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MiR-21-5p Promotes Osteogenic Differentiation and Calcification of Valvular Interstitial Cells by Targeting TGFBI in

Yan Gu1, Rongjin Chen1, Jianxiang Song1

  • 1Department of Cardiothoracic Surgery, The Sixth Affiliated Hospital of Nantong University, Yancheng Third People's Hospital, Yancheng, Jiangsu 224000, China.

Iranian Journal of Public Health
|November 15, 2024
PubMed

Insights

MicroRNA-21-5p promotes calcific aortic valve disease (CAVD) by increasing valve mineralization. Targeting miR-21-5p and its downstream protein, TGFBI, may offer new therapeutic strategies for CAVD.

Area of Science:

  • Cardiovascular Biology
  • Molecular Medicine
  • Biomarkers and Diagnostics

Background:

  • Calcific aortic valve disease (CAVD) is a prevalent condition in the elderly, characterized by high morbidity and mortality.
  • The precise molecular mechanisms driving aortic valve mineralization in CAVD remain incompletely understood.
  • MicroRNAs (miRNAs) are implicated in cardiovascular diseases, and this study focuses on miR-21-5p's role in CAVD.

Purpose of the Study:

  • To investigate the role of miR-21-5p and its downstream targets in the progression of calcific aortic valve disease (CAVD).
  • To elucidate the molecular mechanisms by which miR-21-5p influences aortic valve mineralization.

Main Methods:

  • Human aortic valve (AV) tissues from CAVD patients and adjacent normal tissues were analyzed.
  • Quantitative reverse transcription polymerase chain reaction (RT-qPCR) and Western blotting were used to assess miR-21-5p and protein expression.
  • Alkaline phosphatase (ALP) and alizarin red staining evaluated valve interstitial cell (VIC) mineralization and osteogenic differentiation.

Main Results:

  • miR-21-5p expression was significantly elevated in CAVD tissues, while its target, TGFBI, was downregulated.
  • miR-21-5p directly targets TGFBI, and TGFBI overexpression inhibited miR-21-5p-induced VIC osteogenic differentiation.
  • Results indicate that miR-21-5p promotes VIC osteogenic differentiation and calcification, contributing to CAVD progression via TGFBI.

Conclusions:

  • miR-21-5p plays a crucial role in promoting VIC osteogenic differentiation and aortic valve calcification in CAVD.
  • The miR-21-5p/TGFBI axis represents a potential therapeutic target for managing CAVD.
  • This research provides insights into CAVD mechanisms and suggests novel diagnostic and therapeutic avenues.
Abstract

Keywords:
Calcific aortic valve diseaseOsteogenic differentiationValvular interstitial cells

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