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ANGPTL4 promotes nephrotic syndrome by downregulating podocyte expression of ACTN4 and podocin

Yue Li1, Zichuan Xu1, Hui Deng1

  • 1Nephrology Department, Guangzhou Women and Children's Medical Center, Guangdong Provincial Clinical Research Center for Child Health, Guangzhou City, 510623, China.

Biochemical and Biophysical Research Communications
|December 10, 2022
PubMed
Abstract

Insights

Angiopoietin-like protein 4 (ANGPTL4) worsens nephrotic syndrome in mice by increasing hyperlipidemia and podocyte injury. Knocking out the ANGPTL4 gene alleviates these symptoms, suggesting a therapeutic target.

Area of Science:

  • Nephrology
  • Molecular Biology
  • Biochemistry

Background:

  • Lipopolysaccharide (LPS) induces nephrotic syndrome features like proteinuria and podocyte injury in mice.
  • Angiopoietin-like protein 4 (ANGPTL4) exacerbates renal injury by affecting glomerular basement membrane charge.
  • The precise mechanism of ANGPTL4 in podocyte injury remains unclear.

Purpose of the Study:

  • Investigate ANGPTL4's role in podocyte foot process (FP) fusion.
  • Examine ANGPTL4's impact on podocyte signaling molecules in nephrotic syndrome.

Main Methods:

  • Generated angptl4 gene knockout (KO) C57BL6 mice using CRISPR/Cas9.
  • Induced nephrotic syndrome model using LPS in wild-type and angptl4 KO mice.
  • Assessed glomerular expression of ACTN4, podocin, and TRPC6 via immunohistochemistry.

Main Results:

  • ANGPTL4 KO mice showed significantly reduced hyperlipidemia and proteinuria under nephrotic conditions.
  • Foot process fusion was notably improved in nephrotic mice lacking ANGPTL4.
  • ANGPTL4 deficiency partially preserved ACTN4 and podocin expression in nephrotic glomeruli, unlike wild-type mice.

Conclusions:

  • ANGPTL4 promotes hyperlipidemia and podocyte injury in nephrotic mice, contributing to proteinuria.
  • ANGPTL4's mechanism may involve down-regulating actin cytoskeletal regulators ACTN4 and podocin.
Keywords:
ACTN4Angiopoietin-like protein 4Nephrotic syndromePodocinPodocyte injuryTRPC6

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