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OGT knockdown counteracts high phosphate-induced vascular calcification in chronic kidney disease through autophagy

Tian-Hua Xu1, Zitong Sheng1, Yue Li1

  • 1Department of Nephrology, the First Hospital of China Medical University, Shenyang 110001, PR China.

Life Sciences
|July 22, 2020
PubMed
Abstract

Insights

O-GlcNAc transferase (OGT) silencing suppresses vascular calcification in chronic kidney disease (CKD) by reducing YAP and enhancing autophagy. This highlights OGT as a potential therapeutic target for preventing vascular calcification in CKD patients.

Area of Science:

  • Cardiovascular Biology
  • Nephrology
  • Cellular Metabolism

Background:

  • Pathological vascular calcification (VC) is a significant risk factor for cardiovascular mortality, particularly prevalent in chronic kidney disease (CKD).
  • Autophagy plays a protective role against high phosphate-induced VC.
  • The role of O-GlcNAc transferase (OGT) in mediating autophagy and VC in CKD remains to be fully elucidated.

Purpose of the Study:

  • To investigate the effect of O-GlcNAc transferase (OGT) on high phosphate-induced vascular calcification (VC) in chronic kidney disease (CKD).
  • To explore the role of OGT in mediating autophagy during high phosphate-induced VC.
  • To determine the interaction between OGT and Yes-associated protein (YAP) in the context of VC.

Main Methods:

  • Utilized a rat model of CKD induced by 5/6 nephrectomy and high phosphate diet to study VC.
  • Induced VSMC calcification in vitro using high phosphate treatment.
  • Performed loss-of-function experiments for OGT, co-immunoprecipitation, and GST pull-down assays to assess OGT-YAP interactions.
  • Measured autophagy markers, calcium deposition, and calcium content in response to altered OGT and YAP expression.

Main Results:

  • OGT expression was upregulated in high phosphate-induced VC models (in vitro and in vivo).
  • OGT silencing suppressed high phosphate-induced VC in rat aortas and VSMCs.
  • OGT enhanced YAP stability via glycosylation; overexpressing YAP reduced autophagy.
  • OGT accelerated high phosphate-induced VC by inhibiting autophagy through YAP upregulation.

Conclusions:

  • OGT silencing downregulates YAP, leading to autophagy activation and suppression of high phosphate-induced VC.
  • OGT inhibition presents a promising therapeutic strategy for preventing vascular calcification in CKD.
  • The OGT-YAP-autophagy pathway is a critical mechanism in high phosphate-induced VC in CKD.
Keywords:
AutophagyChronic kidney diseaseGlycosylationHigh phosphateO-GlcNAc transferaseVascular calcificationYes-associated protein

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