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Characterization of smooth muscle microRNA and mRNA genes that are regulated by actin polymerization
Author(s) -
Albinsson Sebastian,
Turczynska Karolina,
Swärd Karl,
Hellstrand Per
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.922.7
Subject(s) - calponin , tropomyosin , actin , myosin , microrna , microbiology and biotechnology , biology , phenotype , gene expression , myosin light chain kinase , gene , chemistry , genetics
The phenotype of vascular smooth muscle cells is regulated by multiple environmental cues including mechanical stretch. We have previously demonstrated that stretch‐induced actin polymerization is an important event for the expression of smooth muscle markers. The aim of this study was to characterize mRNA/proteins and microRNAs (miRNAs) that are regulated by actin polymerization to evaluate the role of this control mechanism for phenotypic modulation and vascular disease. Affymetrix chip gene arrays as well as miScript pathway focused miRNA PCR arrays were performed on smooth muscle cells treated with jasplakinolide, which stabilizes actin filaments. As expected a number of well‐known smooth muscle markers including calponin (Cnn1), myosin heavy chain (Myh11) and tropomyosin (Tpm2) were significantly up‐regulated by jasplakinolide treatment. We also confirmed that transcription of the newly identified smooth muscle markers Lmod1 and Kcnmb1 was induced by actin polymerization. In addition, our array data revealed a number of genes and miRNAs that were significantly affected by actin polymerization but which have not been previously identified as markers of the contractile smooth muscle phenotype. In conclusion, this study will lead to a better understanding of the regulation and importance of contractile smooth muscle markers and phenotypic modulation in the vasculature.