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Meis2 represses the osteoblastic transdifferentiation of aortic valve interstitial cells through the Notch1/Twist1

Cheng Sun1, Hanning Liu1, Ke Si2

  • 1National Clinical Research Center of Cardiovascular Diseases, State Key Laboratory of Cardiovascular Disease, Fuwai Hospital, National Center for Cardiovascular Diseases, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, People's Republic of China; Department of Cardiovascular Surgery, Fuwai Hospital, National Center for Cardiovascular Diseases, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, People's Republic of China.

Biochemical and Biophysical Research Communications
|December 31, 2018
PubMed
Abstract

Insights

Meis2 normally prevents aortic valve calcification by inhibiting osteoblastic changes in cells. Reduced Meis2 levels promote calcific aortic valve disease (CAVD) via the Notch1/Twist1 pathway, suggesting Meis2 as a therapeutic target.

Area of Science:

  • Cardiovascular Biology
  • Cellular Biology
  • Developmental Biology

Background:

  • Calcific aortic valve disease (CAVD) is the most prevalent valvular heart condition globally.
  • Osteoblastic transdifferentiation of aortic valve interstitial cells (VICs) is central to CAVD pathogenesis, yet its molecular drivers remain unclear.
  • Neural crest cells (NCCs) contribute to VIC development through epithelial-to-mesenchymal transition (EMT) and migration, processes influenced by Meis2.

Purpose of the Study:

  • To investigate the role of Meis2 in the development of CAVD.
  • To identify the downstream targets and signaling pathways regulated by Meis2 in aortic valve calcification.

Main Methods:

  • Quantified Meis2 expression in human calcified and normal aortic valve tissues.
  • Utilized siRNA to inhibit Meis2 in porcine aortic VICs in vitro.
  • Assessed the impact of Meis2 inhibition on osteoblastic differentiation and Notch1/Twist1 signaling.

Main Results:

  • Meis2 gene and protein expression were significantly lower in calcified human aortic valves compared to normal valves.
  • Inhibition of Meis2 in vitro led to decreased expression of Notch1 and Twist1.
  • Meis2 suppression promoted osteoblastic transdifferentiation of porcine aortic VICs.

Conclusions:

  • Meis2 acts as a repressor of VIC osteoblastic transdifferentiation through the Notch1/Twist1 signaling pathway.
  • Meis2 is identified as a potential therapeutic target for preventing CAVD progression.
Keywords:
Aortic valve interstitial cellsCalcific aortic valve diseaseMeis2Notch1Osteoblastic transdifferentiation

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