Cerrahpaşa Medical Journal
ORIGINAL ARTICLE

TGF-β1 expression and mesangial alterations in rat glomeruli of an experimental chronic nephrosis model

1.

İstanbul Üniversitesi-Cerrahpaşa, Cerrahpaşa Tıp Fakültesi, Histoloji ve Embriyoloji Anabilim Dalı, İstanbul, Türkiye

2.

İstanbul Üniversitesi-Cerrahpaşa, Cerrahpaşa Tıp Fakültesi, İç Hastalıkları Anabilim Dalı, Nefroloji Bilim Dalı, İstanbul, Türkiye

3.

Ordu Üniversitesi Tıp Fakültesi, Histoloji ve Embriyoloji Anabilim Dalı, Ordu, Türkiye

4.

İstanbul Üniversitesi-Cerrahpaşa, Cerrahpaşa Tıp Fakültesi, Biyokimya Anabilim Dalı, İstanbul, Türkiye

5.

İstanbul Üniversitesi Çapa Tıp Fakültesi, Histoloji ve Embriyoloji Anabilim Dalı, İstanbul, Türkiye

Cerrahpasa Med J 2019; 43: 6-12
DOI: 10.26650/cjm.2019.43.11
Read: 1193 Downloads: 236 Published: 19 September 2019

Objective: Puromycine aminonucleoside nephrosis (PAN) is extensively used as an experimental model of proteinuria following podocyte injury. In PAN animal models, nephrotic syndrome with minimal change disease and focal segmental sclerosis-like nephritis is demonstrated to be similar to that in human; however, the real mechanism of PAN is not yet elucidated. Evidence shows that transforming growth factor-β1 (TGF-β1) plays a key via stimulating matrix protein synthesis of both glomerular epithelial and mesangial cells. In this study, we aimed to examine the relationship between TGF-β expression and accumulation in mesangial matrix (MM) by the changes in renal function and ultrastructure alterations in renal glomeruli of the chronic PAN induced rats.

Methods: Twelve male Wistar albino rats were divided into two groups: control group (n=6), chronic group (n=6). All data was statistically analyzed by One-way ANOVA Test.

Results: Proteinuria levels in the chronic nephrosis groups were greater than the control (p<0.0025) whereas the levels of serum albumin and creatinine clearances were progressively decreased (p<0.05). TGF-β1 expression and MM were both significantly increased in PAN değerlegroup.
Ultrastructural images of glomeruli of PAN showed apoptotic endothelium and mesangial cells, interstitial collagen and macrophages in increased MM.

Conclusion: Our findings suggest that chronic PAN application induces a nephrotic syndrome, leading to renal impairment by TGF-β1 expression in glomeruli, increase in MM, formation of abundant interstitial collagen, and migration of macrophages. We suggest that chronic PAN progressively increases TGF-β1 expression and apoptosis following expansion of mesangial matrix in the affected glomeruli. This study needs further researches to determine the main source and signal pathway of TGF-β1 expression by double staining methods.

Cite this article as: Seçkin İ, Uzunalan M, Ayaz Pekpak M, Köktürk S, Sönmez HA, Güngör ZB. TGF-β1 expression and mesangial alterations in rat glomeruli of an experimental chronic nephrosis model. Cerrahpasa Med J 2019; 43(1): 6-12.

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