Abstract

Our previous work has demonstrated that the cellular phenotype changes of human pulmonary artery smooth muscle cells (PASMCs) play an important role during pulmonary vascular remodelling. However, little is known about the role of PASMCs phenotype modulation in the course of hypoxia-induced migration and its behind molecular mechanisms. In this study, we have shown that cGMP-dependent protein kinase (PKG) Iα transfection significantly attenuated the hypoxia-induced down-regulation of the expressions of SM-α-actin, MHC and calponin. Hypoxia-induced PASMC migration was also suppressed by PKGIα overexpression. Furthermore, this overexpression attenuated ANX A1 upregulation under hypoxic conditions. All those effects were reversed by a PKG inhibitor KT5823. Our data indicate that manipulating upstream entity e.g., PKGIa, may have a potential therapeutic value to prevent hypoxia-associated pulmonary arterial remodeling for pulmonary hypertension development.

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Publisher Full Text

Authors

Yi B, Cui J, Ning J, Gu J, Wang G, Bai L, Qian G, Lu K

Institution

Department of Anesthesia, Southwest Hospital, The Third Military Medical University, Chongqing 400038, China.

Source

Biochemical and biophysical research communications 418:4 2012 Feb 24 pg 598-602

MeSH

Actins
Annexin A1
Calcium-Binding Proteins
Cell Hypoxia
Cell Movement
Cells, Cultured
Cyclic GMP-Dependent Protein Kinases
Down-Regulation
Humans
Hypertension, Pulmonary
Microfilament Proteins
Myocytes, Smooth Muscle
Myosin Heavy Chains
Pulmonary Artery
Transfection

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

22293199