Journal articles: 'Renal tissue regeneration'

1

Tsuji, Kenji, and Shinji Kitamura. "Trophic Factors from Tissue Stem Cells for Renal Regeneration." Stem Cells International 2015 (2015): 1–7. http://dx.doi.org/10.1155/2015/537204.

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Stem cell therapies against renal injury have been advancing. The many trials for renal regeneration are reported to be effective in many kinds of renal injury models. Regarding the therapeutic mechanism, it is believed that stem cells contribute to make regeneration via not only direct stem cell differentiation in the injured space but also indirect effect via secreted factors from stem cells. Direct differentiation from stem cells to renal composed cells has been reported. They differentiate to renal composed cells and make functions. However, regarding renal regeneration, stem cells are discussed to secrete many kinds of growth factors, cytokines, and chemokines in paracrine or autocrine manner, which protect against renal injury, too. In addition, it is reported that stem cells have the ability to communicate with nearby cells via microvesicle-related RNA and proteins. Taken together from many reports, many secreted factors from stem cells were needed for renal regeneration orchestrally with harmony. In this review, we focused on the effects and insights of stem cells and regenerative factors from stem cells.

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Yokote, Shinya, Shuichiro Yamanaka, and Takashi Yokoo. "De NovoKidney Regeneration with Stem Cells." Journal of Biomedicine and Biotechnology 2012 (2012): 1–10. http://dx.doi.org/10.1155/2012/453519.

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Recent studies have reported on techniques to mobilize and activate endogenous stem-cells in injured kidneys or to introduce exogenous stem cells for tissue repair. Despite many recent advantages in renal regenerative therapy, chronic kidney disease (CKD) remains a major cause of morbidity and mortality and the number of CKD patients has been increasing. When the sophisticated structure of the kidneys is totally disrupted by end stage renal disease (ESRD), traditional stem cell-based therapy is unable to completely regenerate the damaged tissue. This suggests that whole organ regeneration may be a promising therapeutic approach to alleviate patients with uncured CKD. We summarize here the potential of stem-cell-based therapy for injured tissue repair andde novowhole kidney regeneration. In addition, we describe the hurdles that must be overcome and possible applications of this approach in kidney regeneration.

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Little, Melissa H., Alexander N. Combes, and Minoru Takasato. "Understanding kidney morphogenesis to guide renal tissue regeneration." Nature Reviews Nephrology 12, no. 10 (August 30, 2016): 624–35. http://dx.doi.org/10.1038/nrneph.2016.126.

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Bruno, Stefania, Stefano Porta, and Benedetta Bussolati. "Extracellular vesicles in renal tissue damage and regeneration." European Journal of Pharmacology 790 (November 2016): 83–91. http://dx.doi.org/10.1016/j.ejphar.2016.06.058.

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Salama, Samir A., Hany H. Arab, and Ibrahim A. Maghrabi. "Troxerutin down-regulates KIM-1, modulates p38 MAPK signaling, and enhances renal regenerative capacity in a rat model of gentamycin-induced acute kidney injury." Food & Function 9, no. 12 (2018): 6632–42. http://dx.doi.org/10.1039/c8fo01086b.

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Piron, Annie, Isabelle Leonard, Denis Nonclercq, Gerard Toubeau, Paul Falmagne, Jeanine-Anne Heuson-Stiennon, and Guy Laurent. "In vitro demonstration of a mitogenic activity in renal tissue extracts during regenerative hyperplasia." American Journal of Physiology-Renal Physiology 274, no. 2 (February 1, 1998): F348—F357. http://dx.doi.org/10.1152/ajprenal.1998.274.2.f348.

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Normal rat kidney (NRK-52E) cells, an established cell line of renal origin, were used as a bioassay system to reveal a possible mitogenic activity in tissue extracts prepared from kidneys undergoing tubular regeneration. Acute tubular injury was induced in female Wistar rats by a 4-day treatment with gentamicin at daily doses of 50 or 100 mg/kg twice daily. Animals were killed either 1 or 4 days after cessation of gentamicin administration. Proximal tubule regeneration in treated animals was confirmed by morphological examination after proliferating cell nuclear antigen staining. Tissue extracts from regenerating kidneys stimulated DNA synthesis in growth-arrested cells to a higher extent than extracts from intact kidneys. Sera from treated and control animals showed no difference with respect to mitogenic activity. The mitogenic effect of tissue extracts was sensitive to the tyrosine kinase inhibitor tyrphostin A46. The cell proliferative response to regenerating kidney extracts, but not that to intact kidney extracts, was partly suppressed by the addition of anti-insulin-like growth factor I (anti-IGF-I) antiserum. These data indicate that nephrogenic repair entails an elevation of biologically active IGF-I in kidney tissue.

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Bussolati, Benedetta, Akito Maeshima, Janos Peti-Peterdi, Takashi Yokoo, and Laura Lasagni. "Renal Stem Cells, Tissue Regeneration, and Stem Cell Therapies for Renal Diseases." Stem Cells International 2015 (2015): 1–2. http://dx.doi.org/10.1155/2015/302792.

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Lee, Sang Jin, Hung-Jen Wang, Tae-Hyoung Kim, Jin San Choi, Gauri Kulkarni, John D. Jackson, Anthony Atala, and James J. Yoo. "In Situ Tissue Regeneration of Renal Tissue Induced by Collagen Hydrogel Injection." STEM CELLS Translational Medicine 7, no. 2 (January 29, 2018): 241–50. http://dx.doi.org/10.1002/sctm.16-0361.

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Cho, Y. S., H. C. Moon, C. Y. Choi, S. S. Kim, B. S. Kim, J. H. Han, K. J. Joo, C. H. Kwon, and H. J. Park. "32 Renal tissue regeneration using cellular transplantation in rats." European Urology Supplements 3, no. 2 (February 2004): 10. http://dx.doi.org/10.1016/s1569-9056(04)90034-6.

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Cho, Young Sam, Hong Chul Moon, Sang Su Kim, Cha Yang Choi, Byung Su Kim, Jeong Ho Han, Kwan lung Joo, Chil Hun Kwon, and Heung Jae Park. "1842: Renal Tissue Regeneration Using Cellular Transplantation in Rats." Journal of Urology 171, no. 4S (April 2004): 487. http://dx.doi.org/10.1016/s0022-5347(18)39034-7.

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Kamil, Amal. "Eruca sativa and Raphanus sativus oils Enhance Hepatic and Renal Tissues Regeneration in White Mice." Al-Mustansiriyah Journal of Science 29, no. 4 (May 6, 2019): 27. http://dx.doi.org/10.23851/mjs.v29i4.404.

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Regeneration is a process of tissue repairing in the body, and according to this process the cells of the body are divided into three types; labile, stable and permanent cells. Objectives: The aims of this study are to evaluate the ability of two herbal seed oils (Eruca sativa and Raphanus sativus) to enhance regeneration and repair in the liver and kidney in the irradiated mice. And to investigate which herbal oil is more effective. Method: Four groups of mice were used in this study. The first three groups were exposed to radiation while the fourth was used as a control. After irradiation the first and second groups were treated with local Eruca sativa and Raphanus sativus oils respectively. While the third group used as a control. Then histopathological investigation was done. Results: Histopathological examination in irradiated groups exhibited that both seed oils could induce regeneration in both hepatic and renal tissues but the activity of Raphanus sativus oil was more effective than Eruca sativa especially in renal tissue. Meanwhile, poor regeneration process appeared in the third group (control). Conclusion: Both local herbal oils had ability to enhance regeneration in the examined tissues but R. sativus seed oil exerted more activity than E. sativa seed oil.

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Tsuji, Kenji, Shinji Kitamura, and Jun Wada. "Secretomes from Mesenchymal Stem Cells against Acute Kidney Injury: Possible Heterogeneity." Stem Cells International 2018 (December 16, 2018): 1–14. http://dx.doi.org/10.1155/2018/8693137.

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A kidney has the ability to regenerate itself after a variety of renal injuries. Mesenchymal stem cells (MSCs) have been shown to ameliorate tissue damages during renal injuries and diseases. The regenerations induced by MSCs are primarily mediated by the paracrine release of soluble factors and extracellular vesicles, including exosomes and microvesicles. Extracellular vesicles contain proteins, microRNAs, and mRNAs that are transferred into recipient cells to induce several repair signaling pathways. Over the past few decades, many studies identified trophic factors from MSCs, which attenuate renal injury in a variety of animal acute kidney injury models, including renal ischemia-reperfusion injury and drug-induced renal injury, using microarray and proteomic analysis. Nevertheless, these studies have revealed the heterogeneity of trophic factors from MSCs that depend on the cell origins and different stimuli including hypoxia, inflammatory stimuli, and aging. In this review article, we summarize the secretomes and regenerative mechanisms induced by MSCs and highlight the possible heterogeneity of trophic factors from different types of MSC and different circumstances for renal regeneration.

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Sokolova, I. B., and G. T. Ivanova. "5/6 nephrectomy: renal tissue regeneration and condition of brain microcirculation." Nephrology (Saint-Petersburg) 24, no. 4 (June 26, 2020): 87–92. http://dx.doi.org/10.36485/1561-6274-2020-24-4-87-92.

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THE AIM. To find out if the level of regeneration of renal tissue after nephrectomy 5/6 kidney mass is sufficient to prevent pathological deterioration of microcirculation in the cerebral cortex. MATERIAL AND METHODS. The method of intravital microscopy was used to study the density of the microvascular network of the pial sheath of the cerebral cortex in Wistar rats 4 months after the removal of 5/6 of the renal tissue mass. At the same time, the level of perfusion and oxygen saturation (SO2) were measured in the cortical tissue using laser Doppler flowmetry. To assess the degree of kidney regeneration after resection, a morphological study of kidney tissue was carried out when staining with hematoxylin-eosin and Masson. RESULTS. It was shown that 4 months after nephrectomy in the pial membrane, the density of the microvascular network decreased by an average of 1.3 times compared with falsely operated animals, and the number of arterial vessels by 1.5 times. The level of tissue perfusion (on average by 20%) and SO2 (on average from 95 to 91%) decreased statistically significantly. On morphological preparations, there were no signs of true regeneration; revealed glomerular hypertrophy, the development of fibrosis, deformation of blood vessels, and tubular structures. CONCLUSION. Renal regeneration 4 months after nephrectomy 5/6 kidney mass is insufficient to normalize its function, and therefore does not prevent the cerebrovascular accident. Significant microcirculation disorders are observed in rat cerebral cortex: a decrease in the density of the microvascular network, a decrease in the rate of cerebral blood flow and tissue oxygen saturation, which are signs of the formation of lacunar strokes.

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Okumura, Noriko, Takafumi Yoshikawa, Akitaka Nonomura, and Yoshinori Takakura. "Organ Regeneration in Porous Hydoroxyapatite." Key Engineering Materials 309-311 (May 2006): 1017–22. http://dx.doi.org/10.4028/www.scientific.net/kem.309-311.1017.

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HA has a high affinity for bone as well as various tissues. In the present study, we investigated an affinity for abdominal organs. Coralline hydroxyapatite ceramic (HA, cubic structure 4x4x4mm, Interpore 500) was used in this experiment. We made two incisions in the lower back of a 5-week-old male nude mouse, and implanted HA blocks. One was placed around the liver at the right side and another one was placed around the kidney at the left side. The organ fibrous capsule was not removed. At 6 weeks after implantation, mice were sacrificed under overanesthesia and HA blocks were retrieved and prepared for histological analysis. In the HE stain of HA blocks around liver, liver tissue is invaded into the HA pore areas. Hepatocyte proliferation in trabecular pattern was seen in contact with the surfaces of many HA pores. Within some pores, hepatic lobular pattern, Glisson sheath or central vein could be detected. In the HA around kidney, renal tissue was observed in many pores. The pore areas of HA were fullfilled with grumerulus and urinary tube tissues. In contact with the surfaces of some HA blocks, the tissue invasion of pancreas and spleen tissue were recognized. These results indicate that porous HA has a high affinity for the celiac organs, and has a stimulatory effect on celiac organ regeneration. Especially, concerning the regeneration of kidney, it has not been reported yet, so this report is very interesting. HA is also very useful as a scaffold of the organ regeneration.

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Jamadar, Abeda, and Reena Rao. "Glycogen Synthase Kinase-3 Signaling in Acute Kidney Injury." Nephron 144, no. 12 (2020): 609–12. http://dx.doi.org/10.1159/000509354.

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Acute kidney injury (AKI) is a common clinical syndrome that involves renal tubular epithelial cell death and leads to acute decline in renal function. Improper tubular regeneration following AKI often leads to CKD. We discuss the role of a serine/threonine protein kinase called glycogen synthase kinase-3 (GSK3) in renal tubular injury and renal fibrosis. We also highlight the importance of GSK3 as a potential drug target in AKI patients and molecular mechanisms promoting tissue regeneration.

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Gobé, Glenda C., Ralph Buttyan, Kate R. L. Wyburn, Maria R. Etheridge, and Peter J. Smith. "Clusterin expression and apoptosis in tissue remodeling associated with renal regeneration." Kidney International 47, no. 2 (February 1995): 411–20. http://dx.doi.org/10.1038/ki.1995.54.

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17

Kramer, J., J. Steinhhoff, L. Fricke, and J. Rohwedel. "ES CELL-DERIVED RENAL CELL TYPES: A TOOL FOR TISSUE REGENERATION?" Transplantation 78 (July 2004): 594. http://dx.doi.org/10.1097/00007890-200407271-01600.

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18

Kim, Yun Ah, So Young Chun, Sung-Bin Park, Eunyoung Kang, Won-Gun Koh, Tae Gyun Kwon, Dong Keun Han, and Yoon Ki Joung. "Scaffold-supported extracellular matrices preserved by magnesium hydroxide nanoparticles for renal tissue regeneration." Biomaterials Science 8, no. 19 (2020): 5427–40. http://dx.doi.org/10.1039/d0bm00871k.

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Fibroblast-derived extracellular matrix-supported scaffolds made up of PLGA were prepared with the enhanced preservation of ECM components by composites with magnesium hydroxide nanoparticles, and were applied for renal tissue regeneration.

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Ratliff, B. B., T. Ghaly, P. Brudnicki, K. Yasuda, M. Rajdev, M. Bank, J. Mares, A. K. Hatzopoulos, and M. S. Goligorsky. "Endothelial progenitors encapsulated in bioartificial niches are insulated from systemic cytotoxicity and are angiogenesis competent." American Journal of Physiology-Renal Physiology 299, no. 1 (July 2010): F178—F186. http://dx.doi.org/10.1152/ajprenal.00102.2010.

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Intrinsic stem cells (SC) participate in tissue remodeling and regeneration in various diseases and following toxic insults. Failure of tissue regeneration is in part attributed to lack of SC protection from toxic stress of noxious stimuli, thus prompting intense research efforts to develop strategies for SC protection and functional preservation for in vivo delivery. One strategy is creation of artificial SC niches in an attempt to mimic the requirements of endogenous SC niches by generating scaffolds with properties of extracellular matrix. Here, we investigated the use of hyaluronic acid (HA) hydrogels as an artificial SC niche and examined regenerative capabilities of encapsulated embryonic endothelial progenitor cells (eEPC) in three different in vivo models. Hydrogel-encapsulated eEPC demonstrated improved resistance to toxic insult (adriamycin) in vitro, thus prompting in vivo studies. Implantation of HA hydrogels containing eEPC to mice with adriamycin nephropathy or renal ischemia resulted in eEPC mobilization to injured kidneys (and to a lesser extent to the spleen) and improvement of renal function, which was equal or superior to adoptively transferred EPC by intravenous infusion. In mice with hindlimb ischemia, EPC encapsulated in HA hydrogels dramatically accelerated the recovery of collateral circulation with the efficacy superior to intravenous infusion of EPC. In conclusion, HA hydrogels protect eEPC against adriamycin cytotoxicity and implantation of eEPC encapsulated in HA hydrogels supports renal regeneration in ischemic and cytotoxic (adriamycin) nephropathy and neovascularization of ischemic hindlimb, thus establishing their functional competence and superior capabilities to deliver stem cells stored in and released from this bioartificial niche.

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Black, Laurence M., Jeremie M. Lever, and Anupam Agarwal. "Renal Inflammation and Fibrosis: A Double-edged Sword." Journal of Histochemistry & Cytochemistry 67, no. 9 (May 22, 2019): 663–81. http://dx.doi.org/10.1369/0022155419852932.

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Renal tissue injury initiates inflammatory and fibrotic processes that occur to promote regeneration and repair. After renal injury, damaged tissue releases cytokines and chemokines, which stimulate activation and infiltration of inflammatory cells to the kidney. Normal tissue repair processes occur simultaneously with activation of myofibroblasts, collagen deposition, and wound healing responses; however, prolonged activation of pro-inflammatory and pro-fibrotic cell types causes excess extracellular matrix deposition. This review focuses on the physiological and pathophysiological roles of specialized cell types, cytokines/chemokines, and growth factors, and their implications in recovery or exacerbation of acute kidney injury.

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Tajima, Kazuki, Kohei Kuroda, Yuya Otaka, Rie Kinoshita, Mizuki Kita, Toshifumi Oyamada, and Kazutaka Kanai. "Decellularization of canine kidney for three-dimensional organ regeneration." Veterinary World 13, no. 3 (2020): 452–57. http://dx.doi.org/10.14202/vetworld.2020.452-457.

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Background and Aim: Kidney regeneration is required for dogs with end-stage renal failure. Decellularization is one of the bioengineering techniques, which involves the removal of all tissue cells and cellular components and conservation of the extracellular matrix (ECM). Studies in rats have shown that decellularized kidney has regenerative potential; however, there are no reports on renal decellularization in dogs. Here, we showed the decellularization of the canine kidney. Materials and Methods: The renal artery of the cadaveric canine kidney was cannulated and the whole kidney was frozen at –80°C. After completely thawing, it was perfused with physiological saline and sodium dodecyl sulfate (0.5%, 6 h) through the cannulated renal artery to achieve decellularization. To assess the efficiency of the decellularization protocol, histological and immunohistochemical analysis of decellularized kidney was performed. Results: The results of hematoxylin and eosin (H and E) staining revealed that the decellularized canine kidney had no apparent cellular components. In addition, 4’,6-diamidino-2-phenylindole (DAPI) staining showed no visible nuclear components within the whole decellularized kidney. Therefore, both H and E and DAPI staining showed decellularization of the canine kidney. Our decellularization protocol also preserved the basement membrane of glomerulus, shown by periodic acid methenamine silver, periodic acid–Schiff, fibronectin, and collagen type IV stain. Conclusion: Our decellularization protocol could eliminate cellular components and remaining native ECM structures of canine kidney. These results could promote further research into canine kidney regeneration, which may be the first small step to regenerate the canine kidney waiting for renal transplantation.

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Gupta, Sandeep, Shunan Li, Md J. Abedin, Lawrence Wang, Eric Schneider, Behzad Najafian, and Mark Rosenberg. "Effect of Notch activation on the regenerative response to acute renal failure." American Journal of Physiology-Renal Physiology 298, no. 1 (January 2010): F209—F215. http://dx.doi.org/10.1152/ajprenal.00451.2009.

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Episodes of acute renal failure (ARF) are not always fully reversible and may lead to chronic disease, due in part to an inadequate regenerative response. The Notch signaling pathway is involved in determining cell fate during development, and tissue maintenance and repair in adult organs. The purpose of this study was to examine the role of the Notch pathway in renal regeneration following ARF. Kidney injury, induced by ischemia-reperfusion, resulted in early activation of the Notch pathway, as evidenced by increased expression of Notch1 and Notch2 intracellular domain (cleaved Notch). The effect of exogenous administration of the Notch ligand Delta-like-4 (DLL4) on recovery from ARF was then studied. Rats were pretreated by intraperitoneal injection of DLL4 or vehicle control. Two days following the last DLL4 dose, ARF was induced by bilateral renal artery clamping for 45 min followed by reperfusion. The severity of renal injury was similar in DLL4 and control rats. Renal recovery was facilitated by DLL4 treatment, as evidenced by faster return of serum creatinine to baseline by 48 h in DLL4-treated rats as against 5 days in vehicle-treated control rats. Cell proliferation was higher in the DLL4-treated group. In conclusion, activation of the Notch pathway occurs following ARF. Pretreatment with the Notch ligand DLL4 enhanced recovery from ARF and represents a potential novel therapeutic option for regenerating the injured kidney.

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Andrianova, Nadezda V., Marina I. Buyan, Ljubava D. Zorova, Irina B. Pevzner, Vasily A. Popkov, Valentina A. Babenko, Denis N. Silachev, Egor Y. Plotnikov, and Dmitry B. Zorov. "Kidney Cells Regeneration: Dedifferentiation of Tubular Epithelium, Resident Stem Cells and Possible Niches for Renal Progenitors." International Journal of Molecular Sciences 20, no. 24 (December 15, 2019): 6326. http://dx.doi.org/10.3390/ijms20246326.

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A kidney is an organ with relatively low basal cellular regenerative potential. However, renal cells have a pronounced ability to proliferate after injury, which undermines that the kidney cells are able to regenerate under induced conditions. The majority of studies explain yielded regeneration either by the dedifferentiation of the mature tubular epithelium or by the presence of a resident pool of progenitor cells in the kidney tissue. Whether cells responsible for the regeneration of the kidney initially have progenitor properties or if they obtain a “progenitor phenotype” during dedifferentiation after an injury, still stays the open question. The major stumbling block in resolving the issue is the lack of specific methods for distinguishing between dedifferentiated cells and resident progenitor cells. Transgenic animals, single-cell transcriptomics, and other recent approaches could be powerful tools to solve this problem. This review examines the main mechanisms of kidney regeneration: dedifferentiation of epithelial cells and activation of progenitor cells with special attention to potential niches of kidney progenitor cells. We attempted to give a detailed description of the most controversial topics in this field and ways to resolve these issues.

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Ahn, H. S., S. S. Kim, C. Y. Choi, J. H. Han, M. H. Park, K. W. Song, Y. S. Kim, et al. "REGENERATION OF KIDNEY TISSUE THROUGH THE TRANSPLANTATION OF EMBRYONIC RENAL CELL IN RAT." European Urology Supplements 5, no. 2 (April 2006): 210. http://dx.doi.org/10.1016/s1569-9056(06)60758-6.

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Margreiter, R., Š. Vitko, J. Whelchel, J. C. Magee, H. Tedesco, J. Eris, J. Pascual, B. Kahan, Z. Wang, and H. Sollinger. "POST-OPERATIVE TISSUE REGENERATION IN RENAL TRANSPLANTATION: COMPARABLE OUTCOME WITH EVEROLIMUS OR MMF." Transplantation 86, Supplement (July 2008): 188. http://dx.doi.org/10.1097/01.tp.0000332215.21482.27.

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Serban, Monica A., Toyin Knight, Richard G. Payne, Joydeep Basu, Elias A. Rivera, Neil Robbins, Darell McCoy, Craig Halberstadt, Deepak Jain, and Timothy A. Bertram. "Cross-linked gelatin microspheres with continuously tunable degradation profiles for renal tissue regeneration." Biotechnology and Applied Biochemistry 61, no. 2 (October 22, 2013): 75–81. http://dx.doi.org/10.1002/bab.1125.

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27

Basile, D. P., J. M. Rovak, D. R. Martin, and M. R. Hammerman. "Increased transforming growth factor-beta 1 expression in regenerating rat renal tubules following ischemic injury." American Journal of Physiology-Renal Physiology 270, no. 3 (March 1, 1996): F500—F509. http://dx.doi.org/10.1152/ajprenal.1996.270.3.f500.

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To gain insight into the role that transforming growth factor-beta 1 (TGF-beta 1) plays in the regeneration of kidneys following acute renal failure, we characterized the expression of TGF-beta 1 mRNA and the expression of active and latent TGF-beta peptide at various times during recovery from acute ischemic injury in rat. Levels of whole kidney TGF-beta 1 mRNA were elevated significantly at 12 h postinjury (1.5-fold vs. sham-operated controls), and by 24 h postinjury were elevated by 3.6-fold. Levels remained elevated for 14 days following ischemia, but were no longer elevated at 28 days postinjury. In situ hybridization demonstrated that the elevated expression of TGF-beta 1 was localized predominantly to cells in the regenerating tubules in the outer medulla. When examined at 14 days postischemia, levels of TGF-beta 1 mRNA were elevated in the outer medulla only in tubules that appeared incompletely regenerated. Immunohistochemical staining localized active TGF-beta to the lumen of proximal tubules in control animals and in desquamated and regenerating tubular epithelial cells following ischemia. TGF-beta 1 latency-associated peptide was present intracellularly in proximal tubules of sham-operated rats and reduced following ischemia. We hypothesize that endogenous renal TGF-beta serves to promote tissue regeneration following acute injury via an autocrine or paracrine mechanism.

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Curtis, Lisa M., Sifeng Chen, Bo Chen, Anupam Agarwal, Christopher A. Klug, and Paul W. Sanders. "Contribution of intrarenal cells to cellular repair after acute kidney injury: subcapsular implantation technique." American Journal of Physiology-Renal Physiology 295, no. 1 (July 2008): F310—F314. http://dx.doi.org/10.1152/ajprenal.90205.2008.

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The kidney is capable of regeneration following injury, particularly following acute insults. Although the mechanisms underlying cellular regeneration are incompletely understood, emerging evidence suggests a role for cells of renal origin in the repair and replacement of damaged renal tubule cells. The overall hypothesis of this study is that native kidney cells that reside in a niche in the kidney provide robust contribution to the repair of kidney tubules following injury. To test this hypothesis, we utilized a model of renal ischemia-reperfusion injury that results in extensive morphological changes, particularly in the outer medulla. Renal tissue obtained from mice constitutively expressing Escherichia coli β-galactosidase (ROSA26) was dissected from the cortex, outer medulla, or papilla and implanted under the renal capsule of the injured mice. Mice were allowed to recover for 7 days. Sections through the injured kidney demonstrated the presence of implant-derived cells in renal tubules in the outer medulla. The implanted renal region that exhibited the most robust response was the papilla, whereas tissue pieces from the cortex and outer medulla showed less contribution to recipient renal tubules. These results provide proof-of-principle evidence that renal-derived reparative cells reside in all regions of the kidney, perhaps more predominantly in the renal papilla. A greater understanding of the cell biology of renal repair by native kidney cells will provide further insight into the design of novel therapies in acute kidney injury, and the subcapsular implant technique described in this study may offer unique advantages to evaluate renal repair mechanisms.

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Kelley, Rusty, Eric S. Werdin, Andrew T. Bruce, Sumana Choudhury, Shay M. Wallace, Roger M. Ilagan, Bryan R. Cox, et al. "Tubular cell-enriched subpopulation of primary renal cells improves survival and augments kidney function in rodent model of chronic kidney disease." American Journal of Physiology-Renal Physiology 299, no. 5 (November 2010): F1026—F1039. http://dx.doi.org/10.1152/ajprenal.00221.2010.

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Established chronic kidney disease (CKD) may be identified by severely impaired renal filtration that ultimately leads to the need for dialysis or kidney transplant. Dialysis addresses only some of the sequelae of CKD, and a significant gap persists between patients needing transplant and available organs, providing impetus for development of new CKD treatment modalities. Some postulate that CKD develops from a progressive imbalance between tissue damage and the kidney's intrinsic repair and regeneration processes. In this study we evaluated the effect of kidney cells, delivered orthotopically by intraparenchymal injection to rodents 4–7 wk after CKD was established by two-step 5/6 renal mass reduction (NX), on the regeneration of kidney function and architecture as assessed by physiological, tissue, and molecular markers. A proof of concept for the model, cell delivery, and systemic effect was demonstrated with a heterogeneous population of renal cells (UNFX) that contained cells from all major compartments of the kidney. Tubular cells are known contributors to kidney regeneration in situ following acute injury. Initially tested as a control, a tubular cell-enriched subpopulation of UNFX (B2) surprisingly outperformed UNFX. Two independent studies (3 and 6 mo in duration) with B2 confirmed that B2 significantly extended survival and improved renal filtration (serum creatinine and blood urea nitrogen). The specificity of B2 effects was verified by direct comparison to cell-free vehicle controls and an equivalent dose of non-B2 cells. Quantitative histological evaluation of kidneys at 6 mo after treatment confirmed that B2 treatment reduced severity of kidney tissue pathology. Treatment-associated reduction of transforming growth factor (TGF)-β1, plasminogen activator inhibitor (PAI)-1, and fibronectin (FN) provided evidence that B2 cells attenuated canonical pathways of profibrotic extracellular matrix production.

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Eftekhari, Aziz, Solmaz Maleki Dizaj, Elham Ahmadian, Agata Przekora, Seyed Mahdi Hosseiniyan Khatibi, Mohammadreza Ardalan, Sepideh Zununi Vahed, et al. "Application of Advanced Nanomaterials for Kidney Failure Treatment and Regeneration." Materials 14, no. 11 (May 29, 2021): 2939. http://dx.doi.org/10.3390/ma14112939.

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The implementation of nanomedicine not only provides enhanced drug solubility and reduced off-target adverse effects, but also offers novel theranostic approaches in clinical practice. The increasing number of studies on the application of nanomaterials in kidney therapies has provided hope in a more efficient strategy for the treatment of renal diseases. The combination of biotechnology, material science and nanotechnology has rapidly gained momentum in the realm of therapeutic medicine. The establishment of the bedrock of this emerging field has been initiated and an exponential progress is observed which might significantly improve the quality of human life. In this context, several approaches based on nanomaterials have been applied in the treatment and regeneration of renal tissue. The presented review article in detail describes novel strategies for renal failure treatment with the use of various nanomaterials (including carbon nanotubes, nanofibrous membranes), mesenchymal stem cells-derived nanovesicles, and nanomaterial-based adsorbents and membranes that are used in wearable blood purification systems and synthetic kidneys.

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Nakajima, T., T. Miyaji, A. Kato, N. Ikegaya, T. Yamamoto, and A. Hishida. "Uninephrectomy reduces apoptotic cell death and enhances renal tubular cell regeneration in ischemic ARF in rats." American Journal of Physiology-Renal Physiology 271, no. 4 (October 1, 1996): F846—F853. http://dx.doi.org/10.1152/ajprenal.1996.271.4.f846.

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Contralateral uninephrectomy attenuates unilateral ischemic renal injury functionally and morphologically. In this study we investigated the effects of uninephrectomy on apoptotic renal cell death and tubular regeneration in ischemic acute renal failure (ARF) in rats. Unilateral ischemic injury was provoked by a 60-min left renal artery occlusion in right-nephrectomized (Nx) and sham-nephrectomized (sham-Nx) rats. Uninephrectomy attenuated tubular damage 48 h following the renal ischemia Apoptotic cells were found in renal tissue as early as 3 h after reperfusion and increased in number by 12 h. The “ladder” pattern of DNA fragments on agarose gel electrophoresis was also apparent in ischemic kidney. Uninephrectomy reduced apoptotic cells and DNA fragmentation. The expression of proliferating cell nuclear antigen (PCNA) could be seen 24 h after reperfusion and progressively increased thereafter PCNA expression in ischemic kidney was greater in Nx than sham-Nx rats at 24 h after renal reperfusion. These data suggest that uninephrectomy reduces apoptotic cells and DNA fragmentation and enhances PCNA expression. The reduced apoptotic cell death and enhanced cell regeneration may be importantly involved in the uninephrectomy-induced attenuation of ischemic acute renal failure in rats.

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Sobreiro‐Almeida, Rita, Rita Quinteira, and Nuno M. Neves. "Renal Regeneration: The Role of Extracellular Matrix and Current ECM‐Based Tissue Engineered Strategies." Advanced Healthcare Materials 10, no. 14 (June 16, 2021): 2100160. http://dx.doi.org/10.1002/adhm.202100160.

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Morais, D. B., M. S. Jesus, A. C. Bonatto, D. W. Silva, and A. Kataoka. "Classification of anemia as to the medullary response through reticulocyte count in dogs attended to in the Veterinary Hospital from Federal University of Mato Grosso, Campus Sinop." Scientific Electronic Archives 13, no. 6 (May 29, 2020): 79. http://dx.doi.org/10.36560/13620201058.

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Anemia is defined as the presence of erythrocytes, hemoglobin concentration and/or hematocrit below the reference values, leading to death if not treated. It is manifested clinically in the presence of pale mucosae, dyspnea, exercise intolerance and increased heart rate due to reduced tissue oxygenation. The aim of this study was to classify the anemia according to the medullar response in regenerative with weak, moderate or intense release and non-regenerative with null response, correlating with its possible causes by reticulocyte count. Thus, 50 blood samples from anemic dogs treated at the Veterinary Hospital of the Universidade Federal de Mato Grosso, Sinop Campus, were evaluated. After collection, blood smears were prepared for reticulocyte counting using supravital staining. Of the 50 animals evaluated, 54% (27/50) showed non-regenerative anemia with null response (<60,000 cells/μL), 36% (18/50) showed regeneration with weak release (60,000 to 150,000 cells/μL) and 10% (5/50) presented moderate to intense regeneration (>150,000 cells/μL). In conclusion, in this study was observed a predominance of non-regenerative anemia and a lower incidence of responsive anemia; the medullary response was more evident in hemoparasitosis anemia and non-regenerative anemia occurred mainly in animals with renal insufficiency, possibly due to insufficient production of erythropoietin

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Melica, Maria Elena, Gilda La Regina, Matteo Parri, Anna Julie Peired, Paola Romagnani, and Laura Lasagni. "Substrate Stiffness Modulates Renal Progenitor Cell Properties via a ROCK-Mediated Mechanotransduction Mechanism." Cells 8, no. 12 (December 3, 2019): 1561. http://dx.doi.org/10.3390/cells8121561.

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Stem cell (SC)-based tissue engineering and regenerative medicine (RM) approaches may provide alternative therapeutic strategies for the rising number of patients suffering from chronic kidney disease. Embryonic SCs and inducible pluripotent SCs are the most frequently used cell types, but autologous patient-derived renal SCs, such as human CD133+CD24+ renal progenitor cells (RPCs), represent a preferable option. RPCs are of interest also for the RM approaches based on the pharmacological encouragement of in situ regeneration by endogenous SCs. An understanding of the biochemical and biophysical factors that influence RPC behavior is essential for improving their applicability. We investigated how the mechanical properties of the substrate modulate RPC behavior in vitro. We employed collagen I-coated hydrogels with variable stiffness to modulate the mechanical environment of RPCs and found that their morphology, proliferation, migration, and differentiation toward the podocyte lineage were highly dependent on mechanical stiffness. Indeed, a stiff matrix induced cell spreading and focal adhesion assembly trough a Rho kinase (ROCK)-mediated mechanism. Similarly, the proliferative and migratory capacity of RPCs increased as stiffness increased and ROCK inhibition, by either Y27632 or antisense LNA-GapmeRs, abolished these effects. The acquisition of podocyte markers was also modulated, in a narrow range, by the elastic modulus and involved ROCK activity. Our findings may aid in 1) the optimization of RPC culture conditions to favor cell expansion or to induce efficient differentiation with important implication for RPC bioprocessing, and in 2) understanding how alterations of the physical properties of the renal tissue associated with diseases could influenced the regenerative response of RPCs.

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Engel, Jason E., and Alejandro R. Chade. "Macrophage polarization in chronic kidney disease: a balancing act between renal recovery and decline?" American Journal of Physiology-Renal Physiology 317, no. 6 (December 1, 2019): F1409—F1413. http://dx.doi.org/10.1152/ajprenal.00380.2019.

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Macrophages are heterogenous cells of the innate immune system that can fluidly modulate their phenotype to respond to their local microenvironment. They are found throughout the renal compartments, where they contribute to homeostasis and function. However, renal injury activates molecular pathways that initially stimulate differentiation of macrophages into a proinflammatory M1 phenotype. Later in the course of healing, abundant apoptotic debris and anti-inflammatory cytokines induce the production of anti-inflammatory M2 macrophages, which contribute to tissue regeneration and repair. Thus, the dynamic balance of M1 and M2 populations may outline the burden of inflammation and process of tissue repair that define renal outcomes, which has been the impetus for therapeutic efforts targeting macrophages. This review will discuss the role of these phenotypes in the progression of chronic renal injury, potential pathogenic mechanisms, and the promise of macrophage-based therapeutic applications for chronic kidney disease.

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Sun, Zejia, Xin Li, Xiang Zheng, Peng Cao, Baozhong Yu, and Wei Wang. "Stromal cell-derived factor-1/CXC chemokine receptor 4 axis in injury repair and renal transplantation." Journal of International Medical Research 47, no. 11 (October 3, 2019): 5426–40. http://dx.doi.org/10.1177/0300060519876138.

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Stem cell therapy has shown promise in treating a variety of pathologies, such as myocardial infarction, ischaemic stroke and organ transplantation. The stromal cell-derived factor-1 (SDF-1)/CXC chemokine receptor-4 (CXCR4) axis plays a key role in stem cell mobilization. This review describes the important role of SDF-1 in tissue injury and how it works in tissue revascularization and regeneration via CXCR4. Furthermore, factors influencing the SDF-1/CXCR4 axis and its clinical potential in ischaemia reperfusion injury, such as renal transplantation, are discussed. Exploring signalling pathways of the SDF-1/CXCR4 axis will contribute to the development of stem cell therapy so that more clinical problems can be solved. Controlling directional homing of stem cells through the SDF-1/CXCR4 axis is key to improving the efficacy of stem cell therapy for tissue injury. CXCR4 antagonists may also be effective in increasing circulating levels of adult stem cells, thereby exerting beneficial effects on damaged or inflamed tissues in diseases that are currently not treated by standard approaches.

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Basile, David P., Daniel R. Martin, and Marc R. Hammerman. "Extracellular matrix-related genes in kidney after ischemic injury: potential role for TGF-β in repair." American Journal of Physiology-Renal Physiology 275, no. 6 (December 1, 1998): F894—F903. http://dx.doi.org/10.1152/ajprenal.1998.275.6.f894.

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The renal expression of transforming growth factor-β1 (TGF-β1) is enhanced following induction of ischemic injury in rat. In cultured renal cells, TGF-β stimulates the synthesis of extracellular matrix. To link TGF-β1 expression with the regulation of extracellular matrix postischemia, we characterized the expression of several genes known to regulate extracellular matrix synthesis at various times during recovery from acute ischemic renal injury in rat. Levels of mRNA for plasminogen activator inhibitor-1 (PAI-1), tissue inhibitor of metalloprotease-1 (TIMP-1), α1(IV) collagen, and fibronectin-EIIIA (FN-EIIIA) mRNAs were significantly enhanced in kidneys within 12 h to 3 days after injury and remained elevated at 7–28 days postischemia relative to levels in kidneys of sham-operated controls. PAI-1 mRNA and peptide were localized in regenerating proximal tubules at 3 and 7 days postischemic injury. α1(IV) Collagen and FN-EIIIA mRNAs were expressed primarily in regenerating proximal tubule cells. Immunoreactivity for FN-EIIIA was enhanced in the tubular basement membrane (TBM) of regenerating proximal tubules, and α1(IV) collagen immunoreactivity was detected in thickened tubulointerstitial spaces. In contrast, TIMP-1 immunoreactivity was enhanced in distal nephron structures postischemia. Immunoneutralization of TGF-β in vivo attenuated the increases in FN-EIIIA, α1(IV) collagen, PAI-1, and TIMP-1 mRNAs by 52%, 73%, 43%, and 27%, respectively. These data are consistent with TGF-β expression postischemic injury participating in renal regeneration of extracellular matrix homeostasis in the proximal TBM.

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Jin, Meiling, Yuansheng Xie, Qinggang Li, and Xiangmei Chen. "Stem Cell-Based Cell Therapy for Glomerulonephritis." BioMed Research International 2014 (2014): 1–15. http://dx.doi.org/10.1155/2014/124730.

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Glomerulonephritis (GN), characterized by immune-mediated inflammatory changes in the glomerular, is a common cause of end stage renal disease. Therapeutic options for glomerulonephritis applicable to all cases mainly include symptomatic treatment and strategies to delay progression. In the attempt to yield innovative interventions fostering the limited capability of regeneration of renal tissue after injury and the uncontrolled pathological process by current treatments, stem cell-based therapy has emerged as novel therapy for its ability to inhibit inflammation and promote regeneration. Many basic and clinical studies have been performed that support the ability of various stem cell populations to ameliorate glomerular injury and improve renal function. However, there is a long way before putting stem cell-based therapy into clinical practice. In the present article, we aim to review works performed with respect to the use of stem cell of different origins in GN, and to discuss the potential mechanism of therapeutic effect and the challenges for clinical application of stem cells.

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Nguan, Christopher Y. C., Qiunong Guan, Martin E. Gleave, and Caigan Du. "Promotion of cell proliferation by clusterin in the renal tissue repair phase after ischemia-reperfusion injury." American Journal of Physiology-Renal Physiology 306, no. 7 (April 1, 2014): F724—F733. http://dx.doi.org/10.1152/ajprenal.00410.2013.

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Renal repair begins soon after the kidney suffers ischemia-reperfusion injury (IRI); however, its molecular pathways are not fully understood. Clusterin (Clu) is a chaperone protein with cytoprotective functions in renal IRI. The aim of this study was to investigate the role of Clu in renal repair after IRI. IRI was induced in the left kidneys of wild-type (WT) C57BL/6J (B6) vs. Clu knockout (KO) B6 mice by clamping the renal pedicles for 28–45 min at the body temperature of 32°C. The renal repair was assessed by histology and confirmed by renal function. Gene expression was examined using PCR array. Here, we show that following IRI, renal tubular damage and Clu expression in WT kidneys were induced at day 1, reached the maximum at day 3, and significantly diminished at day 7 along with normal function, whereas the tubular damage in Clu KO kidneys steadily increased from initiation of insult to the end of the experiment, when renal failure occurred. Renal repair in WT kidneys was positively correlated with an increase in Ki67+ proliferative tubular cells and survival from IRI. The functions of Clu in renal repair and renal tubular cell proliferation in cultures were associated with upregulation of a panel of genes that could positively regulate cell cycle progression and DNA damage repair, which might promote cell proliferation but not involve cell migration. In conclusion, these data suggest that Clu is required for renal tissue regeneration in the kidney repair phase after IRI, which is associated with promotion of tubular cell proliferation.

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Krishnamoorthy, Aparna, Amrendra Kumar Ajay, Dana Hoffmann, Tae-Min Kim, Victoria Ramirez, Gabriela Campanholle, Norma A. Bobadilla, Sushrut S. Waikar, and Vishal S. Vaidya. "Fibrinogen β–derived Bβ15-42 peptide protects against kidney ischemia/ reperfusion injury." Blood 118, no. 7 (August 18, 2011): 1934–42. http://dx.doi.org/10.1182/blood-2011-02-338061.

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AbstractIschemia/reperfusion (I/R) injury in the kidney is a major cause of acute kidney injury (AKI) in humans and is associated with significantly high mortality. To identify genes that modulate kidney injury and repair, we conducted genome-wide expression analysis in the rat kidneys after I/R and found that the mRNA levels of fibrinogen (Fg)α, Fgβ, and Fgγ chains significantly increase in the kidney and remain elevated throughout the regeneration process. Cellular characterization of Fgα and Fgγ chain immunoreactive proteins shows a predominant expression in renal tubular cells and the localization of immunoreactive Fgβ chain protein is primarily in the renal interstitium in healthy and regenerating kidney. We also show that urinary excretion of Fg is massively increased after kidney damage and is capable of distinguishing human patients with acute or chronic kidney injury (n = 25) from healthy volunteers (n = 25) with high sensitivity and specificity (area under the receiver operating characteristic of 0.98). Furthermore, we demonstrate that Fgβ-derived Bβ15-42 peptide administration protects mice from I/R-induced kidney injury by aiding in epithelial cell proliferation and tissue repair. Given that kidney regeneration is a major determinant of outcome for patients with kidney damage, these results provide new opportunities for the use of Fg in diagnosis, prevention, and therapeutic interventions in kidney disease.

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Dai, Chunsun, Junwei Yang, and Youhua Liu. "Single Injection of Naked Plasmid Encoding Hepatocyte Growth Factor Prevents Cell Death and Ameliorates Acute Renal Failure in Mice." Journal of the American Society of Nephrology 13, no. 2 (February 2002): 411–22. http://dx.doi.org/10.1681/asn.v132411.

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ABSTRACT. Hepatocyte growth factor (HGF) is a pleiotrophic factor that plays an important role in tissue repair and regeneration after injury. The expression of both HGF and its c-met receptor genes is rapidly upregulated after acute renal injury induced by folic acid. In this study, the role of exogenous HGF in preventing acute renal failure by systemic administration of naked plasmid containing human HGF cDNA driven under the cytomegalovirus promoter (pCMV-HGF) was examined in mice. Intravenous injection of pCMV-HGF plasmid produced substantial levels of human HGF protein in mouse kidneys. Simultaneous injection of HGF plasmid DNA significantly ameliorated renal dysfunctions and accelerated recovery from the acute injury induced by folic acid. Of interest, preadministration of HGF plasmid 24 h before folic acid injection dramatically protected renal epithelial cells from both apoptotic and necrotic death and preserved the structural and functional integrity of renal tubules. Expression of HGF transgene activated protein kinase B/Akt kinase and preserved prosurvival Bcl-xL protein expression in vivo. These results indicate that a single, intravenous injection of naked plasmid containing HGF gene not only promotes renal regeneration after injury but also protects tubular epithelial cells from the initial injury and cell death in the first place. These data suggest that HGF gene therapy may provide a new avenue for exploring a novel therapeutic strategy for clinical acute renal failure.

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Morrow, Carla M. K., Victor E. Valli, Petra A. Volmer, and Paul A. Eubig. "Canine Renal Pathology Associated with Grape or Raisin Ingestion: 10 Cases." Journal of Veterinary Diagnostic Investigation 17, no. 3 (May 2005): 223–31. http://dx.doi.org/10.1177/104063870501700302.

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Ten dogs suffered acute renal failure after ingesting ≥3 g/kg (dry matter) of grapes or raisins. All dogs had degeneration or necrosis (or both) of proximal renal tubules with basement membranes remaining intact, and epithelial regeneration was observed in 5 out of 10 cases. Mineralized tubular debris or granular to proteinaceous casts (or both) were present in all cases. A golden-brown, globular, intracellular pigment of varying amounts and sizes was observed in 6 out of 10 cases with variable reaction with Prussian blue. Multifocal fibrinous arteritis of the large colon was seen in 2 out of 5 cases with globulin insudation of vessel wall demonstrated by immunohistochemical staining for immunoglobulin (Ig)G and IgM. Mineral analysis on frozen renal tissue from 2 out of 2 cases revealed mildly elevated Ca:P ratio in both. Clinically significant observations were preservation of the integrity of basement membranes after grape-induced tubular injury and presence of early epithelial regeneration. Thus, recovery may be possible if anuria is aggressively managed. With respect to potential pathophysiologic mechanisms, further research into the roles of calcium homeostasis, vascular reactivity, and the significance of the golden-brown pigment is indicated.

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Schaudies, R. P., D. Nonclercq, L. Nelson, G. Toubeau, J. Zanen, J. A. Heuson-Stiennon, and G. Laurent. "Endogenous EGF as a potential renotrophic factor in ischemia-induced acute renal failure." American Journal of Physiology-Renal Physiology 265, no. 3 (September 1, 1993): F425—F434. http://dx.doi.org/10.1152/ajprenal.1993.265.3.f425.

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The time course for the increases in soluble renal epidermal growth factor (EGF) after ischemia has been established. These elevated levels of EGF have been compared with the degree of tissue injury as well as the extent of cell proliferation in the recovering tissue. Levels of soluble immunoreactive EGF (irEGF) in control animals were 9.74 +/- 1.1 ng/g wet wt (n = 4-8 for all values) and rose to 83.9 +/- 30 ng/g within 12 h after injury. Soluble irEGF content peaked at 88.8 +/- 15 ng/g at 24 h postinjury and returned to control values by 72 h. We previously reported that trypsin digestion of crude renal membranes (CRM) generates rat EGF that is indistinguishable from that isolated from the submandibular gland. Initial levels of trypsin-releasable membrane-associated irEGF were 439 +/- 26 ng/g. These levels fell to 46.6 +/- 9.6 ng/g at 48 h after injury. The total renal EGF demonstrated an 80% decline 48 h after injury but returned to 50% of the initial values after 72 h representing significant new synthesis of EGF-containing proteins between 48 and 72 h postinjury. Immunohistochemical staining of kidney paraffin sections for EGF immunoreactivity demonstrated staining intensities that paralleled the amount of irEGF in the trypsin-digested CRM fraction, suggesting that the membrane-associated irEGF is the predominant form detected by this technique. Regenerative hyperplasia subsequent to tubular insult was monitored by immunostaining nuclei of S phase cells after pulse labeling with the thymidine analogue 5-bromo-2'-deoxyuridine. Cell proliferation was particularly prominent in the outer stripe of outer medulla of kidneys exposed to ischemia and reached a maximum (19-fold higher than the baseline value) 48 h after reperfusion. Renal cell turnover returned to control values by day 7. The observation that the peak in soluble EGF levels (24 h) precedes the peak in tubular regeneration (48 h) by 24 h is consistent with the hypothesis that EGF is one of the mitogenic signals triggering regenerative hyperplasia after renal injury.

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Morin, N. J., G. Laurent, D. Nonclercq, G. Toubeau, J. A. Heuson-Stiennon, M. G. Bergeron, and D. Beauchamp. "Epidermal growth factor accelerates renal tissue repair in a model of gentamicin nephrotoxicity in rats." American Journal of Physiology-Renal Physiology 263, no. 5 (November 1, 1992): F806—F811. http://dx.doi.org/10.1152/ajprenal.1992.263.5.f806.

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Epidermal growth factor (EGF) is a potent mitogen for renal tubular cells that possess specific high-affinity binding sites for this polypeptide. However, actual function of EGF within the kidney remains to be elucidated. We evaluated the effect of exogenous EGF administration on the rate of tubular regeneration in an experimental model of gentamicin (GT) nephrotoxicity. Female Sprague-Dawley rats were anesthetized, and a miniosmotic pump filled with mouse EGF or saline was implanted subcutaneously. Twenty-four hours later, GT (40 mg.kg-1 x 12 h-1 ip) was given for 4 and 8 days. Groups of treated animals and controls were killed either the day after cessation of treatment (days 5 and 9) or 4 and 8 days after the end of 8-day GT administration (days 12 and 16). Cortical GT levels of groups killed at days 5, 9, 12, and 16 were similar in animals infused with saline or EGF. Serum creatinine levels were significantly higher in GT-treated animals infused with EGF or saline and killed at days 9 and 12 compared with saline-treated animals infused with EGF or saline alone (P < 0.01). Blood urea nitrogen (BUN) also increased as a result of GT administration. However, in animals receiving GT and EGF and killed at day 16, mean BUN level was significantly lower (P < 0.01) compared with rats dosed with GT alone. In treated rats, the extent of tubular regeneration, evaluated by the rate of [3H]thymidine incorporation into renal cortical DNA or by the frequency of S-phase cells (histoautoradiography), was increased in a dose- and time-dependent fashion.(ABSTRACT TRUNCATED AT 250 WORDS)

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Toson, Elshahat Abo-Mosalam, Hanaa Hamdy Ahmed, Hatem Abdel Moneim El-mezayen, Laila Ahmed Rashed, and Eslam Samy Elsherbiny. "Possible Renal Repairing Mechanisms of Mesenchymal Stem Cells in Cyclosporine-Mediated Nephrotoxicity: Endothelial Viability and Hemodynamics." Indonesian Biomedical Journal 11, no. 2 (August 1, 2019): 145–51. http://dx.doi.org/10.18585/inabj.v11i2.617.

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BACKGROUND: Stem cell-based therapy may represent the first realistic option for tissue repairing and regeneration. Mesenchymal stem cells (MSCs) are proved to be involved in the regeneration of many tissues which are subjected to different types of injury. Cyclosporine (CsA) in spite of its use as immune suppressive drug during kidney transplantation, it was considered as important model of nephropathy specially, during long-term administration.METHODS: Isolation and preparation of MSCs using Dulbecco's modified Eagle's medium (DMEM), in vitro differentiation through adipogenesis chondrogenesis and osteogenesis was confirmed by using Alizarin Red S stain, Oil Red O stain and Alcian Blue stain, respectively, characterization using flow cytometry technique to detect cluster of differentiation (CD)34, CD44 and CD105 surface markers and homing of MSCs using polymerase chain reaction (PCR) Sry gene assay, were executed. Serum levels of vascular endothelial growth factor (VEGF), endothelin-1 (ET-1) and endothelial nitric oxide synthase (eNOS) were quantified using enzyme-linked immunosorbent assay (ELISA) kits based on the principle of double-antibody sandwich technique. The structural organization of kidney tissue was examined using histological procedures.RESULTS: Single intravenous dose of MSCs is capable to boost kidney repairment process as indicated by the significant decrease in serum ET-1 level paralleled by significant increase in VEGF and eNOS. Moreover, histological findings revealed the improvement of focal hemorrhage in between the degenerated tubules, congestion in the cortical blood vessels, vacuolization in the endothelial cells lining the glomerular tufts and focal perivascular inflammatory cells aggregation.CONCLUSION: This study demonstrated the favorable influence of MSCs in repressing cyclosporine-induced nephropathy in rats. This could be achieved through angiogenic and anti-arteriolopathic mechanisms.KEYWORDS: angiogenesis, cyclosporine, endothelin-1, MSCs, nephropathy

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Lih, Eugene, Wooram Park, Ki Wan Park, So Young Chun, Hyuncheol Kim, Yoon Ki Joung, Tae Gyun Kwon, Jeffrey A. Hubbell, and Dong Keun Han. "A Bioinspired Scaffold with Anti-Inflammatory Magnesium Hydroxide and Decellularized Extracellular Matrix for Renal Tissue Regeneration." ACS Central Science 5, no. 3 (January 25, 2019): 458–67. http://dx.doi.org/10.1021/acscentsci.8b00812.

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Miya, Masaaki, Akito Maeshima, Keiichiro Mishima, Noriyuki Sakurai, Hidekazu Ikeuchi, Takashi Kuroiwa, Keiju Hiromura, Hideaki Yokoo, and Yoshihisa Nojima. "Enhancement of in vitro human tubulogenesis by endothelial cell-derived factors: implications for in vivo tubular regeneration after injury." American Journal of Physiology-Renal Physiology 301, no. 2 (August 2011): F387—F395. http://dx.doi.org/10.1152/ajprenal.00619.2010.

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Renal proximal tubular epithelium can regenerate after various insults. To examine whether the tubular repair process is regulated by surrounding peritubular capillaries, we established an in vitro human tubulogenesis model that mimics in vivo tubular regeneration after injury. In this model, HGF, a potent renotropic factor, dose dependently induced tubular structures in human renal proximal tubular epithelial cells cultured in gels. Consistent with regenerating tubular cells after injury, HGF-induced tubular structures expressed a developmental gene, Pax-2, and a mesenchymal marker, vimentin, and formed a lumen with aquaporin-1 expression. Electron microscopic analysis showed the presence of microvilli on the apical site of the lumen, suggesting that these structures are morphologically equivalent to renal tubules in vivo. When cocultured with human umbilical vein endothelial cells (HUVEC), HGF-induced tubular formation was significantly enhanced. This could not be reproduced by the addition of VEGF, basic FGF, or PDGF. Protein array revealed that HUVEC produced various matrix metalloproteinases (MMPs). The stimulatory effects of coculture with HUVEC or HUVEC-derived conditional medium were almost completely abolished by addition of the tissue inhibitor of metalloproteinase (TIMP)-1 or TIMP-2. These data suggest that endothelial cell-derived factors including MMPs play a critical role in tubulogenesis and imply a potential role of peritubular capillary endothelium as a source of factor(s) required for tubular recovery after injury.

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Nakagawa, Shunsaku, Tomohiro Omura, Atsushi Yonezawa, Ikuko Yano, Takayuki Nakagawa, and Kazuo Matsubara. "Extracellular nucleotides from dying cells act as molecular signals to promote wound repair in renal tubular injury." American Journal of Physiology-Renal Physiology 307, no. 12 (December 15, 2014): F1404—F1411. http://dx.doi.org/10.1152/ajprenal.00196.2014.

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Acute kidney injury (AKI) often correlates with poor prognosis and is followed by various severe unfavorable systemic outcomes. It is important to understand the pathophysiology of AKI for the development of novel therapeutic approaches toward promoting renal regeneration after injury. Recent studies have indicated that AKI-induced tubular cell death plays an active role in the onset of tissue regeneration; however, the mechanisms underlying renal tubular repair after injury have yet to be understood. In the present study, we explored molecules that might serve as “danger” signals in mediating tubular regeneration. Kidneys of rats systemically administered the nephrotoxicant cisplatin (to induce AKI) exhibited massive cell proliferation. The proportion of proliferating cells in the total cell distribution was highest in the outer stripe of the outer medulla coincided with where the tubular damage was the most severe in this study. This finding suggests that soluble factors may have been released from damaged cells to stimulate the proliferation of neighboring tubular epithelial cells. In elucidating the mechanism of dying cell-to-surviving cell communication using normal rat kidney NRK-52E epithelial cells, we found a significant increase in ATP levels in supernatants of these cells after the induction of cell death using ultraviolet irradiation. Furthermore, treatment of conditioned supernatants with apyrase or suramin, which inhibits purinergic signaling, resulted in significant decreases in cell proliferation and migration activities. These results demonstrate a novel role for extracellular nucleotides, probably as danger signals in aggravating tubular regeneration after AKI.

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Magnasco, Alberto, Mirko Corselli, Roberta Bertelli, Adalberto Ibatici, Monica Peresi, Gabriele Gaggero, Valentina Cappiello, et al. "Mesenchymal Stem Cells Protective Effect in Adriamycin Model of Nephropathy." Cell Transplantation 17, no. 10-11 (October 2008): 1157–67. http://dx.doi.org/10.3727/096368908787236567.

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Mesenchymal stem cells (MSCs) may be of value in regeneration of renal tissue after damage; however, lack of biological knowledge and variability of results in animal models limit their utilization. We studied the effects of MSCs on podocytes in vitro and in vivo utilizing adriamycin (ADR) as a model of renal toxicity. The in vivo experimental approach was carried out in male Sprague-Dawley rats (overall 60 animals) treated with different ADR schemes to induce acute and chronic nephrosis. MSCs were given a) concomitantly to ADR in tail vein or b) in aorta and c) in tail vein 60 days after ADR. Homing was assessed with PKH26-MSCs. MSCs rescued podocytes from apoptosis induced by ADR in vitro. The maximal effect (80% rescue) was obtained with MSCs/podocytes coculture ratio of 1:1 for 72 h. All rats treated with ADR developed nephrosis. MSCs did not modify the clinical parameters (i.e., proteinuria, serum creatinine, lipids) but protected the kidney from severe glomerulosclerosis when given concomitantly to ADR. Rats given MSCs 60 days after ADR developed the same severe renal damage. Only a few MSCs were found in renal tubule-interstitial areas 1–24 h after injection and no MSCs were detected in glomeruli. MSCs reduced apoptosis of podocytes treated with ADR in vitro. Early and repeated MSCs infusion blunted glomerular damage in chronic ADR-induced nephropathy. MSCs did not modify proteinuria and progression to renal failure, which implies lack of regenerative potential in this model.

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Kunduzova, Oxana R., Pascale Bianchi, Nathalie Pizzinat, Ghislaine Escourrou, Marie‐Helene Seguelas, Angelo Parini, and Claudie Cambon. "Regulation of JNK/ERK activation, cell apoptosis, and tissue regeneration by monoamine oxidases after renal ischemia‐reperfusion." FASEB Journal 16, no. 9 (May 21, 2002): 1129–31. http://dx.doi.org/10.1096/fj.01-1008fje.

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Journal articles on the topic 'Renal tissue regeneration'

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