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
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Czech description
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Classification
Type
J<sub>imp</sub> - Article in a specialist periodical, which is included in the Web of Science database
CEP classification
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OECD FORD branch
30105 - Physiology (including cytology)
Result continuities
Project
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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
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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