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Heat shock protein 60 involvement in vascular smooth muscle cell proliferation

The result's identifiers

  • Result code in IS VaVaI

    <a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F67985823%3A_____%2F18%3A00489952" target="_blank" >RIV/67985823:_____/18:00489952 - isvavai.cz</a>

  • Result on the web

    <a href="http://dx.doi.org/10.1016/j.cellsig.2018.03.011" target="_blank" >http://dx.doi.org/10.1016/j.cellsig.2018.03.011</a>

  • DOI - Digital Object Identifier

    <a href="http://dx.doi.org/10.1016/j.cellsig.2018.03.011" target="_blank" >10.1016/j.cellsig.2018.03.011</a>

Alternative languages

  • Result language

    angličtina

  • Original language name

    Heat shock protein 60 involvement in vascular smooth muscle cell proliferation

  • Original language description

    Heat shock protein 60 (Hsp60) is a mediator of stress-induced vascular smooth muscle cell (VSMC) proliferation. This study will determine, first, if the mitochondrial or cytoplasmic localization of Hsp60 is critical to VSMC proliferation and, second, the mechanism of Hsp60 induction of VSMC proliferation with a focus on modification of nucleocytoplasmic trafficking. Hsp60 was overexpressed in primary rabbit VSMCs with or without a mitochondrial targeting sequence (AdHsp60(mito-)). Both interventions induced an increase in VSMC PCNA expression and proliferation. The increase in VSMC PCNA expression and growth was not observed after siRNA-mediated knockdown of Hsp60 expression. Nuclear protein import in VSMC was measured by fluorescent microscopy using a microinjected fluorescent import substrate. Nuclear protein import was stimulated by both AdHsp60 and AdHsp60(mito-) treatments. AdHsp60 treatment also induced increases in nucleoporin (Nup) 62, Nup153, importin-alpha, importin-beta and Ran expression as well as cellular ATP levels compared to control. AdHsp60(mito-) treatment induced an up-regulation in importin-alpha, importing) and Ran expression compared to control. Hsp60 knockdown did not change nuclear protein import nor the expression of any nuclear transport receptors or nucleoporins. Both heat shock treatment and Hsp60 overexpression promoted the interaction of Ran with Hsp60. VSMC proliferation can be modulated via an Hsp60 dependent, cytosol localized mechanism that in part involves a stimulation of nuclear protein import through an interaction with Ran. This novel cellular signaling role for Hsp60 may be important in growth-based vascular pathologies like atherosclerosis and hypertension.

  • Czech name

  • Czech description

Classification

  • Type

    J<sub>imp</sub> - Article in a specialist periodical, which is included in the Web of Science database

  • CEP classification

  • OECD FORD branch

    30105 - Physiology (including cytology)

Result continuities

  • Project

  • Continuities

    I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Others

  • Publication year

    2018

  • Confidentiality

    S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Data specific for result type

  • Name of the periodical

    Cellular Signalling

  • ISSN

    0898-6568

  • e-ISSN

  • Volume of the periodical

    47

  • Issue of the periodical within the volume

    Jul

  • Country of publishing house

    US - UNITED STATES

  • Number of pages

    8

  • Pages from-to

    44-51

  • UT code for WoS article

    000433643600005

  • EID of the result in the Scopus database

    2-s2.0-85044588949