1. Results of this study suggest that ASCs were able to improve cardiac function of infarcted rat hearts. Paracrine effect may be the mechanism underlying the improved cardiac function and increased capillary density.
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Weisel, John W., Tatiana Lebedeva, Chandrasekaran Nagaswami, Vincent M. Hayes, Walter Massefski, Rustem I. Litvinov, Lubica Rauova, Thomas J. Lowery, and Douglas B. Cines. "Polyhedrocytes: Compressed Polyhedral Erythrocytes In Contracted Blood Clots and Thrombi." Blood 122, no. 21 (November 15, 2013): 452. http://dx.doi.org/10.1182/blood.v122.21.452.452.
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Background Contraction of blood clots is necessary for hemostasis, wound healing and to restore flow past obstructive thrombi. However, little has been known about the structure of contracted clots and mechanisms of contraction. Erythrocytes, biconcave cells that are highly deformable to allow their passage through the microvasculature, are abundant in venous thrombi, and to a lesser extent in arterial thrombi. Erythrocytes promote hemostasis, but their participation in clot contraction has not been reported. Here we study the mechanisms of clot contraction and the roles of erythrocytes, platelets and fibrin, and show that erythrocyte shape change into compressed polyhedrocytes allows tight packing consistent with the major function of clots to stem bleeding. Methods Whole blood was clotted by recalcification and addition of thrombin or kaolin, while following the process of clotting, including contraction, with a new technique using T2 magnetic resonance. We examined the structure and composition of contracted whole blood clots by scanning electron microscopy and confocal light microscopy. Results Contracted clots display a remarkable structure, with a close-packed, tessellated array (or mosaic tiling of space) of compressed polyhedral erythrocytes (called polyhedrocytes) on the interior and a meshwork of fibrin and platelet aggregates on the exterior. Little fibin and few platelets were found on the interior of the contracted clots. The same results were obtained with both thrombin and kaolin as activators of clotting and also with reconstituted human blood and clots prepared from mouse blood. Confocal microscopy of hydrated clots confirms the results of scanning electron microscopy. The mechanical nature of this shape change was confirmed by polyhedrocyte formation from the forces of centrifugation of blood without clotting. Platelets (with their cytoskeletal motility proteins) and fibrin(ogen) (as the substrate bridging platelets for contraction) are required to generate the forces necessary to segregate platelets/fibrin from erythrocytes and to compress erythrocytes into a closely packed polyhedral array. To assess the density of packing of the polyhedral erythrocytes, we replaced the water surrounding the clots with D2O and observed by T2 magnetic resonance that hydrogen/deuterium exchange for the contracted clots was very slow, consistent with their very tightly packed, almost impermeable structure. The same polyhedrocyte structures were observed from in vivo thrombi aspirated by cardiologists from the coronary arteries of ST-elevation myocardial infarction patients. Summary/Conclusions We have observed a previously undiscovered, naturally occurring erythrocyte function and morphology, closely packed polyhedra, in contracted clots and thrombi, and an unexpected spatial redistribution of platelets and fibrin that occurs during contraction. Clot contraction is an essential part of hemostasis, since both human genetic disorders of platelet myosin IIA and megakaryocyte myosin IIA-knock out mice show a bleeding phenotype. These observations on contracted clots imply that they are stiff, rigid structures that can form an impermeable, watertight seal. On the one hand, contraction of clots within the vasculature may relieve obstruction of blood vessels and allow recanalization, especially in the venous system. On the other hand, these results account for long-standing clinical observations that fibrinolysis is greatly prolonged following clot contraction, since perfusion or diffusion of lytic enzymes into these tightly packed polyhedral erythrocytes would be nearly impossible. These results suggest a vital role for erythrocytes and clot contraction in hemostasis and wound healing. Disclosures: No relevant conflicts of interest to declare.
Dissertations / Theses on the topic "Myocardial infarction. Fibrin. Stem cells"
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Murphy, Megan K. "Fibrin microthreads promote stem cell growth for localized delivery in regenerative therapy." Worcester, Mass. : Worcester Polytechnic Institute, 2008. http://www.wpi.edu/Pubs/ETD/Available/etd-090208-143505/.
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Elmestiri, Mostafa Mohamed. "Dynamic changes in haematopiotic stem cells after myocardial infarction." Thesis, University of British Columbia, 2008. http://hdl.handle.net/2429/2469.
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Objective
Increases in the number of CD34+ stem cells and progenitor cells in blood and infarcted areas after acute myocardial infarction (AMI) are a documented phenomenon. However, no study has yet reported on the dynamic changes in specific populations of adult stem cells, such as c-kit +Lin- cells or ckit + Lin - Sca1 + (KLS cells), following AMI. This study investigated the dynamic changes in these cells in multiple systems/organs following MI in mice.
Methods
The C57BU6J mice received either no surgery (normal control, n=6) or surgical ligation of the left anterior descending coronary artery to create AMI (n=24). On day-1 (n=7), -3 (n=5), -6 (n=6), and -12 (n=6) after AMI, mononuclear cells were isolated from theblood, spleen, and bone marrow, and stained with Lineage-PEcy7, c-kit-PE, and Sca1-APC antibodies. The c-kit +Lin - cell and KLS cell populations in the mononuclear cells were analyzed by FACS flowcytometry.
Results
The pattern of changes in the c-kit + Lin - cells was very similar to that in the KLS cells in the bone marrow, circulating blood, and spleen following AMI. There was a significant increase in these cells on day-3 in the bone marrow (c-kit +Lin- cells: 1.470 ± 0.094% vs control 1.127 ± 0.019%, and KLS cells: 0.365 ± 0.012 % vs control 0.1848 ± 0.019%, p<0.05), which then slowly declined from day-6 to -12. In the blood, these cells, particularly the KLS cells, decreased slightly from day-1 to -12. On day-3, -6, and -12 the cells increased continuously and significantly in the spleen, (on day 3, c-kit +Lin-cells: 0.253 ± 0.0107 % vs control 0.1305 ± 0.014 %; it was 0.3212 ± 0.028 % on day-6). (on day-6 KLS cells: 0.1078 ± 0.076 % vs control 0.0425 ± 0.0064 % while on day 12 it was 0.1174 ± 0.035 % p<0.05).
Conclusion
This study provides for the first time the longest observation of the dynamic changes of specific sub-groups of adult stem cells (c-kit +Lin- cells and KLS cells) in multiple systems following AMI. The study demonstrates that AMI results in significant changes, or mobilization, of these cells in the bone marrow, spleen, and blood. Significant and continuous accumulation of the cells in the spleen occurs following AMI, despite the decreased level of the cells in the blood. The role of the spleen in stem cell mobilization after AMI is unclear and requires further investigation.
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Malandraki-Miller, Sophia. "Enhancing progenitor cells for cell therapy after myocardial infarction." Thesis, University of Oxford, 2016. https://ora.ox.ac.uk/objects/uuid:205043f4-e3e0-4947-9afc-b43f1543e0bd.
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Based on data from the World Healthcare Organisation, cardiovascular diseases are the primary cause of disease-related death globally, with myocardial infarction (MI) being the most prevalent. If not treated effectively, MI can progress to heart failure (HF). With 70 million prescriptions for HF in 2014 and 515 people in the UK being hospitalised daily with MI, the British Heart Foundation calls for novel robust treatments. Even though cardiac stem cell (CSC) therapy for MI has been under investigation for more than a decade, there still has not been a consensus over the identity of the adult endogenous CSC. Recent clinical trials, using selected Ckit+ cells or the cardiosphere-derived cells (CDCs) have shown moderate results. The aim of this thesis was to develop a digestion-based method for isolation of cardiac progenitor cells (CPCs) from the mouse atria. The resulting "CTs" were isolated by collagenase/trypsin (where their name has resulted from) digestion with a prolonged period step for cell attachment. CTs were compared to isolated CDCs for their marker expression, using RT-PCR and Immunocytochemistry, showing cells with a mesenchymal phenotype which expressed SCA1 and CKIT. The CDCs had more of a fibroblast phenotype with higher Ddr2 and Wt1 expression. Using a TGF-β1 differentiation protocol, the CTs could be differentiated more effectively to a CM lineage than could the CDCs. In addition, Oleic acid (OA) supplementation stimulated the Peroxisome proliferator-activated receptor alpha pathway and led to maturation of the CT cells, both before and after differentiation. The differentiated CTs begin to express Tnnt2, while OA led to Myh7 increase and upregulated their oxidative metabolism. Finally, the CTs were more able to survive under serum-starvation than the CDCs, and transfection with miR-210 could enhance CT survival under these conditions and increased VEGF secretion. By digestion of the whole atria and allowing a prolonged time for attachment, we have developed a novel isolation protocol which generates a cell population containing a range of progenitors. Cells within this population can survive under serum starvation and can be differentiated to a CM lineage, making them a promising therapeutic population.
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Nussbaum, Jeannette. "Embryonic stem cells for myocardial infarct repair /." Thesis, Connect to this title online; UW restricted, 2004. http://hdl.handle.net/1773/6312.
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Fakharzadeh, Michael. "Delivering Stem Cells to the Heart." Digital WPI, 2010. https://digitalcommons.wpi.edu/etd-theses/677.
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Myocardial infarction is a prominent medical problem in the world today. Current treatments are limited and do not strive to regenerate the myocardial tissue that is lost post-infarction. Human mesenchymal stem cells (hMSCs) have been shown to improve cardiac function when implanted post-infarction. The effectiveness of stem cell therapy largely depends on the delivery method. Current delivery methods are insufficient due to their low cell engraftment rate and inability to target the endocardium, where most myocardial infarctions occur. Biological microthreads are a promising new local cell delivery method that may improve upon these current limitations. We hypothesize that biological microthreads will increase efficiency of hMSC delivery to the beating rat heart compared to intramyocardial injection. To test our hypothesis we seeded biological microthreads in vitro with 100 ìL of cell suspension (100,000 hMSCs). After one day, an average of 11,806 ± 3,932 hMSCs were counted on the biological microthreads. The biological microthreads were attached to suture needles to allow targeted delivery to the rat heart (in the left ventricular wall). Human mesenchymal stem cells were loaded with quantum dots prior to seeding the biological microthread bundles or delivery to the rat heart via injection. For intramyocardial injection, a cell suspension containing 10,000 hMSCs (35 ìL) was injected into the myocardial wall using a 100 ìL syringe. The delivery efficiency of each method was determined by sectioning the heart into 8 µm thick sections and analyzing three sections every sixty sections (24 µm every 480 µm) for quantum dot loaded hMSCs. These sections were stained with Hoechst dye and quantum dot loaded cells in the heart sections were manually counted. The delivery efficiency of each biological microthread implantation was calculated by dividing the number of counted quantum dot loaded hMSCs in the heart wall by the average number of hMSCs on the biological microthread bundles (normalized to the length that was implanted in the heart wall) after 24 hours. The delivery efficiency of intramyocardial injection was calculated by dividing the number of counted quantum dot loaded hMSCs in the heart wall by 10,000 (the number of cells injected). Biological microthread mediated hMSC delivery had a significantly higher delivery efficiency (66.6 ± 11.1%) compared to intramyocardial injection (11.8 ± 6.25%) after 1 hour (p < 0.05). Biological microthread implantation tracking illustrated that we were able to deliver hMSCs to the myocardium and endocardium of the left ventricular wall for hMSC delivery. This study illustrates that biological microthreads can serve as an efficient means of delivering hMSCs to the infarcted heart. Unlike the currently utilized delivery methods, biological microthreads can target the infarcted layer of the left ventricular wall and maximize hMSC engraftment to that layer.
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Fiumana, Emanuela <1975>. "Stem Cells as a therapy for myocardial infarction in animal models." Doctoral thesis, Alma Mater Studiorum - Università di Bologna, 2008. http://amsdottorato.unibo.it/643/.
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Advances in stem cell biology have challenged the notion that infarcted myocardium is
irreparable. The pluripotent ability of stem cells to differentiate into specialized cell lines began
to garner intense interest within cardiology when it was shown in animal models that
intramyocardial injection of bone marrow stem cells (MSCs), or the mobilization of bone
marrow stem cells with spontaneous homing to myocardium, could improve cardiac function and
survival after induced myocardial infarction (MI) [1, 2]. Furthermore, the existence of stem cells
in myocardium has been identified in animal heart [3, 4], and intense research is under way in an
attempt to clarify their potential clinical application for patients with myocardial infarction. To
date, in order to identify the best one, different kinds of stem cells have been studied; these have
been derived from embryo or adult tissues (i.e. bone marrow, heart, peripheral blood etc.).
Currently, three different biologic therapies for cardiovascular diseases are under investigation:
cell therapy, gene therapy and the more recent “tissue-engineering” therapy .
During my Ph.D. course, first I focalised my study on the isolation and characterization of
Cardiac Stem Cells (CSCs) in wild-type and transgenic mice and for this purpose I attended, for
more than one year, the Cardiovascular Research Institute of the New York Medical College, in
Valhalla (NY, USA) under the direction of Doctor Piero Anversa. During this period I learnt
different Immunohistochemical and Biomolecular techniques, useful for investigating the
regenerative potential of stem cells.
Then, during the next two years, I studied the new approach of cardiac regenerative medicine
based on “tissue-engineering” in order to investigate a new strategy to regenerate the infracted
myocardium. Tissue-engineering is a promising approach that makes possible the creation of
new functional tissue to replace lost or failing tissue. This new discipline combines isolated
functioning cells and biodegradable 3-dimensional (3D) polymeric scaffolds. The scaffold
temporarily provides the biomechanical support for the cells until they produce their own
extracellular matrix. Because tissue-engineering constructs contain living cells, they may have
the potential for growth and cellular self-repair and remodeling. In the present study, I examined
whether the tissue-engineering strategy within hyaluron-based scaffolds would result in the
formation of alternative cardiac tissue that could replace the scar and improve cardiac function
after MI in syngeneic heterotopic rat hearts. Rat hearts were explanted, subjected to left coronary
descending artery occlusion, and then grafted into the abdomen (aorta-aorta anastomosis) of
receiving syngeneic rat. After 2 weeks, a pouch of 3 mm2 was made in the thickness of the
ventricular wall at the level of the post-infarction scar. The hyaluronic scaffold, previously
engineered for 3 weeks with rat MSCs, was introduced into the pouch and the myocardial edges
sutured with few stitches. Two weeks later we evaluated the cardiac function by M-Mode
echocardiography and the myocardial morphology by microscope analysis.
We chose bone marrow-derived mensenchymal stem cells (MSCs) because they have shown
great signaling and regenerative properties when delivered to heart tissue following a myocardial
infarction (MI). However, while the object of cell transplantation is to improve ventricular
function, cardiac cell transplantation has had limited success because of poor graft viability and
low cell retention, that’s why we decided to combine MSCs with a biopolimeric scaffold.
At the end of the experiments we observed that the hyaluronan fibres had not been
substantially degraded 2 weeks after heart-transplantation. Most MSCs had migrated to the
surrounding infarcted area where they were especially found close to small-sized vessels. Scar
tissue was moderated in the engrafted region and the thickness of the corresponding ventricular
wall was comparable to that of the non-infarcted remote area. Also, the left ventricular
shortening fraction, evaluated by M-Mode echocardiography, was found a little bit increased
when compared to that measured just before construct transplantation. Therefore, this study
suggests that post-infarction myocardial remodelling can be favourably affected by the grafting
of MSCs delivered through a hyaluron-based scaffold
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Kujanpää, K. (Kirsi). "Mechanisms behind stem cell therapy in acute myocardial infarction." Doctoral thesis, Oulun yliopisto, 2016. http://urn.fi/urn:isbn:9789526212920.
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Abstract Ischemic heart disease is one of the leading cause of death in the Western world. There is convincing evidence that stem cell therapy improves cardiac function and reduces the scar formation following an acute myocardial infarction (AMI). The mechanisms involved in the recovery remain partly unknown. Direct injection of stem cells into myocardium is a widely used transplantation technique though there are few details available about the behavior of cells after transplantation. A cardiac explant culture model simulating tissue stress was developed in this study to examine in detail the properties of the stem cells after their transplantation. The migration range in myocardium and the number of adherent stem cells increased with time. In vitro and in vivo studies revealed that after their administration, the stem cells became localized in the slit-like spaces, such as in the capillaries. Even though the study outcomes regarding the impact of stem cell therapy in recovery after AMI have been largely promising, the results of the clinical studies have proved to be more controversial. If one wishes to evaluate the true contribution of the stem cell therapy to the recovery, it is essential to devise a reliable study method for cell targeting. Here, iron labeled stem cells in combination with magnetic resonance imaging (MRI) were used. The MRI data corresponded to the histological results. Thus, it is concluded that MRI is a feasible method for monitoring the effectiveness of cell targeting. Stem cell treatment was shown to increase cardiac function at three weeks after AMI. If there was a high number of stem cells in cardiac tissue after transplantation, this predicted a greater improvement in cardiac function. Improper stem cell injection may lead to leakage of the stem cells out of the myocardium, leading to unreproducible study results. Inflammation modulating factors secreted by the stem cells are considered as key mechanisms in the recovery after AMI. There were differences in the cytokine levels between the stem cell treated and control groups in a clinical and in vivo animal study i.e. stem cell therapy exerted a balancing effect on the inflammatory process, a crucial component in the optimal recovery after AMI. The present study reveals many properties of stem cells, importance of cell targeting and the influence of stem cell therapy on cytokine levels after AMITiivistelmä Iskeeminen sydänsairaus on yksi yleisimmistä kuolinsyistä länsimaissa. Tutkimusten mukaan kantasoluterapia parantaa sydämen toimintakykyä ja pienentää akuutin sydäninfarktin jälkeen sydämeen muodostuvan arpikudoksen määrää. Paranemiseen liittyvät mekanismit ovat edelleen osittain tuntemattomia. Kantasolujen ruiskutus suoraan sydämeen on paljon käytetty menetelmä, vaikka solujen käyttäytymistä ei tunneta tarkkaan.Tutkimuksessa kehitetyn kudoksen stressitilaa simuloivan sydänkudoksen kasvatusmenetelmän avulla tutkittiin siirrettyjen kantasolujen toimintaa yksityiskohtaisesti. Kantasolujen vaeltaman matkan sydänkudoksessa ja kiinnittyneiden kantasolujen lukumäärä havaittiin kasvavan ajan kuluessa. In vitro ja in vivo tutkimuksissa havaittiin kantasolujen sijaitsevan ruiskutuksen jälkeen rakomaisissa paikoissa kuten pienissä verisuonissa. Vaikka tutkimustulokset kantasoluterapian hyödyistä paranemisen suhteen ovat pääosin lupaavia, kliinisten tutkimusten tulokset ovat ristiriitaisia. Todellisen kantasoluhoidon vaikutuksen arvioimiseksi tarvitaan luotettava menetelmä varmistamaan kantasolujen hakeutuminen vaurioalueelle. Tässä tutkimuksessa rautaleimattujen kantasolujen paikantamisessa käytetty magneettikuvantaminen vastasi histologisia löydöksiä. Magneettikuvantaminen todettiin käyttökelpoiseksi menetelmäksi solujen paikallistamisessa. Kantasoluhoidon osoitettiin parantavan sydämen toimintakykyä kolme viikkoa akuutin sydäninfarktin jälkeen. Suuri kantasolumäärä sydänkudoksessa siirron jälkeen ennusti parempaa toipumista. Puutteellisesti suoritettu kantasoluruiskutus voi johtaa kantasolujen vuotamiseen pois sydänkudoksesta aiheuttaen vaihtelevuutta tutkimustuloksiin. Kantasolujen erittämiä tulehdusta sääteleviä tekijöitä pidetään tärkeimpänä mekanismina paranemisprosessissa. Tutkimus osoitti eroavaisuuksia kantasoluhoidetun ja kontrolliryhmän välillä. Kliinisessä ja koe-eläintutkimuksessa kantasolusiirrolla todettiin tulehdusreaktiota tasapainottava vaikutus, mikä on tärkeää optimaalisen sydänlihaskudoksen paranemisen kannalta akuutin sydäninfarktin jälkeen. Tutkimus toi esiin monia kantasolujen ominaisuuksia, solujen paikantamisen tärkeyden ja kantasoluhoidon vaikutuksen sytokiinipitoisuuksiin akuutin sydäninfarktin jälkeen
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Miettinen, J. (Johanna). "Studies on bone marrow-derived stem cells in patients with acute myocardial infarction." Doctoral thesis, Oulun yliopisto, 2011. http://urn.fi/urn:isbn:9789514293924.
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Abstract Intracoronary administration of autologous bone marrow derived stem cells (BMC) has been postulated to repair the myocardial damage in patients who have suffered acute ST-elevation myocardial infarction (STEMI). The aim of this study was to find determinants for the left ventricular functional recovery after BMC treatment of STEMI and to study the effect of BMC treatment on different biochemical and clinical parameters associated with the outcome of STEMI patients. In this study, STEMI patients treated with thrombolysis were randomly assigned to receive either intracoronary BMC (n=39) or placebo (n=39) into the infarct related artery at the time of percutaneous coronary intervention. The efficacy of the BMC treatment was assessed by measurement of the change of left ventricular ejection fraction (LVEF) from baseline to six months after STEMI. Two-dimensional echocardiography was used to assess PA pressure, LV systolic and diastolic function. Blood samples were drawn for biochemical determinations at several time points and BMCs were cultured in the laboratory for in vitro analyses. In the BMC group, the most powerful determinant of the change of LVEF was the baseline LVEF. Patients with baseline LVEF at or below the median (≤62.5%) experienced a more marked improvement of LVEF than those above the median. Elevated levels of N-terminal probrain natriuretic peptide (NT-proBNP) and N-terminal proatrial natriuretic peptide (NT-proANP) were also associated with an improvement of LVEF in the BMC group. However, no difference was observed between the BMC group and the placebo group in the changes of the levels of NT-proANP, NT-proBNP or any of the inflammatory markers measured. The BMC group showed a trend toward a reduction of peak PA pressure, while the placebo group had a significant increase of peak PA pressure at 6 months. In addition, there was a greater improvement in the LV diastolic function, assessed in quartiles, in the BMC group. The in vitro studies of BMCs revealed that exposure to tumor necrosis factor alpha (TNF-α) significantly enhanced the proliferation of BMCs and resulted in activation of immunosuppression by altering the expression of several immunosuppressive proteins. In conclusion, low baseline LVEF as well as high levels of natriuretic peptides NT-proANP and NT-proBNP, which reflect the severity of the hemodynamic and neurohumoral reactions evoked by the myocardial damage, have a considerable association to a better response to stem cell therapy after an acute STEMI. BMC therapy also prevents the increase of PA pressure and improves the cardiac diastolic function. Based on in vitro studies, the inflammatory cytokine TNF-α seems to evoke an enhanced proliferation of the bone marrow-derived mesenchymal stem cells and activation of several immunosuppressive defence mechanismsTiivistelmä Sydäninfarktipotilaiden sepelvaltimoon pallolaajennuksen yhteydessä injektoitujen kantasolujen tiedetään parantavan hieman sydämen pumppauskykyä, mutta taustalla olevaa mekanismia ei tunneta. Kantasoluhoidon onnistumiseen vaikuttavia tekijöitä on tutkittu vasta vähän, eikä myöskään sitä tiedetä, miksi kaikki potilaat eivät hyödy kantasoluhoidosta. Tämän tutkimuksen tavoitteena oli selvittää infarktialueelle annetun kantasoluhoidon vaikutuksia äkillisen ST-nousuinfarktin (STEMI) sairastaneissa potilaissa, ja etsiä hoidon onnistumiseen vaikuttavia tekijöitä. Tutkimuksessa käytettiin potilasaineistoa, johon otettiin 78 äkilliseen sydäninfarktiin sairastunutta potilasta, jotka hoidettiin liuotushoidolla ja sen jälkeen pallolaajennuksella. Puolet potilaista satunnaistettiin saamaan lumeliuosta ja puolet omaa luuydinsolukkoaan (BMC), joka ruiskutettiin pallolaajennuksen yhteydessä sepelvaltimon kautta infarktialueelle. Hoidon vaikusta tutkittiin mittaamalla angiografian avulla vasemman kammion ejektiofraktion (LVEF) muutosta lähtötilanteen ja kuuden kuukauden seurannan välillä. Lisäksi sydämen ultraäänitutkimuksella määritettiin keuhkovaltimopainetta ja vasemman kammion systolista ja diastolista toimintaa. Potilaista otettiin lisäksi verinäytteitä, joista määritettiin erilaisia tulehdusmerkkiaineita ja natriureettisia peptidejä. Lisäksi potilaista kerättyjä luuydinkantasoluja viljeltiin laboratoriossa in vitro-analyyseja varten. Tutkimuksessa todettiin, että LVEF ennen kantasoluhoitoa oli voimakkain ennustetekijä suotuisalle LVEF:n muutokselle kantasoluhoidon jälkeen. Potilaat, joilla LVEF oli ennen kantasoluhoitoa alle mediaaniarvon (≤62.5%), hyötyivät kantasoluhoidosta enemmän kuin potilaat, joilla LVEF oli yli mediaanin. Myös natriureettisten peptidien NT-proBNP:n ja NT-proANP:n korkea taso infarktin jälkeen oli yhteydessä suurempaan LVEF:n paranemiseen BMC-potilailla. Natriureettisten peptidien ja tulehdusmerkkiaineiden pitoisuuksien muutoksissa kantasoluhoidon jälkeen ei kuitenkaan todettu eroa BMC- ja kontrolliryhmän välillä. Sydämen diastolisen toiminnan havaittiin paranevan enemmän BMC-ryhmässä kuin kontrolliryhmässä. Lisäksi BMC-ryhmässä havaittiin lievää laskua keuhkovaltimopaineessa, kun taas kontrolliryhmässä se nousi merkittävästi. In vitro-tutkimukset luuytimestä erilaistetuilla mesenkymaalisilla kantasoluilla puolestaan osoittivat, että tuumorinekroositekijä alfa (TNF-α)-altistus lisäsi solujakautumista ja monien immunosupressiivisten proteiinien tuottoa soluissa. Matala LVEF sekä natriureettisten peptidien NT-proBNP:n ja NT-proANP:n korkea taso sydäninfarktin jälkeen kuvaavat infarktivaurion aiheuttamien hemodynaamisten ja neurohumoraalisten reaktioiden vakavuutta, ja tässä tutkimuksessa niiden osoitettiin olevan vahvasti yhteydessä äkillisen ST-nousuinfarktin jälkeen annetun kantasoluhoidon hyötyyn. Kantasoluhoito saattaa myös suojata infarktipotilaita haitalliselta keuhkovaltimopaineen nousulta ja parantaa sydämen diastolista toimintaa. Tulehdusvälittäjäaine TNF-α näytti in vitro-kokeiden perusteella lisäävän luuytimen mesenkymaalisten kantasolujen jakautumista ja aktivoivan niissä monia immunosuppressiivisia puolustusmekanismeja tulehdusta vastaan
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Tan, Yew Liang Terence Clinical School St George Hospital Faculty of Medicine UNSW. "Differentiation and migration of Sca-1+/CD 31-cardiac side population cells in a mouse infarction model." Publisher:University of New South Wales. Clinical School - St George Hospital, 2009. http://handle.unsw.edu.au/1959.4/43387.
Full textAbstract:
Myocardial infarction is the most common cause of heart failure and remains one of the leading causes of morbidity and mortality in humans. Stem cells are important in the maintenance and repair of adult tissues. Hoechst effluxing cells, termed side population cells are a rare subset of cells found in adult tissues that are highly enriched for stem and progenitor cell activity. Recent studies have suggested that Sca-1+/CD31- cardiac side population cells are capable of differentiation into cardiomyocytes in vitro. However, the response of cardiac side population cells to myocardial injury remains unknown in vivo. In this study, we directly transplanted Sca-1+/CD31- cardiac side population cells into an acutely infarcted mouse heart. After two weeks, the transplanted cells were found to express cardiomyocyte or endothelial cell markers. Importantly, when these cells were transplanted into a remote nonischemic part of the heart after MI, they were able to migrate to the damaged myocardium. Consistent with these cells homing property, we found that SDF-1α, a chemotactic chemokine and its receptor, CXCR4 were up-regulated in the damaged myocardium and on Sca-1+/CD31- cardiac SP cells respectively following an acute myocardial infarction. We further showed that SDF-1α was able to induce migration of Sca-1+/CD31- cardiac side population cells in vitro. Our results have therefore suggested that Sca-1+/CD31- cardiac side population cells are able to migrate to damaged myocardium from non-ischemic myocardium and differentiate into cardiomyocytes as well as endothelial cells in the acutely infarcted mouse heart. We postulate that the SDF-1α/CXCR4 interaction may play an important role in the migration of these cells. Understanding and enhancing these processes may hold enormous potential possibilities for therapeutic myocardial regeneration for the treatment of cardiovascular disease.
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Mayfield, Audrey. "Encapsulation of Cardiac Stem Cells to Enhance Cell Retention and Cardiac Repair." Thesis, Université d'Ottawa / University of Ottawa, 2014. http://hdl.handle.net/10393/31500.
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Despite advances in treatment, heart failure remains one of the top killers in Canada. This recognition motivates a new research focus to harness the fundamental repair properties of the human heart, with human cardiac stem cells (CSCs) emerging as a promising cell candidate to regenerate damaged myocardium. The rationale of this approach is simple with ex vivo amplification of CSCs from clinical grade biopsies, followed by delivery to areas of injury, where they engraft and regenerate the heart. Currently, outcomes are limited by modest engraftment and poor long-term survival of the injected CSCs due to on-going cell loss during transplantation. As such, we explored the effect of cell encapsulation to increase CSC engraftment and survival after myocardial injection. Transcript and protein profiling of human atrial appendage sourced CSCs revealed strong expression the pro-survival integrin dimers αVβ3 and α5β1- thus rationalizing the integration of fibronectin and fibrinogen into a supportive intra-capsular matrix. Encapsulation maintained CSC viability and expression of pro-survival transcripts when compared to standard suspended CSCs. Media conditioned by encapsulated CSCs demonstrated superior production of pro-angiogenic/ cardioprotective cytokines, angiogenesis and recruitment of circulating angiogenic cells. Intra-myocardial injection of encapsulated CSCs after experimental myocardial infarction favorably affected long-term retention of CSCs, reduced scar burden and improved overall cardiac function. Taken together, cell encapsulation of CSCs prevents detachment induced cell death while boosting the mechanical retention of CSCs to enhance repair of damaged myocardium.
Books on the topic "Myocardial infarction. Fibrin. Stem cells"
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E, Harding Sian, and SpringerLink (Online service), eds. Myocardial Tissue Engineering. Berlin, Heidelberg: Springer-Verlag Berlin Heidelberg, 2011.
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Cardiac Regeneration and Repair : Volume 2: Biomaterials and Tissue Engineering. Elsevier Science & Technology, 2014.
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Boccaccini, Aldo R., and Sian Harding. Myocardial Tissue Engineering. Springer, 2011.
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Cardiac Regeneration and Repair : Volume 1: Pathology and Therapies. Elsevier Science & Technology, 2014.
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(Editor), Nabil Dib, Doris A. Taylor (Editor), and Edward B. Diethrich (Editor), eds. Stem Cell Therapy and Tissue Engineering for Cardiovascular Repair: From Basic Research to Clinical Applications. Springer, 2005.
Find full textBook chapters on the topic "Myocardial infarction. Fibrin. Stem cells"
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ter Horst, Kasper W. "Bone Marrow-Derived Stem Cell Therapy for Myocardial Infarction." In Stem Cells and Cancer Stem Cells, Volume 1, 163–71. Dordrecht: Springer Netherlands, 2011. http://dx.doi.org/10.1007/978-94-007-1709-1_20.
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Angeli, Franca S., and Yerem Yeghiazarians. "Bone Marrow Cell Therapy for Acute Myocardial Infarction: A Clinical Trial Review." In Stem Cells & Regenerative Medicine, 265–77. Totowa, NJ: Humana Press, 2010. http://dx.doi.org/10.1007/978-1-60761-860-7_16.
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Kraitchman, Dara L., Dorota A. Kedziorek, and Jeff W. M. Bulte. "MR Imaging of Transplanted Stem Cells in Myocardial Infarction." In Methods in Molecular Biology, 141–52. Totowa, NJ: Humana Press, 2010. http://dx.doi.org/10.1007/978-1-60761-901-7_10.
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Henning, Robert J. "Stem Cells in the Treatment of Myocardial Infarction and Cardiomyopathy." In Translational Medicine Research, 277–316. Dordrecht: Springer Netherlands, 2015. http://dx.doi.org/10.1007/978-94-017-7273-0_12.
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Janssens, Stefan P. "Cell Therapy of Acute Myocardial Infarction and Ischemic Cardiomyopathy: From Experimental Findings to Clinical Trials." In Adult and Pluripotent Stem Cells, 113–41. Dordrecht: Springer Netherlands, 2014. http://dx.doi.org/10.1007/978-94-017-8657-7_7.
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Su, Weijun, Liang Leng, Zhongchao Han, Zuoxiang He, and Zongjin Li. "Bioluminescence Imaging of Human Embryonic Stem Cell-Derived Endothelial Cells for Treatment of Myocardial Infarction." In Imaging and Tracking Stem Cells, 203–15. Totowa, NJ: Humana Press, 2013. http://dx.doi.org/10.1007/7651_2013_15.
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Panfilov, Ilia Alexander, Renate de Jong, Shin-ichiro Takashima, and Henricus J. Duckers. "Clinical Study Using Adipose-Derived Mesenchymal-Like Stem Cells in Acute Myocardial Infarction and Heart Failure." In Methods in Molecular Biology, 207–12. Totowa, NJ: Humana Press, 2013. http://dx.doi.org/10.1007/978-1-62703-511-8_16.
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Maltabe, Violetta A., Theofilos M. Kolettis, and Panos Kouklis. "Challenges in stem cell-based approaches for myocardial regeneration after myocardial infarction." In Stem Cells, 17–50. WORLD SCIENTIFIC, 2020. http://dx.doi.org/10.1142/9789811205538_0002.
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Renneberg, Reinhard, Viola Berkling, and Vanya Loroch. "Myocardial Infarction, Cancer, and Stem Cells." In Biotechnology for Beginners, 311–42. Elsevier, 2017. http://dx.doi.org/10.1016/b978-0-12-801224-6.00009-6.
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Chacko, Simi, and Periannan Kuppusamy. "Hypoxic Preconditioning of Stem Cells to Treat Myocardial Infarction." In Cardiovascular Diseases, 199–210. CRC Press, 2013. http://dx.doi.org/10.1201/b14663-15.
Full textConference papers on the topic "Myocardial infarction. Fibrin. Stem cells"
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Discher, Dennis, and Adam Engler. "Mesenchymal Stem Cell Injection After Myocardial Infarction Improves Myocardial Compliance." In ASME 2007 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2007. http://dx.doi.org/10.1115/sbc2007-176754.
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Cellular therapy for myocardial injury has improved ventricular function in both animal and clinical studies, though the mechanism of benefit is unclear. This study was undertaken to examine the effects of cellular injection after infarction on myocardial elasticity. Coronary artery ligation of Lewis rats was followed by direct injection of human mesenchymal stem cells (MSC) into the acutely ischemic myocardium. Two weeks post-infarct, myocardial elasticity was mapped by atomic force microscopy. MSC-injected hearts near the infarct region were two-fold stiffer than myocardium from non-infarcted animals but softer than myocardium from vehicle-treated infarcted animals. After eight weeks, the following variables were evaluated: MSC engraftment and left ventricular geometry by histologic methods; cardiac function with a pressure-volume conductance catheter; myocardial fibrosis by Masson trichrome staining; vascularity by immunohistochemistry; and apoptosis by TUNEL assay. The human cells engrafted and expressed a cardiomyocyte protein but stopped short of full differentiation and did not stimulate significant angiogenesis. MSC-injected hearts showed significantly less fibrosis than controls, as well as less left ventricular dilation, reduced apoptosis, increased myocardial thickness, and preservation of systolic and diastolic cardiac function. In summary, MSC injection after myocardial infarction did not regenerate contracting cardiomyocytes but reduced the stiffness of the subsequent scar and attenuated post-infarction remodeling, preserving some cardiac function. Improving scarred heart muscle compliance could be a functional benefit of cellular cardiomyoplasty.
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Guyette, Jacques, Zewei Tao, Angelica DeMartino, Melissa Kuhn, Marsha Rolle, George Pins, and Glenn R. Gaudette. "Delivering Stem Cells to the Heart on Biological Sutures: Effects on Regional Mechanical Function." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53680.
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Heart failure (HF) affects over 5 million people in the US alone,1 costs society over $10B per year in medical care costs,2 and is the single most common hospital discharge diagnosis.3 Despite our advances in many areas of cardiovascular disease, we have made little progress in treating HF,4 largely due to the fact that few treatments actually aim to treat myocardial infarction (MI), which is the underlying cause of most cases of HF. Once a patient exhibits HF, their long-term survival is in jeopardy, exhibiting less than 50% probability of survival 5 years after diagnosis.4
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Engler, Adam J. "Probing Mechanisms of Mechano-Sensitive Differentiation in Mesenchymal Stem Cells." In ASME 2010 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2010. http://dx.doi.org/10.1115/sbc2010-19184.
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Adult mesenchymal stem cells (MSCs) have recently been shown to be responsive to the properties of their adjacent extracellular niche, most notably physical parameters such as topography and elasticity. Elasticity varies dramatically between tissues that MSCs inhibit, which drives elasticity-based differentiation into neurons, muscle, bone, etc. However within tissues, distinct elasticity gradients, brought on by pathological conditions, e.g. myocardial infarction ∼ 8.67 ± 1.50 kPa/mm, or through normal tissue variation, e.g. 0.58 ± 0.88 kPa/mm, could drive MSC migration. In fact, MSCs appear to undergo directed migration up elasticity gradients, or “durotax,” as shallow as 0.96 kPa/mm, indicating a ‘differentiation hierarchy’ since when given the choice, MSCs will durotax into the stiffest regions of the niche and then differentiate based on niche elasticity. As cells move up the gradient, they do so by deforming their niche to determine it’s elasticity, but the molecular mechanism that converts this biophysical signal into a biochemical one which the nucleus can interpret is yet unresolved. We have identified several focal adhesion-related proteins may be capable of force-induced conformational changes, e.g. vinculin. Upon the application of different amounts of traction stress in situ by MSCs, an appropriate amount of stretching results in the exposure of cryptic MAPK binding sites within vinculin and suggests that vinculin, among other focal adhesion proteins, may be sensitive to physical ECM properties and thus able to relay information leading to differentiation of stem cells.
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Barminko, Jeffrey, Jean Pierre Dolle, Rene Schloss, Martin Grumet, and Martin L. Yarmush. "Encapsulated Mesenchymal Stem Cells for Central Nervous System Repair." In ASME 2010 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2010. http://dx.doi.org/10.1115/sbc2010-19712.
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Mesenchymal stromal cells (MSC) have long been regarded as a cell source with the potential to provide therapies for various different tissue pathologies. They were originally identified for their ability to adhere to tissue culture plastic and gained favor due to their tremendous ability to propagate[1]. It was this finding as well as their ability to differentiate into lineages of mesoderm which have long made MSC a potential tool for autologous cellular replacement therapies [2, 3]. More recently, their cyto-protective role has been realized and been implicated in the benefit achieved in treating various different tissue pathologies. MSC have been found to secrete several different cytokines and growth factors in vitro. Furthermore, these factors can be modulated based on the environment MSC are exposed to. MSC have shown therapeutic benefits in models of GVHD, myocardial infarction, fulminant hepatic failure, central nervous system trauma and others, without any apparent cellular replacement. These advances propelled MSC to the fore front of potential cellular therapies and many are seeking to take advantage of their tissue protective properties. However, several draw backs in current methods of MSC implantation limit the ability to carry out safe and controlled clinical trials. Limitation with current MSC implantation approaches include; 1) directly transplanted MSCs exposed to the complex injury environment may be affected themselves early in the treatment processes, 2) MSC may also migrate to undesired tissue locations and 3) may differentiate into undesired end stage cells. These issues severally limit the translatability of MSC treatments in clinical settings; they make controlling experiments very difficult. There becomes a need to develop engineered methods for delivering these cells in a controlled manner. In order to circumvent these potential problems, we propose to use an alginate microencapsulation system as a vehicle for MSC delivery taking advantage of the soluble factors MSC provide.
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Wan, Chen-rei, Seok Chung, Ryo Sudo, and Roger D. Kamm. "Induction of Cardiomyocyte Differentiation From Mouse Embryonic Stem Cells in a Confined Microfluidic Environment." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-203995.
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Embryonic stem cell derived cardiomyocytes are deemed an attractive treatment option for myocardial infarction. Their clinical efficacy, however, has not been unequivocally demonstrated. There is a need for better understanding and characterization of the cardiogenesis process. A microfluidic platform in vitro is used to dissect and better understand the differentiation process. Through this study, we find that while embryoid bodies (EBs) flatten out in a well plate system, differentiated EBs self-assemble into complex 3D structures. The beating regions of EBs are also different. Most beating areas are observed in a ring pattern on 2D well plates around the center, self-assembled beating large 3D aggregates are found in microfluidic devices. Furthermore, inspired by the natural mechanical environment of the heart, we applied uniaxial cyclic mechanical stretch to EBs. Results suggest that prolonged mechanical stimulation acts as a negative regulator of cardiogenesis. From this study, we conclude that the culture environments can influence differentiation of embryonic stem cells into cardiomycytes, and that the use of microfluidic systems can provide new insights into the differentiation process.
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Rodriguez, Marita L., Charles E. Murry, and Nathan J. Sniadecki. "Assessment of Induced Pluripotent Stem Cell-Derived Cardiomyocyte Contractility Using Micropost Arrays." In ASME 2013 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/sbc2013-14640.
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Cardiovascular stem cell therapies have shown increasing promise as a potential therapeutic means for reversing the effects of a myocardial infarction [1]. Out of the currently available sources of human stem cells, human induced pluripotent stem cells (hiPSCs) are very promising in that: the number of cell lines that can be induced to the pluripotent state is extremely vast, they serve as a potential source for patient-specific cardiomyocytes, and their use is non-controversial. However, before they can be used feasibly in a clinical setting, the functional engraftment of these cells into the host tissue must be improved [2]. It is hypothesized that the structural and functional maturity of the stem-cell derived cardiomyocytes prior to implantation, may significantly affect the ability of these cells to engraft with resident heart tissue [3]. One of the most important functional characteristics of a cardiomyocyte is its ability to produce contractile forces. However, assessing the contractile properties of single iPS-CMs is a difficult task. iPS-CMs generally have relatively unorganized cytoskeletons, with stress fibers in multiple directions. This trait renders one or two-point force assays ineffectual in determining total cell forces. Furthermore, iPS-CMs don’t spread well on tissue culture surfaces, which make two-dimensional force measurements almost impossible.
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Marklein, Ross A., and Jason A. Burdick. "Spatial and Temporal Control of Stem Cell Behavior in 3D Sequentially Crosslinked Macroporous Hydrogels." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80064.
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The effect of matrix mechanics on stem cell behavior has received considerable attention due to the implications of tissue mechanics as not only a consequence but also a contributor to the development of certain pathologies. For example, a significant increase in matrix mechanics (“tissue stiffening”) is a hallmark of post-myocardial infarction [1], as well as heart valve calcification [2]. Recently, human mesenchymal stem cells (hMSCs) have been implemented in post-infarct therapeutic strategies due to their potential ability to contribute to tissue healing through differentiation and trophic factor secretion. However, due to aberrant mechanics and other microenvironment cues, studies have reported deleterious effects of hMSC implantation, such as ectopic calcification [3], which agrees well with previous reports on hMSC differentiation in response to mechanics [4]. Although not as well documented as stem cell differentiation in response to mechanics, there has been some initial evidence in support of the influence of mechanics on stem cell trophic factor secretion [5].
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Fusler, V., L. Badimon, V. Turitto, JJ Badimon, PC Adams, and JH Chesebro. "PATHOGENETIC AND ANGIOGRAPHIC FEATURES IN UNSTABLE ANGINAAND OTHER ACUTE CORONARY SYNDROMES." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643710.
Full textAbstract:
Angiography in patients with unstable angina or myocardial infarction with subtotal coronary occlusions reveals eccentric stenoses with irregularborders suggesting ruptured atherosclerotic plaques. In addition, the closer the angiogram is to the time of chest pain the higher is the likelihoodof observing a thrombotic filling defect distal to the stenotic region. Thus, we: 1) have investigated the relationship among platelet-vessel wall interaction, rheology, andthrombogenicsubstrate and 2) propose a hypothesisaccounting for thrombosis in the acute coronary syndromes.1) Platelet Vessel Wall Interactions, Rheology and Substrate - We have studied substrate and rheology in both an 'ex vivo' perfusion chamber and 'in vivo'swine model. Qur results, combinedwith those of others, show the following:-Platelet Vessel Wall Interaction and Thrombus Formation - a) In superficial arterial injury plateletsadherevia platelet membrane glycoprotein (GP) lb to the vessel wall to form a monolayer. Von Willebrand Factor (vWF), a high molecular weight glycoprotein found in plasma, platelets, and endothelial cells, binds GPIb and supports platelet adhesion. Platelet derived growth factors(PDGF) from these adherent platelets may contribute to atherogenesis. b) In deep arterial injury, plateletsare stimulated by three pathways -arachidonate, ADP and the "third pathway" -leading to exposure of platelet receptors (GPIIb/IIIa), and subsequent aggregation. Fibrinogenand vWF participate in aggregation bybinding to GPIIb/IIIa. Simultaneously, thrombin stimulates aggregation andthe formation of fibrin that stabilizes platelet aggregates, c) Both a platelet monolayer and aggregation with thrombosis, produce vasoconstriction due to release of platelet products (serotonin, thromboxane A2,and PDGF).- Rheology - a) Stenotic lesions produce a high local shear rate, whichenhances platelet-vessel wall interaction and, in the presence of acute rupture, platelet deposition and subsequent thrombus formation, b) Platelet deposition and thrombosis are particularly favored if the site of rupture includes the stenosis with its high shear rate,while the stasis in the post-stenotic region favors proprogationof thrombus.- Substrate - a) Plaque rupture produces a rough surface and exposes collagen and fat to flowing blood. Thisstimulates mural thrombosis, b) Such thrombus is either fixed or labile depending on the degree of plaque rupture or damage.2) Acute and Subacute Coronary Syndromes - The above observations in the swine model, coupled with recent clinical and pathological observations support the following:-Unstable Angina - Mild or restricted plaque rupture with or without activated mural thrombus, by increasingthe stenosis, explains the increase in exertional angina; subsequent labile thrombosis with platelet-related vasoconstriction explains the resting angina.-Q Wave Myocardial Infarction - The thrombus is occlusive and fixed or persistent because the damage to the vessel wall or to the plaque is more severe or extensive than in unstable angina.-Non-Q Wave Myocardial Infarction -In this syndrome, intermediate between unstable angina and Q wave myocardial infarction, the occlusive thrombus is more transient than in Q wave infarction because of less substrate exposure or damage.
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Honda, T., M. Aosaki, T. Tanaka, M. Aosaki, T. Uchida, S. Kimata, K. Hirosawa, Y. Horikawa, S. Ishizuka, and K. Ohki. "EFFECTS OF INTRAVENOUS ADMINISTRATIONOF A TISSUE-TYPE PLASMINOGEN ACTIVATOR (AK-124) IN ACUTE MYOCARDIAL INFARCTION, INCLUDING CHANGES IN BLOOD COAGULATION AND FIBRINOLYTIC ACTIVITY.- PRELIMINARY REPORT." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644894.
Full textAbstract:
We administered a tissue-type plasminogen activator (t-PA) intravenously to 10 patients with acute myocardial infarction (AMI), within 6 hours after the onset of symptoms, and then examined the state of reperfusion by coronary arterio graphy (CAG), and observed changes in blood coagulation and fibrinolytic activity to evaluate the drug effects. AK-124 (produced by Asahi Chemical Industry and Kowa Co., Ltd.in collaboration), a t-PA produced the by tissue cultureof normal human lung cells, was given in a dosage of48,000_576,000 A.K. units by intravenous infusionover 30_45 minutes. In 7 patients who received t-PA, areflow or improved flow was detected on CAG. In t-PAtreated patients, euglobulin lysis activity clearly increased, euglobulin lysis time clearly shortened, and D-dimer increased. After t-PA treatment, the levels of circulating fibrinogen and a2-plasmin inhibitor decreased by an average of 12%, and 14% of base-line values respectively, but plasminogen showed no detectable change. A hematoma at the site of the catheter insertion was observed in one patient. These observations suggest that t-PA has a higher specificity for fibrin bound plasminogen than for plasma plasminogen, and produces coronary thrombolysis without causing systemic fibrinolysis, at least with the above dosage.