THE INFLUENCE OF ANGIOPOIETIN-LIKE PROTEIN 3 ON MACROPHAGES POLARIZATION AND ITS EFFECT ON THE PODOCYTE EMT IN DIABETIC NEPHROPATHY

E-Poster

https://storage.unitedwebnetwork.com/files/184/38fcf7d9e01dd032322c6a161c995cfe.pdf

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Co-author 1

Yanli Ma 907434662@qq.com Shanghai Fourth People’s Hospital, Tongji University School of Medicine Pediatrics Shanghai

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Yu Chen nancy97368@163.com Shanghai Fourth People’s Hospital, Tongji University School of Medicine Pediatrics Shanghai

Co-author 3

Hong Xu Hongxu202110@163.com Children’s Hospital of Fudan University Nephrology Shanghai

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Ni Du duni2007@foxmail.com Chongqing University Three Gorges Hospital Nephrology Chongqing

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Introduction

Podocyte injury, which involves the podocyte epithelialmesenchymal transition (EMT) process, is a crucial factor contributing to theprogression of diabetic nephropathy (DN) and proteinuria. Our study aimed toexamine the protective properties of Angiopoietin-like protein 3 (Angptl3)knockout on podocyte damage and macrophage polarization in DN mice andpodocytes treated with HG. Furthermore, we also sought to investigate theunderlying molecular mechanism responsible for these effects.

Methods

DN was induced in B6;129S5 mice through intraperitoneal injection of40 mg/kg of streptozotocin (STZ). Subsequently, the changes in renal function,podocyte apoptosis, inflammatory factors (tumor necrosis factor-a [TNF-a],interleukin-6 [IL-6], and interleukin-1b [IL-1b]), IL-10, TGF-b1, IL-1Ra, IL-10Ra,and nephrin were evaluated. Moreover, we investigated the mechanismunderlying the role of Angptl3 in macrophages polarization, podocyte injury,podocyte EMT.

Results

Our findings revealed that Angptl3 knockout significantly attenuatedSTZ or HG-induced renal dysfunction and podocyte EMT. In both in vivo and invitro studies, Angptl3 knockout led to (1) promote the transformation of M1 typemacrophages into M2 type macrophages; (2) amelioration of the reducedexpression of nephrin, synaptopodin, and podocin; (3) inhibition of NLRP3inflammasome activation and release of IL-1b; and (4) regulation of a-SMAexpression via the macrophage polarization. (5) After HG treatment, there wasan increase in pro-inflammatory factors and foot cell damage. These changeswere reversed upon Angptle knockdown.

Conclusions

Our study suggests that the knockout of Angptl3 alleviatespodocyte EMT and podocyte injury by regulating macrophage polarization.

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