Journal
EXPERIMENTAL CELL RESEARCH
Volume 385, Issue 1, Pages -Publisher
ELSEVIER INC
DOI: 10.1016/j.yexcr.2019.111670
Keywords
Podocyte; TGF-beta 1; Autophagy; Decorin; Mesangial cell proliferation
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Funding
- Science and Technology Commission of Shanghai Municipality [4DZ2260200]
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IgA nephropathy (IgAN) is a mesangial proliferative glomerulonephritis which often shows proteinuria, an indicator for podocyte damage. TGF-beta 1 has been known to contribute to podocyte injury by inducing apoptosis, cytoskeleton relocation or cytoskeleton loss. And Decorin, a small proteoglycan known to neutralize TGF-beta 1, was reported to induce autophagy in vascular endothelial cells. However, it remains unknown how TGF-beta 1 and Decorin can affect podocyte autophagy in mesangial proliferative glomerulonephritis. In this study, we used in vivo and in vitro models to find out the effect of TGF-beta 1 and Decorin on podocyte autophagy. P-rpS6 and p-ULK1 were detected by Western blot to show the activation of mTORC1 pathway following TGF-beta 1 treatment. Also, we collected serum from IgAN patients and anti-Thy1.1 nephritis, and quantified TGF-beta 1 and Decorin using ELISA. Together, we showed that TGF-beta 1 could activate mTORC1 and inhibit autophagy, while Decorin has precisely the opposite effect. As the mesangial cells (MCs) proliferate, TGF-beta 1 increases and Decorin decreases in the serum of IgAN and anti-Thy1.1 nephritis. This finding deepened our understanding regarding how MC proliferation could finally result in podocyte dysfunction.
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