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The cell membrane repair protein MG53 modulates transcription factor NF-κB signaling to control kidney fibrosis

Haichang Li1, Pu Duann2, Zhongguang Li1

  • 1Department of Surgery, Davis Heart and Lung Research Institute, The Ohio State University, Columbus, Ohio, USA.

Kidney International
|November 10, 2021
PubMed

Insights

The cell membrane repair protein MG53 protects against kidney fibrosis and inflammation. MG53 deficiency exacerbates kidney fibrosis, while enhancing MG53 levels offers therapeutic potential for chronic kidney disease.

Area of Science:

  • Nephrology
  • Cell Biology
  • Biochemistry

Background:

  • Kidney fibrosis is a key factor in the progression of acute kidney injury to chronic kidney disease.
  • MG53, a cell membrane repair protein, has demonstrated protective effects against kidney epithelial cell injury and acute kidney injury.
  • The role of MG53 in kidney fibrosis, particularly in aging and disease models, requires further investigation.

Purpose of the Study:

  • To investigate the role of MG53 in modulating kidney fibrosis in aging mice.
  • To evaluate the impact of MG53 deficiency on kidney fibrosis and inflammation in a mouse model of unilateral ureteral obstruction (UUO).
  • To explore the therapeutic potential of MG53 in mitigating kidney fibrosis and inflammation.

Main Methods:

  • Assessed kidney fibrosis and interstitial fibrosis in aging mice with and without MG53 using histological analysis.
  • Utilized the unilateral ureteral obstruction (UUO) model in MG53-deficient and MG53-intact mice to evaluate fibrosis and inflammation.
  • Conducted in vitro experiments to determine MG53's interaction with NF-κB signaling in proximal tubular epithelial cells.
  • Administered enhanced MG53 expression or recombinant protein to UUO mice to assess therapeutic effects.

Main Results:

  • Mice lacking MG53 exhibited increased interstitial fibrosis with age compared to controls.
  • MG53 deficiency exacerbated kidney fibrosis and inflammation in the UUO model.
  • In vitro studies showed MG53 enters proximal tubular cell nuclei and interacts with p65 subunit of NF-κB.
  • Enhanced MG53 levels reduced NF-κB activation, inflammation, and attenuated kidney fibrosis in UUO mice.

Conclusions:

  • MG53 plays a protective role against kidney fibrosis and inflammation.
  • MG53 deficiency leads to heightened inflammation and fibrosis, potentially through interaction with NF-κB signaling.
  • Augmenting MG53 levels presents a potential therapeutic strategy for chronic kidney inflammation and fibrosis, offering protection against chronic kidney disease progression.
Keywords:
TRIM72chronic kidney diseasecytokineinflammationmyokine

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