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MiR-339 inhibits proliferation of pulmonary artery smooth muscle cell by targeting FGF signaling.

Physiol Rep. 2017 Sep;5(18)
Jidong Chen 1 , Xiaolei Cui 2 , Li Li 2 , Junle Qu 1 , J Usha Raj 3 , Deming Gou 4
Jidong Chen 1 , Xiaolei Cui 2 , Li Li 2 , Junle Qu 1 , J Usha Raj 3 , Deming Gou 4
+ et al

[No authors listed]

Author information
  • 1 Key Laboratory of Optoelectronic Devices, Systems of Ministry of Education and Guangdong Province, College of Optoelectronic Engineering, Shenzhen University, Shenzhen, Guangdong, China.
  • 2 Shenzhen Key Laboratory of Marine Bioresource and Eco-environmental Science, Shenzhen Key Laboratory of Microbial Genetic Engineering, College of Life Sciences, Shenzhen University, Shenzhen, Guangdong, China.
  • 3 Department of Pediatrics, University of Illinois at Chicago, Chicago, Illinois.
  • 4 Shenzhen Key Laboratory of Marine Bioresource and Eco-environmental Science, Shenzhen Key Laboratory of Microbial Genetic Engineering, College of Life Sciences, Shenzhen University, Shenzhen, Guangdong, China dmgou@szu.edu.cn.

摘要

Pulmonary artery hypertension (PAH) is a fatal disorder. Recent studies suggest that microRNA (miRNA) plays an important role in regulating proliferation of pulmonary artery smooth muscle cells (PASMC), which underlies the pathology of PAH However, the exact mechanism of action of miRNAs remains elusive. In this study, we found that miR-339 was highly expressed in the cardiovascular system and was downregulated by a group of cytokines and growth factors, especially PDGF-BB and FGF2. Functional analyses revealed that miR-339 can inhibit proliferation of PASMC Also, miR-339 inhibited FGF2-induced proliferation, but had no effect on proliferation induced by PDGF-BB The fibroblast growth factor receptor substrate 2 (FRS2) was identified as a potential direct target of miR-339. Consistent with the actions of miR-339, knockdown of FRS2 only inhibited FGF2- but not PDGF-BB-induced proliferation of PASMC In addition, our results showed that inhibition of ERK and PI3K abrogated the downregulation of miR-339 induced by PDGF-BB Finally, miR-339 expression was found to be decreased in the pulmonary arteries of rats with MCT-induced PAH Our study is the first report on the biological role of miR-339 in regulating proliferation of PASMC by targeting FGF signaling, providing new mechanistic insights into PASMC proliferation and pathogenesis of PAH.

KEYWORDS: PASMC , FGF2, FRS2, PDGF‐BB, miR‐339, proliferation

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