ISSN 2415-3060 (print), ISSN 2522-4972 (online)
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JMBS 2021, 6(2): 37–43
https://doi.org/10.26693/jmbs06.02.037
Experimental Medicine and Morphology

Characteristic of Connective Tissue Fibers and Myofibroblasts Interstitium of the Kidneys in Rats Offspring Born to Females with Experimental Metabolic Syndrome

Hryhoryeva O. A., Korotchuk Ye. V.
Abstract

According to a number of studies, it is known that a woman's diet during pregnancy may be one of factors in the violation of nephrogenesis. Obesity in pregnancy may increase markers of fibrosis and the accumulation of extracellular matrix in the kidneys. The purpose of the study is to investigate the dynamics of the content of collagen fibers and myofibroblasts in the cortical and medulla of the kidneys of rat offspring. Materials and methods. The research was based according to the international bioethical regulations, 120 albino rats were involved in the study. The first group is experimental (MC-1): rats born to females with an experimental metabolic syndrome and after the start of self-feeding received a high-calorie diet up to 120 days of age. The second group is experimental (MC-2): rats that were obtained from females with an experimental metabolic syndrome, but after switching to self-feeding received a standard diet. The third group is a control group of rats with a standard diet and water regime ad libitum. Mason-tricolor histochemical staining was used to determine collagen fibers, and immunohistochemical reaction using mouse Smooth Muscle Actin monoclonal antibodies (αSMA) was used to detect myofibroblasts. Results and discussion. It was found that the content of collagen fibers in the kidneys of the studied groups gradually increases with increasing of observation period, reaching maximum values on the 120th day of the study, with a statistically significant predominance of values in animals of group MC-1 over control animals in cortical and cerebral matter. Also, control and experimental groups are characterized by a gradual increase in the relative area occupied by αSMA+ cells from the total area of the organ, with maximum values at the end of the study. At the same time, there was a statistically significant predominance of the experimental groups MC-1 and MC-2 in the cortical substance in comparison with control animals. Conclusion. The gradual growth of collagen fibers in the cortical and cerebral substance is probably associated with an increase in the content of αSMA+ myofibroblasts, which according to research are markers of fibrosis

Keywords: metabolic syndrome, kidneys, rats, collagen fibers, myofibroblasts

Full text: PDF (Ukr) 336K

References
  1. Childhood overweight and obesity. World Health Organization. 2018. Available from: www.who.int/dietphysicalactivity/childhood/
  2. Batysheva TT, Platonova AN, Bykova OV, Bakhtyna EA. Metabolycheskyy syndrom v detskom y podrostkovom vozraste kak faktor ryska ynsulta [Metabolic syndrome in childhood and adolescence as a risk factor for stroke]. Medytsyna: teoryya y praktyka. 2019; 4: 83–84. [Russian]
  3. Langley-Evans SC. Developmental programming of health and disease. Proc Nutr. Soc. 2006; 65: 97–105.
  4. Wood-Bradley RJ, Barrand S, Giot A, Armitage JA. Understanding the role of maternal diet on kidney development; an opportunity to improve cardiovascular and renal health for future generations. Nutrients. 2015; 7: 1881–1905.
  5. Glastras SJ, Chen H, McGrath RT, Zaky AA, Gill AJ, Pollock CA, et al. Effect of GLP-1 receptor activation on offspring kidney health in a rat model of maternal obesity. Sci Rep. 2016; 6: 23525. https://doi.org/10.1038/srep23525
  6. Djudjaj S, Boor P. Cellular and molecular mechanisms of kidney fibrosis. Molecular Aspects of Medicine. 2019; 65: 16-36. https://doi.org/10.1016/j.mam.2018.06.002
  7. Nogueira A, Pires MJ, Oliveira PA. Pathophysiological mechanisms of renal fibrosis: a review of animal models and therapeutic strategies. In vivo. 2017; 31(1): 1-22. https://doi.org/10.1016/j.mam.2018.06.002
  8. Lovisa S, LeBleu V, Tampe B. Epithelial-to-mesenchymal transition induces cell cycle arrest and parenchymal damage in renal fibrosis. Nat Med. 2015; 21(9): 998–1009. https://doi.org/10.1038/nm.3902
  9. Grande MT, Sánchez-Laorden B, López-Blau C, De Frutos CA, Boutet A, Arévalo M, et al. Snail1-induced partial epithelial-to-mesenchymal transition drives renal fibrosis in mice and can be targeted to reverse established disease. Nat Med. 2015; 21(9): 989–997. https://doi.org/10.1038/nm.3901
  10. Bradding P, Pejler G. The controversial role of mast cells in fibrosis. Immunological Reviews. 2018; 282(1): 198–231. https://doi.org/10.1111/imr.12626
  11. Cherng S, Young J, Ma H. Alpha-smooth muscle actin (α-SMA). J Am Sci. 2008; 4(4): 7-9.
  12. Xiao Q, Guan Y, Li C, Liu L, Zhao D, Wang H. Decreased expression of transforming growth factor-β1 and α-smooth muscle actin contributes to the protection of lotensin against chronic renal failure in rats. Ren Fail. 2018; 40(1): 583-589. https://doi.org/10.1080/0886022X.2018.1496934
  13. Sun KH, Chang Y, Reed NI, Sheppard D. α-Smooth muscle actin is an inconsistent marker of fibroblasts responsible for force-dependent TGFβ activation or collagen production across multiple models of organ fibrosis. American Journal of Physiology-Lung Cellular and Molecular Physiology. 2016; 310(9): L824-L836.
  14. Meran S, Steadman R. Fibroblasts and myofibroblasts in renal fibrosis. International journal of experimental pathology. 2011; 92(3): 158-167. https://doi.org/10.1111/j.1365-2613.2011.00764.x
  15. Strutz F, Zeisberg M. Renal fibroblasts and myofibroblasts in chronic kidney disease. Journal of the American Society of Nephrology. 2006; 17(11): 2992-2998. https://doi.org/10.1681/ASN.2006050420
  16. Genovese F, Manresa AA, Leeming DJ, Karsdal MA, Boor P. The extracellular matrix in the kidney: a source of novel non-invasive biomarkers of kidney fibrosis? Fibrogenesis Tissue Repair. 2014; 7(1): 4. https://doi.org/10.1186/1755-1536-7-4
  17. Qureshi OS, Bon H, Twomey B, Holdsworth G, Ford K, Bergin M, et al. An immunofluorescence assay for extracellular matrix components highlights the role of epithelial cells in producing a stable, fibrillar extracellular matrix. Biol. Open. 2017; 6: 1423–1433. https://doi.org/10.1242/bio.025866
  18. Korotchuk YV, Hryhoriyeva OA. Dynamica morphometrychnyh pokaznykiv nyrky shchuriv, otrymanykh vid materiv z eksperymentalnym metabolichnym syndromom [Dynamics of morphometric parameters of rats` kidneys obtained from mothers with experimental metabolic syndrome]. Visnyk problem biologiyi i medytsyny. 2020; 2(156): 266–271. https://doi.org/10.29254/2077-4214-2020-2-156-266-271
  19. Mack M, Yanagita M. Origin of myofibroblasts and cellular events triggering fibrosis. Kidney international. 2015; 87 (2): 297-307. https://doi.org/doi.org/10.1038/ki.2014.287
  20. Syvolap VD, Lashkul DA. Markery fibrozu u khvorykh na khronichnu sertsevu nedostatnist ishemichnogo genezu ta nyrkovu dysfunktsiyu [Markers of fibrosis in ischemic chronic heart failure and renal dysfunction]. Zaporozhskyy medytsynskyy zhurnal. 2015; 3: 24-28. https://doi.org/10.14739/2310-1210.2015.3.4445