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Related Experiment Video

Updated: Jun 24, 2025

Isolation of Primary Patient-specific Aortic Smooth Muscle Cells and Semiquantitative Real-time Contraction Measurements In Vitro

Isolation of Primary Patient-specific Aortic Smooth Muscle Cells and Semiquantitative Real-time Contraction Measurements In Vitro

Published on: February 15, 2022

Smooth Muscle Ythdf2 Abrogation Ameliorates Pulmonary Vascular Remodeling by Regulating Myadm Transcript Stability.

Jie Wang^1,2, Yueyao Shen¹, Yuhui Zhang¹

¹Department of Forensic Medicine (J.W., Y.S., Y.Z., D.L., Y.Y., F.C., L.H.), Nanjing Medical University, China.

Hypertension (Dallas, Tex. : 1979)

|June 4, 2024

Summary

Increased Ythdf2 promotes pulmonary hypertension (PH) by stabilizing Myadm mRNA, leading to PASMC proliferation. Targeting Ythdf2 offers a potential therapeutic strategy for PH.

Keywords:

N-methyladenosine RNA methylation hypertension, pulmonary myocytes, smooth muscle pulmonary artery

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Last Updated: Jun 24, 2025

Isolation of Primary Patient-specific Aortic Smooth Muscle Cells and Semiquantitative Real-time Contraction Measurements In Vitro

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Published on: February 15, 2022

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Isolation of Pulmonary Artery Smooth Muscle Cells from Neonatal Mice

Isolation of Pulmonary Artery Smooth Muscle Cells from Neonatal Mice

Published on: October 19, 2013

Area of Science:

Molecular Biology
Cardiovascular Research
Epigenetics

Background:

N6-methyladenosine (m⁶A) RNA modification and its regulators are implicated in pulmonary hypertension (PH) pathogenesis.
Ythdf2 (YTH N6-methyladenosine RNA binding protein 2) degrades m⁶A-modified mRNAs and is linked to PH and pulmonary artery smooth muscle cell (PASMC) proliferation.
The specific roles of Ythdf2 in PASMCs and its downstream targets in PH development require clarification.

Purpose of the Study:

To investigate the expression and function of Ythdf2 in PASMCs during PH.
To identify downstream targets of Ythdf2 in PASMCs in the context of PH.
To elucidate the molecular mechanisms by which Ythdf2 contributes to PH.

Main Methods:

Investigated Ythdf2 expression and function in human and rodent PH-PASMCs.
Utilized smooth muscle cell-specific Ythdf2-deficient mice for in vivo studies.
Employed proteomic analysis, m⁶A sequencing, and RNA immunoprecipitation to identify downstream targets.

Main Results:

Ythdf2 was upregulated in PH-PASMCs; its deficiency ameliorated PH development and PASMC proliferation.
Ythdf2 stabilized Myadm mRNA in an m⁶A-dependent manner, promoting PASMC proliferation and PH.
Loss of Ythdf2 decreased Myadm expression, and silencing Myadm inhibited Ythdf2-dependent PASMC hyperproliferation via p21 upregulation.

Conclusions:

Identified a novel m⁶A/Myadm/p21 pathway where increased Ythdf2 drives PH-PASMC proliferation.
Ythdf2 targeting in PASMCs presents a potential therapeutic strategy for pulmonary hypertension.