Počet záznamů: 1

Excitation-contraction coupling and excitation-transcription coupling in blood vessels: their possible interactions in hypertensive vascular remodeling

  1. 1.
    0461577 - FGU-C 2017 RIV CZ eng J - Článek v odborném periodiku
    Misárková, Eliška - Behuliak, Michal - Bencze, Michal - Zicha, Josef
    Excitation-contraction coupling and excitation-transcription coupling in blood vessels: their possible interactions in hypertensive vascular remodeling.
    Physiological Research. Roč. 65, č. 2 (2016), s. 173-191 ISSN 0862-8408
    Grant CEP: GA MZd(CZ) NV15-25396A
    Institucionální podpora: RVO:67985823
    Klíčová slova: vascular smooth muscle cells * contractile VSMC phenotype * proliferative VSMC phenotype * cell Ca2+ handling * intracellular signaling pathways
    Kód oboru RIV: FA - Kardiovaskulární nemoci vč. kardiochirurgie
    Impakt faktor: 1.461, rok: 2016

    Vascular smooth muscle cells (VSMC) display considerable phenotype plasticity which can be studied in vivo on vascular remodeling which occurs during acute or chronic vascular injury. In differentiated cells, which represent contractile phenotype, there are characteristic rapid transient changes of intracellular Ca2+ concentration ([Ca2+]i), while the resting cytosolic [Ca2+]i concentration is low. It is mainly caused by two components of the Ca2+ signaling pathways: Ca2+ entry via L-type voltagedependent Ca2+ channels and dynamic involvement of intracellular stores. Proliferative VSMC phenotype is characterized by long-lasting [Ca2+]i oscillations accompanied by sustained elevation of basal [Ca2+]i. During the switch from contractile to proliferative phenotype there is a general transition from voltagedependent Ca2+ entry to voltage-independent Ca2+ entry into the cell. These changes are due to the altered gene expression which is dependent on specific transcription factors activated by various stimuli. It is an open question whether abnormal VSMC phenotype reported in rats with genetic hypertension (such as spontaneously hypertensive rats) might be partially caused by a shift from contractile to proliferative VSMC phenotype.
    Trvalý link: http://hdl.handle.net/11104/0261188