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Vascular smooth muscle cell phenotype is defined by C a 2+ ‐dependent transcription factors
Author(s) -
Kudryavtseva Olga,
Aalkjær Christian,
Matchkov Vladimir V.
Publication year - 2013
Publication title -
the febs journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.981
H-Index - 204
eISSN - 1742-4658
pISSN - 1742-464X
DOI - 10.1111/febs.12414
Subject(s) - vascular smooth muscle , microbiology and biotechnology , transcription factor , biology , intracellular , phenotype , angiogenesis , extracellular , transcription (linguistics) , gene , endocrinology , biochemistry , genetics , smooth muscle , linguistics , philosophy
C a 2+ is an important second messenger in vascular smooth muscle cells ( VSMC s). Therefore, VSMC s exercise tight control of the intracellular Ca 2+ concentration ([Ca 2+ ] i ) by expressing a wide repertoire of Ca 2+ channels and transporters. The presence of several pathways for Ca 2+ influx and efflux provides many possibilities for controlling [Ca 2+ ] i in a spatial and temporal manner. Intracellular Ca 2+ has a dual role in VSMC s; first, it is necessary for VSMC contraction; and, second, it can activate multiple transcription factors. These factors are c AMP response element‐binding protein, nuclear factor of activated T lymphocytes, and serum response factor. Furthermore, it was recently reported that the C ‐terminus of voltage‐dependent L ‐type C a 2+ calcium channels can regulate transcription in VSMC s. Transcription regulation in VSMC s modulates the expression patterns of genes, including genes coding for contractile and cytoskeleton proteins, and those promoting proliferation and cell growth. Depending on their gene expression, VSMC s can exist in different functional states or phenotypes. The majority of healthy VSMC s show a contractile phenotype, characterized by high contractile ability and a low proliferative rate. However, VSMC s can undergo phenotypic modulation with different physiological and pathological stimuli, whereby they start to proliferate, migrate, and synthesize excessive extracellular matrix. These events are associated with injury repair and angiogenesis, but also with the development of cardiovascular pathologies, such as atherosclerosis and hypertension. This review discusses the currently known Ca 2+ ‐dependent transcription factors in VSMC s, their regulation by Ca 2+ signalling, and their role in the VSMC phenotype.