Relevant bibliographies by topics / Human Aortic Smooth Muscle Cell

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers

Academic literature on the topic 'Human Aortic Smooth Muscle Cell'

Author: Grafiati
Published: 4 June 2021
Last updated: 11 February 2022

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Journal articles on the topic "Human Aortic Smooth Muscle Cell"

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Belkin, V. M., A. M. Belkin, and V. E. Koteliansky. "Human smooth muscle VLA-1 integrin: purification, substrate specificity, localization in aorta, and expression during development." Journal of Cell Biology 111, no. 5 (November 1, 1990): 2159–70. http://dx.doi.org/10.1083/jcb.111.5.2159.

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A membrane glycoprotein complex was isolated and purified from human smooth muscle by detergent solubilization and affinity chromatography on collagen-Sepharose. The complex was identified as VLA-1 integrin and consisted of two subunits of 195 and 130 kD in SDS-PAGE. Liposomes containing the VLA-1 integrin adhered to surfaces coated with type I, II, III, and IV collagens, Clq subcomponent of the first component of the complement, and laminin. The liposomes specifically adhered to these proteins in a Ca2+, Mg2(+)-dependent manner, but did not bind to gelatin, fibronectin, and thrombospondin substrates. The expression of VLA-1 integrin in different human tissues and cell types, and during aorta smooth muscle development was studied by SDS-PAGE, and subsequent quantitative immunoblotting was performed with antibodies recognizing alpha 1 and beta 1 subunits of the VLA-1 integrin. A high level of VLA-1 integrin expression was an exceptional feature of smooth muscles. Fibroblasts, endothelial cells, keratinocytes, striated muscles, and platelets contained trace amounts of VLA-1 integrin. In the 10-wk-old human fetal aorta, VLA-1 integrin was found only in smooth muscle cells whereas mesenchymal cells, surrounding aortic smooth muscle cells, were VLA-1 integrin negative. By the 24th wk of gestation, the amount of VLA-1 integrin was significantly reduced in the aortic media (4.3-fold for alpha 1 subunit and 2.5-fold for beta 1 subunit) compared with that in the 10-wk-old aortic smooth muscle cells. After birth, the expression of VLA-1 integrin increased and in the 1.5-yr-old child aorta the VLA-1 integrin level was almost the same as in adult aortic media. Smooth muscle cells from intimal thickening of adult aorta express five times less alpha 1 subunit of VLA integrin that smooth muscle cells from adult aortic media. In primary culture of aortic smooth muscle cells, the content of the VLA-1 integrin was dramatically reduced and subcultured cells did not contain VLA-1 integrin at all.
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Glukhova, M. A., S. P. Domogatskii, A. E. Kabakov, V. R. Muzykantov, O. I. Ornatskaya, D. V. Sakharov, and M. G. Frid. "Red blood cell targeting to human aortic smooth muscle cells." Bulletin of Experimental Biology and Medicine 102, no. 5 (November 1986): 1550–52. http://dx.doi.org/10.1007/bf00854687.

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Chotani, Maqsood A., Srabani Mitra, Baogen Y. Su, Sheila Flavahan, Ali H. Eid, K. Reed Clark, Christine R. Montague, Hervé Paris, Diane E. Handy, and Nicholas A. Flavahan. "Regulation of α2-adrenoceptors in human vascular smooth muscle cells." American Journal of Physiology-Heart and Circulatory Physiology 286, no. 1 (January 2004): H59—H67. http://dx.doi.org/10.1152/ajpheart.00268.2003.

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This study analyzed the regulation of α2-adrenoceptors (α2-ARs) in human vascular smooth muscle cells (VSMs). Saphenous veins and dermal arterioles or VSMs cultured from them expressed high levels of α2-ARs (α2C > α2A, via RNase protection assay) and responded to α2-AR stimulation [5-bromo- N-(4,5-dihydro-1 H-imidazol-2-yl)-6-quinoxalinamine (UK-14,304, 1 μM)] with constriction or calcium mobilization. In contrast, VSMs cultured from aorta did not express α2-ARs and neither cultured cells nor intact aorta responded to UK-14,304. Although α2-ARs (α2C >> α2A) were detected in aortas, α2C-ARs were localized by immunohistochemistry to VSMs of adventitial arterioles and not aortic media. In contrast with aortas, aortic arterioles constricted in response to α2-AR stimulation. Reporter constructs demonstrated higher activities for α2A- and α2C-AR gene promoters in arteriolar compared with aortic VSMs. In arteriolar VSMs, serum increased expression of α2C-AR mRNA and protein but decreased expression of α2A-ARs. Serum induction of α2C-ARs was reduced by inhibition of p38 mitogen-activated protein kinase (MAPK) with 2 μM SB-202190 or dominant-negative p38 MAPK. UK-14,304 (1 μM) caused calcium mobilization in control and serum-stimulated cells: in control VSMs, the response was inhibited by the α2A-AR antagonist BRL-44408 (100 nM) but not by the α2C-AR antagonist MK-912 (1 nM), whereas after serum stimulation, MK-912 (1 nM) but not BRL-44408 (100 nM) inhibited the response. These results demonstrate site-specific expression of α2-ARs in human VSMs that reflects differential activity of α2-AR gene promoters; namely, high expression and function in venous and arteriolar VSMs but no detectable expression or function in aortic VSMs. We found that α2C-ARs can be dramatically and selectively induced via a p38 MAPK-dependent pathway. Therefore, altered expression of α2C-ARs may contribute to pathological changes in vascular function.
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Gown, A. M., A. M. Vogel, D. Gordon, and P. L. Lu. "A smooth muscle-specific monoclonal antibody recognizes smooth muscle actin isozymes." Journal of Cell Biology 100, no. 3 (March 1, 1985): 807–13. http://dx.doi.org/10.1083/jcb.100.3.807.

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Injection of chicken gizzard actin into BALB/c mice resulted in the isolation of a smooth muscle-specific monoclonal antibody designated CGA7. When assayed on methanol-Carnoy's fixed, paraffin-embedded tissue, it bound to smooth muscle cells and myoepithelial cells, but failed to decorate striated muscle, endothelium, connective tissue, epithelium, or nerve. CGA7 recognized microfilament bundles in early passage cultures of rat aortic smooth muscle cells and human leiomyosarcoma cells but did not react with human fibroblasts. In Western blot experiments, CGA7 detected actin from chicken gizzard and monkey ileum, but not skeletal muscle or fibroblast actin. Immunoblots performed on two-dimensional gels demonstrated that CGA7 recognizes gamma-actin from chicken gizzard and alpha- and gamma-actin from rat colon muscularis. This antibody was an excellent tissue-specific smooth muscle marker.
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Tang, Yangfeng, Shangyi Yu, Yang Liu, Jiajun Zhang, Lin Han, and Zhiyun Xu. "MicroRNA-124 controls human vascular smooth muscle cell phenotypic switch via Sp1." American Journal of Physiology-Heart and Circulatory Physiology 313, no. 3 (September 1, 2017): H641—H649. http://dx.doi.org/10.1152/ajpheart.00660.2016.

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Phenotypic switch of vascular smooth muscle cells (VSMCs) plays an important role in the pathogenesis of atherosclerosis and aortic dissection. However, the mechanisms of phenotypic modulation are still unclear. MicroRNAs have emerged as important regulators of VSMC function. We recently found that microRNA-124 (miR-124) was downregulated in proliferative vascular diseases that were characterized by a VSMC phenotypic switch. Therefore, we speculated that the aberrant expression of miR-124 might play a critical role in human aortic VSMC phenotypic switch. Using quantitative RT-PCR, we found that miR-124 was dramatically downregulated in the aortic media of clinical specimens of the dissected aorta and correlated with molecular markers of the contractile VSMC phenotype. Overexpression of miR-124 by mimicking transfection significantly attenuated platelet-derived growth factor-BB-induced human aortic VSMC proliferation and phenotypic switch. Furthermore, we identified specificity protein 1 (Sp1) as the downstream target of miR-124. A luciferase reporter assay was used to confirm direct miR-124 targeting of the 3′-untranslated region of the Sp1 gene and repression of Sp1 expression in human aortic VSMCs. Furthermore, constitutively active Sp1 in miR-124-overexpressing VSMCs reversed the antiproliferative effects of miR-124. These results demonstrated a novel mechanism of miR-124 modulation of VSMC phenotypic switch by targeting Sp1 expression. NEW & NOTEWORTHY Previous studies have demonstrated that miR-124 is involved in the proliferation of a variety of cell types. However, miRNAs are expressed in a tissue-specific manner. We first identified miR-124 as a critical regulator in human aortic vascular smooth muscle cell differentiation, proliferation, and phenotype switch by targeting the 3′-untranslated region of specificity protein 1.
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Pedroza, Albert J., Yasushi Tashima, Rohan Shad, Paul Cheng, Robert Wirka, Samantha Churovich, Ken Nakamura, et al. "Single-Cell Transcriptomic Profiling of Vascular Smooth Muscle Cell Phenotype Modulation in Marfan Syndrome Aortic Aneurysm." Arteriosclerosis, Thrombosis, and Vascular Biology 40, no. 9 (September 2020): 2195–211. http://dx.doi.org/10.1161/atvbaha.120.314670.

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Objective: To delineate temporal and spatial dynamics of vascular smooth muscle cell (SMC) transcriptomic changes during aortic aneurysm development in Marfan syndrome (MFS). Approach and Results: We performed single-cell RNA sequencing to study aortic root/ascending aneurysm tissue from Fbn1 C1041G/ + (MFS) mice and healthy controls, identifying all aortic cell types. A distinct cluster of transcriptomically modulated SMCs (modSMCs) was identified in adult Fbn1 C1041G/ + mouse aortic aneurysm tissue only. Comparison with atherosclerotic aortic data (ApoE −/− mice) revealed similar patterns of SMC modulation but identified an MFS-specific gene signature, including plasminogen activator inhibitor-1 ( Serpine1 ) and Kruppel-like factor 4 ( Klf4 ). We identified 481 differentially expressed genes between modSMC and SMC subsets; functional annotation highlighted extracellular matrix modulation, collagen synthesis, adhesion, and proliferation. Pseudotime trajectory analysis of Fbn1 C1041G/ + SMC/modSMC transcriptomes identified genes activated differentially throughout the course of phenotype modulation. While modSMCs were not present in young Fbn1 C1041G/ + mouse aortas despite small aortic aneurysm, multiple early modSMCs marker genes were enriched, suggesting activation of phenotype modulation. modSMCs were not found in nondilated adult Fbn1 C1041G/ + descending thoracic aortas. Single-cell RNA sequencing from human MFS aortic root aneurysm tissue confirmed analogous SMC modulation in clinical disease. Enhanced expression of TGF-β (transforming growth factor beta)-responsive genes correlated with SMC modulation in mouse and human data sets. Conclusions: Dynamic SMC phenotype modulation promotes extracellular matrix substrate modulation and aortic aneurysm progression in MFS. We characterize the disease-specific signature of modSMCs and provide temporal, transcriptomic context to the current understanding of the role TGF-β plays in MFS aortopathy. Collectively, single-cell RNA sequencing implicates TGF-β signaling and Klf4 overexpression as potential upstream drivers of SMC modulation.
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Ferri, Nicola, Federica Panariti, Chiara Ricci, Giuseppe Maiocchi, and Alberto Corsini. "Aliskiren inhibits prorenin-induced human aortic smooth muscle cell migration." Journal of the Renin-Angiotensin-Aldosterone System 16, no. 2 (July 27, 2014): 284–91. http://dx.doi.org/10.1177/1470320314528364.

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Wiskirchen, Jakub, Helmut Dittmann, Rainer Kehlbach, Jens Vogel-Claussen, Regina Gebert, Bernhard M. Dohmen, Wolfgang Schöber, et al. "Rhenium-188 for inhibition of human aortic smooth muscle cell proliferation." International Journal of Radiation Oncology*Biology*Physics 49, no. 3 (March 2001): 809–15. http://dx.doi.org/10.1016/s0360-3016(00)01452-8.

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Huang, Hayden, Roger D. Kamm, Peter T. C. So, and Richard T. Lee. "Receptor-Based Differences in Human Aortic Smooth Muscle Cell Membrane Stiffness." Hypertension 38, no. 5 (November 2001): 1158–61. http://dx.doi.org/10.1161/hy1101.096456.

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Govatati, Suresh, Prahalathan Pichavaram, Jagadeesh Janjanam, Liang Guo, Renu Virmani, and Gadiparthi N. Rao. "Myristoylation of LMCD1 Leads to Its Species-Specific Derepression of E2F1 and NFATc1 in the Modulation of CDC6 and IL-33 Expression During Development of Vascular Lesions." Arteriosclerosis, Thrombosis, and Vascular Biology 40, no. 5 (May 2020): 1256–74. http://dx.doi.org/10.1161/atvbaha.120.314147.

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Objective: In view of our previous observations on differential expression of LMCD1 (LIM and cysteine-rich domains 1) in human versus rodents, we asked the question whether LMCD1 plays a species-specific role in the development of vascular lesions. Approach and Results: A combination of genetic, molecular, cellular, and disease models were used to test species-specific role of LMCD1 in the pathogenesis of vascular lesions. Here, we report species-specific regulation of LMCD1 expression in mediating vascular smooth muscle cell proliferation and migration during vascular wall remodeling in humans versus mice. Thrombin induced LMCD1 expression in human aortic smooth muscle cells but not mouse aortic smooth muscle cells via activation of Par1 (protease-activated receptor 1)-Gαq/11 (Gα protein q/11)-PLCβ3 (phospholipase Cβ3)-NFATc1 (nuclear factor of activated T cells 1) signaling. Furthermore, although LMCD1 mediates thrombin-induced proliferation and migration of both human aortic smooth muscle cells and mouse aortic smooth muscle cells via influencing E2F1 (E2F transcription factor 1)-mediated CDC6 (cell division cycle 6) expression and NFATc1-mediated IL (interleukin)-33 expression, respectively, in humans, it acts as an activator, and in mice, it acts as a repressor of these transcriptional factors. Interestingly, LMCD1 repressor activity was nullified by N-myristoyltransferase 2–mediated myristoylation in mouse. Besides, we found increased expression of LMCD1 in human stenotic arteries as compared to nonstenotic arteries. On the other hand, LMCD1 expression was decreased in neointimal lesions of mouse injured arteries as compared to noninjured arteries. Conclusions: Together, these observations reveal that LMCD1 acts as an activator and repressor of E2F1 and NFATc1 in humans and mice, respectively, in the induction of CDC6 and IL-33 expression during development of vascular lesions. Based on these findings, LMCD could be a potential target for drug development against restenosis and atherosclerosis in humans.
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Dissertations / Theses on the topic "Human Aortic Smooth Muscle Cell"

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Adedoyin, Oreoluwa O. "MECHANISMS OF CYCLOOXYGENASE-2-DEPENDENT HUMAN AORTIC SMOOTH MUSCLE CELL PHENOTYPIC MODULATION." UKnowledge, 2014. http://uknowledge.uky.edu/pharmacy_etds/34.

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Abdominal aortic aneurysm (AAA) is a disease of the aorta characterized by pathological remodeling and progressive weakening of the vessel resulting in the increased risk of rupture and sudden death. In a mouse model of the disease induced by chronic Angiotensin II (AngII) infusion, progression of AAAs is associated with reduced differentiation of smooth muscle cells (SMCs) at the site of lesion development. In the mouse model, the effectiveness of cyclooxygenase-2 (COX-2) inhibition for attenuating AAA progression is associated with maintenance of a differentiated SMC phenotype. However, the safety of COX-2 inhibitors is currently in question due to the increased risk of adverse cardiovascular events. Thus, it is crucial to identify mediators downstream of COX-2 that may provide new targets for treatment of this disease. Recent studies in humans and mouse models have suggested that the microsomal prostaglandin E synthase (mPGES-1) enzyme, which acts downstream of COX-2, may also be involved in the pathogenesis of the disease. We hypothesized that increased prostaglandin E2 (PGE2) synthesis resulting from the induction of both COX-2 and mPGES-1 may result in reduced differentiation of SMCs, and that disruption of this pathway would preserve the differentiated phenotype. To test this hypothesis, human aortic smooth muscle cells (hASMCs) were utilized to examine the effects of a variety of agents involved in AAA development and the COX-2 pathway. My findings suggest that one of the effects of exposing hASMCs to AngII involves a specific induction of mPGES-1 expression. Furthermore, although different COX-2-derived products may have opposing effects, mPGES-1-derived PGE2 may be the primary prostanoid synthesized by SMCs which functions to attenuate differentiation. Therefore, mPGES-1 inhibition may provide inhibition of PGE2 that is more specific than COX-2 inhibitor treatment and may serve as a therapeutic target for attenuating AAA progression by maintaining a differentiated SMC phenotype.
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MURAKAMI, Ryuichiro, Fukushi KAMBE, Hirohito MITSUYAMA, Kenji OKUMURA, Satoru NIWATA, Ryohei YAMAMOTO, and Hisao SEO. "Effect of Epidermal Growth Factor and Cyclosporin A on InterIeukin-8 Gene Expression in Human Aortic Smooth Muscle Cells." Research Institute of Environmental Medicine, Nagoya University, 2002. http://hdl.handle.net/2237/2781.

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Simmers, Phillip Charles. "Benefits of Nitric Oxide Cues to Matrix Synthesis by Healthy and Aneurysmal Human Smooth Muscle Cells within 3D Cocultures." Cleveland State University / OhioLINK, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=csu1399977973.

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Jagadesham, Vamshi Pulloori. "NK cell mediated lysis of vascular smooth muscle cells in abdominal aortic aneurysms." Thesis, University of Leeds, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.578645.

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Abdominal aortic aneurysms (AAA) are characterised by a chronic inflammatory infiltrate within the abdominal aortic wall and aortic smooth muscle cell (AoSMC) apoptosis. It is postulated that the inflammatory infiltrate causes AoSMC apoptosis, with resultant aortic wall weakening and aneurysmal degeneration. This putative immune-mediated reaction against aortic wall component suggests that AAA may have features of an auto immune disease. It has been previously demonstrated that natural killer (NK) cells are elevated in the peripheral blood (PB) of AAA patients and display increased cytotoxicity against AoSMC. This study aimed to identify the molecular basis of the increased NK cell cytotoxicity and why an immune-mediated reaction occurs against AoSMC. Using multi-parametric flow cytometry (FC), expression of the activatory receptors NKp30, NKp44, NKp46 and NKG2D were analysed on PB NK cells from AAA patients and age-sex-matched healthy controls. No difference in activatory receptor expression or cell surface density (ΔMFI) existed between the two groups. Region specific (intra-luminal blood and AAA tissue) activatory receptor phenotypes were also investigated in AAA patients. The significant finding was a reduction in the ΔMFI of NKG2D on tissue NK cells, suggesting an interaction between this receptor and potential cognate ligands within the aortic wall. Characterised AoSMC explanted from AAA tissue were subjected to analysis using qRT-PCR and FC to identify the expression of death receptors (Fas, TRAIL-RI and TRAIL R2) and NKG2D ligands (MICA, MICB, ULBPI-3). AoSMC expressed mRNA for all NKG2D ligands. FC confirmed the cell-surface expression of NKG2D ligands and the death receptors. A significantly greater percentage of NK cells from AAA patients were CD107a+ when co-cultured with AAA AoSMC, thus accounting for the increased cytotoxicity in this group. Despite using anti-NKG2D it was not possible to inhibit NK cell degranulation in response to the NKG2D ligands on AoSMC. This work has demonstrated that AoSMC from AAA express death receptors and NKG2D ligands, potentially accounting for the NK cell molecular mechanism that leads to AoSMC apoptosis. The expression of NKG2D ligands, which have been demonstrated in other auto immune diseases, favours the hypothesis that AAA are an immune-mediated process directed against the abdominal aortic wall.
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Rowe, Daniel Thomas David. "Calcium stores and human vascular smooth muscle cell proliferation." Thesis, University of Bristol, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.392964.

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Kemp, Christian R. W. "Mechanical influences on human vascular smooth muscle cell growth." Thesis, University of Leicester, 2001. http://hdl.handle.net/2381/29397.

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The leading cause of death in Western countries is cardiovascular disease with over 1 million people dying each year as a result in the United States alone. One condition identified as a risk factor for cardiovascular disease is an increased blood pressure or "hypertension" which has been shown to result in morphological changes in blood vessels at different sites around the body, including narrowing of pre-capillary "resistance" vessels. This thesis has sought to investigate whether or not this narrowing of resistance vessels might result from the increased physical forces of hypertension exerted upon the vascular smooth muscle cells of the vessel wall and to investigate the intracellular signalling mechanisms initiating this cellular response. Results indicate that cultured human vascular smooth muscle cells undergo cellular proliferation in response to chronic cyclical mechanical strain but only in the presence of suitable concentrations of soluble growth factors. Furthermore, these growth factors do not originate from the cells in response to the mechanical strain. Therefore, the proliferation is a direct response proportional to the strain applied but dependent upon the concentration of growth factors in the overlying media. In addition the magnitude of human vascular smooth muscle cell proliferation in response to mechanical strain is dependent upon interactions between the cells and specific extracellular matrix proteins and involves activation of the mitogen-activating protein kinase intracellular signalling cascade. In conclusion, these results suggest that the narrowing of resistance vessels observed in hypertension subjects may be a direct result of the increased physical forces exerted upon the vascular smooth muscle cells in conjunction with circulating growth factors. This biological response is mediated via specific cell/matrix interactions and involves specific intracellular signalling pathways, which may provide new targets for the effective treatment and/or management of these structural alterations observed in hypertension individuals.
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Refson, Jonathan Simon. "Vein graft stenosis and the human vascular smooth muscle cell." Thesis, Imperial College London, 2000. http://hdl.handle.net/10044/1/7763.

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Beattie, David Keith. "The influence of altered haemodynamics on human smooth muscle cell behaviour." Thesis, Imperial College London, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.369122.

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Sweeney, David. "Human airway smooth muscle cell Ca2+ dynamics in asthma and health." Thesis, University of Leicester, 2011. http://hdl.handle.net/2381/10130.

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The funding for this research project was kindly provided by the Medical Research Council (MRC) and the British Thoracic Society (BTS)Intracellular Ca2+ homeostasis and handling were investigated in passaged human airway smooth muscle, hASM, cells from asthma and normal donors. Temporal changes in fluorescence of Ca2+-sensitive indicator fura-2 loaded into quiescent sub-confluent hASM cells were monitored using epifluorescence video microscopy. Spontaneous amplitude changes in basal fluorescence of temporal waveforms, or Ca2+ oscillations, were measured. Also, spectral analysis using the FFT transform generated a Ca2+ oscillation dominant frequency (CODF) variable. Neither amplitude nor CODF were significantly different in asthma compared to normal hASM cell donors. However, there was a significant difference (P<0.0001) between CODF in airflow obstruction (AFO), defined as FEV1/FVC<70% and FEV1< 80%, and non-AFO donors, making CODF a strong phenotypic predictor of AFO. hASM cell Ca2+ handling was investigated by Ca2+ uncaging using confocal microscopy and by bradykinin stimulation using epifluorescence microscopy. Basal Ca2+ level, Ca2+ handling exponential decay rate constants (K), SERCA activity and expression, and SOCE after a SR Ca2+-store depletion event, all demonstrated that Ca2+ handling was not significantly different between hASM cells from asthma or normal donors. There was no correlation between FEV1 and K, however there was an emerging correlation between FEV1/FVC and K for bradykinin. The postulate that Ca2+ homeostasis and handling are intrinsically dysfunctional in hASM cells from asthma compared to normal donors is ergo not supported by these data. Caffeine was found to decrease basal Ca2+ and inhibit Ca2+ oscillations in hASM cells. Future work using freshly dispersed hASM cells is required to understand in vivo Ca2+ dynamics using the methods described in this thesis. Since CODF correlates with FEV1, pattern recognition of Ca2+ oscillation frequency spectra has the potential to help define clinical asthma phenotypes. Inevitably, a post-genomic approach to comparative protein expression in asthma and normal hASM cell donors will accelerate understanding of Ca2+ dynamics.
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Comer, Brian S. "Cyclooxygenase-2 expression in asthmatic human airway smooth muscle cells." Thesis, University of South Alabama, 2014. http://pqdtopen.proquest.com/#viewpdf?dispub=3608829.

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Asthmatic human airway smooth muscle cells (hASMCs) exhibit enhanced expression of numerous cytokine-responsive genes but this trend has not been observed for cyclooxygenase-2 (COX-2) expression despite knowledge that conserved regulatory mechanisms exist for cytokine-responsive gene expression. Enhanced expression of cytokine-responsive genes in asthmatic hASMCs has been attributed to differences in histone post-translational modifications and microRNA (miR or miRNA) expression. COX-2 expression is of interest because it serves as a model cytokine-responsive gene and is regulated by epigenetic mechanisms. In other cell types, miR-146a represses COX-2 and Interleukin (IL)-1β expression, directly and indirectly, respectively. Due to sequence homology, miR-146b is predicted to repress the expression of COX-2 and IL-1β. I investigated COX-2 expression in asthmatic and non-asthmatic hASMCS treated with cytomix (IL-1β, tumor necrosis factor (TNF)-α, and interferon (IFN)-γ). Also, I chose to compare histone acetylation, transcription factor binding, and miR-146a/b expression in asthmatic and non-asthmatic hASMCs to identify any correlations with COX-2 expression. A major goal of this project was to help identify new treatment targets for asthma therapeutics . I hypothesized that asthmatic hASMCs treated with cytomix express more COX-2 and secrete more prostaglandinE2 (PGE2) than non-asthmatic hASMCs due to differences in COX-2 epigenetic regulation. It is reported here that asthmatic hASMCs treated with cytomix expressed more COX-2 (mRNA/protein), and secreted more PGE2 than non-asthmatic hASMCs. Histone H3/H4 pan-acetylation at the COX-2 promoter did not increase with cytomix treatment and was not different in asthmatic and non-asthmatic hASMCs. Treatment of hASMCs with cytomix increased RNA Polymerase II and nuclear factor-κB binding at the COX-2 promoter with no difference between asthmatic and non-asthmatic hASMCs. Treatment of hASMCs with cytomix increased miR-146a and miR-146b expression with greater miR-146a expression in asthmatic. MiR-146a/b expression in asthmatic hASMCs treated with cytomix did not negatively correlate with COX-2 expression. These results led me to investigate whether miR-146a/b were capable of negatively regulating COX-2 and IL-1β expression in hASMCs. MiR-146a and miR-146b mimics reduced COX-2 and IL-1β mRNA/protein, and PGE2 secretion in hASMCs. MiR-146a and miR-146a/b combination inhibition increased COX-2 and pro-IL-1β protein in hASMCs but not miR-146b inhibition alone. In conclusion, elevated miR-146a expression and histone acetylation are not responsible for increased COX-2 expression in asthmatic hASMCs. MiR-146a is a minor negative regulator of COX-2 and IL-1β expression in hASMCs at physiological expression levels but mimics are capable of antagonizing cytokine-responsive gene expression profoundly. These results coupled with other evidence from the literature indicate that miR-146a/b should be investigated in animal models of asthma to determine if they are relevant asthma drug target in patients that do not respond to current anti-inflammatory therapies.

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Books on the topic "Human Aortic Smooth Muscle Cell"

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Hamel, Kenneth Carl. The role of activin in aortic smooth muscle cell growth. Ottawa: National Library of Canada, 1993.

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Lutgens, Esther, Marie-Luce Bochaton-Piallat, and Christian Weber. Atherosclerosis: cellular mechanisms. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198755777.003.0013.

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Atherosclerosis is a lipid-driven, chronic inflammatory disease of the large and middle-sized arteries that affects every human being and slowly progresses with age. The disease is characterized by the presence of atherosclerotic plaques consisting of lipids, (immune) cells, and debris that form in the arterial intima. Plaques develop at predisposed regions characterized by disturbed blood flow dynamics, such as curvatures and branch points. In the past decades, experimental and patient studies have revealed the role of the different cell-types of the innate and adaptive immune system, and of non-immune cells such as platelets, endothelial, and vascular smooth muscle cells, in its pathogenesis. This chapter highlights the roles of these individual cell types in atherogenesis and explains their modes of communication using chemokines, cytokines, and co-stimulatory molecules.
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Book chapters on the topic "Human Aortic Smooth Muscle Cell"

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Smirnov, V. N., and A. N. Orekhov. "Smooth Muscle Cells from Adult Human Aorta." In Cell Culture Techniques in Heart and Vessel Research, 271–89. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-75262-9_18.

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Gallet, Carole, Stéphanie Blaie, Sylviane Lévy-Toledano, and Aïda Habib. "Thromboxane-Induced Erk Phosphorylation in Human Aortic Smooth Muscle Cells." In Advances in Experimental Medicine and Biology, 71–73. Boston, MA: Springer US, 2003. http://dx.doi.org/10.1007/978-1-4419-9194-2_14.

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Kawaguchi, Hideaki, Noriteru Morita, Takeshi Murakami, and Kenji Iizuka. "Signal Transduction System in Human Aortic Smooth Muscle Cell Stimulated by Pure Pressure." In Signal Transduction and Cardiac Hypertrophy, 57–67. Boston, MA: Springer US, 2003. http://dx.doi.org/10.1007/978-1-4615-0347-7_5.

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Matsumoto, Kengo, Ken-ichi Hirano, Shuichi Nozaki, Makoto Nishida, Takeshi Ohya, Mohamed Janabi Yakub, Tohru Funahashi, Shizuya Yamashita, and Yuji Matsuzawa. "Expression of CD36 in Cultured Human Aortic Smooth Muscle Cells (HASMCs)." In Lipoprotein Metabolism and Atherogenesis, 272–74. Tokyo: Springer Japan, 2000. http://dx.doi.org/10.1007/978-4-431-68424-4_59.

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Martelli, Alma, Valentina Citi, and Vincenzo Calderone. "Vascular Effects of H2S-Donors: Fluorimetric Detection of H2S Generation and Ion Channel Activation in Human Aortic Smooth Muscle Cells." In Methods in Molecular Biology, 79–87. New York, NY: Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4939-9528-8_6.

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Proudfoot, Diane, and Catherine Shanahan. "Human Vascular Smooth Muscle Cell Culture." In Methods in Molecular Biology, 251–63. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61779-367-7_17.

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Ramos, Kenneth S., K. McMahon, C. Alipui, and D. Demick. "Modulation of Aortic Smooth Muscle Cell Prolifertion by Dinitrotoluene." In Advances in Experimental Medicine and Biology, 805–8. Boston, MA: Springer New York, 1991. http://dx.doi.org/10.1007/978-1-4684-5877-0_110.

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Masuda, Tsuyoshi, Kazuhiro Ohmi, Hideki Yamaguchi, Kazuhide Hasegawa, Tomoyasu Sugiyama, Yuzuru Matsuda, Masamitsu Lino, and Yoshiaki Nonomura. "Growing and differentiating characterization of aortic smooth muscle cell line, p53LMAC01 obtained from p53 knock out mice." In Muscle Physiology and Biochemistry, 99–104. Boston, MA: Springer US, 1999. http://dx.doi.org/10.1007/978-1-4615-5543-8_13.

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Kubin, Thomas, Sabina Vogel, Jutta Wetzel, Stefan Hein, Frederic Pipp, Jörg Herold, Matthias Heil, et al. "Porcine aortic endothelial cells show little effects on smooth muscle cells but are potent stimulators of cardiomyocyte growth." In Cardiac Cell Biology, 39–45. Boston, MA: Springer US, 2003. http://dx.doi.org/10.1007/978-1-4757-4712-6_6.

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Angelini, G. D., and A. C. Newby. "Smooth Muscle Cell Proliferation Responses in Organ Cultures of Human Saphenous Vein." In Coronary Artery Graft Disease, 212–27. Berlin, Heidelberg: Springer Berlin Heidelberg, 1994. http://dx.doi.org/10.1007/978-3-642-78637-2_13.

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Conference papers on the topic "Human Aortic Smooth Muscle Cell"

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Kanthou, C., C. Parker, D. E. Huber, P. Stroobant, V. V. Kakkar, N. Pringle, and W. Richardson. "PLATELET-DERIVED GROWTH FACTORA-CHAIN GENE ACTIVATION AND GROWTH FACTOR PRODUCTION BY HUMAN AORTIC SMOOTH MUSCLE CELLS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643751.

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The many contributory factors leading to the development of cardiovascular disease are currently thought to induce a common pathological change involving smooth muscle cells, which migrate from the vessel wall, proliferate,accumulate at the sites of endothelial cell damage, and then secrete connective tissue proteins and lipids which contribute to the plaque which results in the occlusion of the vessel. According to the recently modified hypothesis of Ross (1), a key event in the development of atheroma may be the abnormal release of a number of growth modulatory polypeptides,including platelet-derived growth factor (PDGF), which can potentially originate from platelets, endothelial cells, monocytes or macrophages, and smooth muscle cells themselves.We have isolated smooth muscle cell lines from 25 samples of human aorta, using digestion with collagenase and elastase. With DNA synthesis and Northern blot techniques, we examined them for both the production of PDGF-like proteins, and for the possible activation of the PDGF A-chain and B-chain genes. Severallines secreted a growth factor and were stillviable after culture for 57 days in serum-free medium. Parallel experiments using Northernblot analysis revealed the activation of the PDGF A-chain gene in all lines examined with no detectable B-chain gene transcripts.These data raise the possibility that vascular damage may activate the gene encoding the A-chain of PDGF in adjacent smooth muscle cells. Such cells might then become capable ofautonomous growth, in an analogous manner tocells transformed by Simian Sarcoma Virus, whose sis oncogene encodes the B-chain of PDGF.
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Gruber, Matthew J., Varun Krishnamurthy, D. A. Narmoneva, and Robert B. Hinton. "Elastin Haploinsufficiency Is Associated With Altered Interstitial Phenotype and Progressive Aortopathy." In ASME 2008 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2008. http://dx.doi.org/10.1115/sbc2008-192891.

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Supravalvular aortic stenosis (SVAS) [1] is a disease of the cardiovascular system that leads to narrowing of the large arteries in humans. Studies have shown [2] that SVAS is caused by mutations or deletions in the elastin gene resulting in elastin haploinsufficiency. Elastin haploinsufficiency results in systemic hypertension [3], thinner and more numerous elastic lamellae [4], and altered arterial mechanics [5]. Genetically modified elastin deficient mice (ELN+/-) recapitulates the human phenotype including obstructive arterial disease and decreased arterial compliance [1,3]. Elastin deficiency in these mice is associated with changes in the mechanical microenvironment in the vascular wall [6], including enhanced wall thickness, increased smooth muscle cell (SMC) proliferation [7] and stiffening of arteries [8]. However, the molecular mechanisms for these changes are not fully understood. Also from a developmental perspective, no information is available regarding initiation and progression of aortic pathology in ELN+/− mice with time. The objectives of this study were to determine the temporal effects of elastin haploinsufficiency on the functional properties of aortic tissue and the aortic cell phenotype, using the elastin deficient mouse model (ELN+/-). We hypothesized that elastin haploinsufficiency will result in progressive abnormalities in aortic stiffness and dynamic alterations in aortic smooth muscle cell phenotype.
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Haskett, Darren, Greg Johnson, and Jonathan Vande Geest. "Age and Location Dependent Microstructural and Biomechanical Characterization of Human Aortas." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-206676.

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The stiffening of the aorta with age is well documented in humans [1]. Collagen, elastin and smooth muscle cells are primarily responsible for the load bearing functionality of the human aorta, and it is generally accepted that imbalances in the organization of these components occur with age and in the presence of disease [2]. While a detailed account of the structural organization of the human aorta has been reported by a few investigators, none of these quantify simultaneously the organization of both collagen and elastin and how these change with age and location along the aortic tree. Additionally, none of these studies accurately assess how these changes result in corresponding alterations in the biomechanical function of the aorta.
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AlDisi, Sara, and Ali Eid. "Origanum Syriacum Inhibits Proliferation, Migration, Invasion and Induces Differentiation of Human Aortic Smooth Muscle Cells." In Qatar Foundation Annual Research Conference Proceedings. Hamad bin Khalifa University Press (HBKU Press), 2016. http://dx.doi.org/10.5339/qfarc.2016.hbsp3060.

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Tremblay, Dominique, Raymond Cartier, Louis Leduc, Rosaire Mongrain, and Richard Leask. "Circumferential Variation of Mechanical Properties of Ascending Aorta (AA): A Comparative Study of Healthy and Dilated AA." In ASME 2007 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2007. http://dx.doi.org/10.1115/sbc2007-176709.

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The biomechanics within the ascending aorta (AA) characterizes the pressure and flow for the entire vascular system. In the aortic wall, it is the structured medial layer that is responsible for the mechanical properties of the AA. The mechanical properties are determined to a large extent by the composition of elastin, collagen and smooth muscle cells (SMCs). Changes in AA biomechanics that arise with age and/or disease can lead to cardiovascular complications and death. Most studies that have investigated the biomechanics of these diseases have assumed homogeneous and isotropic aortic wall properties. Very little work has been done in vitro to determine the local mechanical properties of human vascular tissue. In order to better understand the biomechanics of the human AA, the local properties of pathologic AA tissue from both tricuspid and bicuspid aortic valve patients have been studied and compared with the properties of healthy aortas.
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Elgenaidi, Ismail, and J. Paul Spiers. "5 HIF-1α dependent and independent regulation of PP2A in human aortic smooth muscle cells under hypoxia." In The Scottish Cardiovascular Forum 2018, 3rd February 2018, Trinity Biomedical Science Institute, Trinity College Dublin Ireland. BMJ Publishing Group Ltd and British Cardiovascular Society, 2018. http://dx.doi.org/10.1136/heartjnl-2018-scf.5.

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Ferdous, Zannatul, Hanjoong Jo, and Robert M. Nerem. "Differential Osteogenic Marker Expression by Human Vascular and Valvular Cells in Tissue-Engineered Collagen Constructs." In ASME 2010 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2010. http://dx.doi.org/10.1115/sbc2010-19424.

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Atherosclerosis and aortic stenosis are two of the most prevalent cardiovascular disorders and a major cause of death in elderly population. In atherosclerosis, plaques and calcium deposits build up inside major arteries, which lead to narrowing of the vessel lumens and limits or completely blocks blood flow. Similarly, in calcific aortic stenosis, calcium deposits on valve cusps and valve ring result in narrowing of valve lumen, eventually leading to impaired function and even valve failure. As the disease progresses, both diseases thus require expensive replacement/repair surgeries in most patients. However, in spite of the high prevalence, the causes and mechanisms of these diseases are still not clearly understood. Due to the similarities in diseased tissue pathology, atherosclerosis and aortic stenosis have been suggested to be continuum of the same disease [1] and mainly have been investigated for atherosclerosis. However, the prevalence of both diseases is not concurrent in most patients. Likewise, valvular interstitial cells (VICs) were thought to behave in a similar manner as smooth muscle cells (SMCs), but some recent studies suggest differences between the two cell types [2]. Therefore, unique mechanisms might be involved in how VICs and SMCs respond to an osteogenic environment.
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Du, Wei, Kenneth M. Pryse, Judy A. Fee, Elliot L. Elson, and Ruth J. Okamoto. "Vascular Smooth Muscle Cell Mechanics During Cyclic Stretch: Effect of Serum and a Serum Substitute." In ASME 2007 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2007. http://dx.doi.org/10.1115/sbc2007-176205.

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Remodeling of arteries in response to altered loads is an area of intense interest to cardio-vascular clinicians and researchers. In humans, changes due to cardiovascular diseases (e.g. aortic dilatation) may occur slowly over many years, and mathematical models that describe the remodeling response are needed for predicting the course, and possible treatment, of these diseases. Recently, Humphrey and co-workers have proposed constrained mixture models [1] that consider local stresses in the arterial wall to be the sum of contributions from collagen, elastic fibers, and vascular smooth muscle cells (VSMCs). While numerous studies (e.g., [2]) have considered the active response of VSMCs in large arteries under quasi-static conditions, little is known about the mechanical response of VSMCs to continuous cyclic stretch. We have chosen 3-D bio-artificial tissue constructs as a model system in which to study the response of VSMCs to continuous cyclic stretch. However, VSMCs undergo a shift from a contractile phenotype to a de-differentiated phenotype during culture [3]. Some investigators have suggested that serum deprivation can induce re-differentiation toward a more contractile phenotype [4, 5]. The goal of our study was to compare the effect of incubation conditions on the active responses of VSMCs in 3-D tissue constructs to continuous cyclic stretch.
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Whitton, Andrew, David J. Flint, and Richard A. Black. "Development of a Compliant Electrospun Polyurethane Vascular Graft." In ASME 2010 5th Frontiers in Biomedical Devices Conference. American Society of Mechanical Engineers, 2010. http://dx.doi.org/10.1115/biomed2010-32070.

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Synthetic vascular grafts are an integral tool in vascular surgery. However, the consistent failure of small diameter grafts is one of the main limitations of these devices. For this reason electrospun polyurethane has been investigated for its suitability as a vascular substitute material in this present study. Aligned and random mesh electrospun polyurethane materials were produced and analysed in vitro by investigating the effect of using both materials as a substrate for the culture of human aortic smooth muscle cells. Immunofluorescence analysis showed that cells cultured on electrospun polyurethane maintained a contractile phenotype to a much greater extent than those cultured on cast polyurethane membranes. This contractile phenotype is associated with the state in which a cell would normally reside in a healthy vessel, suggesting that electrospun polyurethane may provide a suitable vascular substitute material.
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Ferruzzi, J., M. S. Enevoldsen, and J. D. Humphrey. "On the Mechanical Behavior of Healthy and Aneurysmal Abdominal Aorta." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53852.

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Abdominal aortic aneurysm (AAA) is a pathological condition of the infrarenal aorta characterized by a local dilatation of the arterial wall. The main histopathologic features of an AAA are smooth muscle cell death and loss of elastin. The biomechanical behavior of AAAs has been widely studied to determine the rupture potential according to the principles of material failure. However, most prior approaches are limited by the use of data from uniaxial tensile testing and by the assumption of material isotropy, leading to inaccurate characterization of the 3D multiaxial mechanical response of the aneurysmal tissue. To date, the best data available on the behavior of human abdominal aorta (AA) and AAA to planar biaxial testing are the ones reported by Vande Geest et al. [1,2]. In a recent work [3], we considered a structurally motivated four-fiber family strain energy function (SEF) [4] to capture the biaxial behavior of the human AA and AAA from Vande Geest et al. [1,2]. We showed that this constitutive relation fits human data better than prior models and most importantly it captures the stiffening of the arterial wall related to both aging and aneurysmal development. These changes in mechanical behavior are mirrored by changes in the best-fit values of the parameters, with a progressive decrease of the isotropic part attributed to elastin and a parallel increase in values associated with the families of collagen fibers.
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