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Target of selective cyclic nucleotide phosphodiesterases differentially regulates arterial myocyte migration (1065.3)
Author(s) -
Brzezinska Paulina,
Hubert Fabien,
Rampersad Sarah,
Wudwud Alie,
Freitag Silja,
Umana M,
Maurice Donald
Publication year - 2014
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.28.1_supplement.1065.3
Subject(s) - microbiology and biotechnology , regulator , phosphodiesterase , cell migration , vascular smooth muscle , myocyte , cardiac myocyte , biology , chemistry , medicine , endocrinology , in vitro , biochemistry , gene , enzyme , smooth muscle
Vascular myocyte (VSMC) migration is a vital process allowing for the regulation of vascular development, tissue repair and the modulation of pathophysiological conditions including atherosclerosis. Atherosclerosis induced damage to the vascular endothelium results in medial VSMC migration into the intima to promote vessel repair. If unregulated, it may exacerbate atherosclerosis related stenosis. cAMP is a regulator of VSMC migration and cAMP‐elevating agents inhibit VSMC migration in vitro and reduce neointimal thickening in vivo. However, these agents promote the formation of integrin‐based adhesions and leading edge structures, which are necessary events for directional cellular migration. The localization of several distinct pools of cAMP generated by distinct cyclic nucleotide phosphodiesterases (PDEs) may explain the differential effects of VSMC migration regulated by cAMP. We used a modified migration assay to visualize and quantitate the formation of leading edge structures by VSMCs during migration. Here, we report differential migration related effects through the target of selective cAMP pools generated by distinct PDEs. Grant Funding Source : Canadian Institutes of Health Research