Heat shock protein 60 involvement in vascular smooth muscle cell proliferation

Kód výsledku v 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>

Výsledek na webu

<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>

Jazyk výsledku

angličtina

Název v původním jazyce

Heat shock protein 60 involvement in vascular smooth muscle cell proliferation

Popis výsledku v původním jazyce

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.

Název v anglickém jazyce

Heat shock protein 60 involvement in vascular smooth muscle cell proliferation

Popis výsledku anglicky

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.

Druh

J_imp - Článek v periodiku v databázi Web of Science

CEP obor

—

OECD FORD obor

30105 - Physiology (including cytology)

Projekt

—

Návaznosti

I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Rok uplatnění

2018

Kód důvěrnosti údajů

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

Název periodika

Cellular Signalling

ISSN

0898-6568

e-ISSN

—

Svazek periodika

47

Číslo periodika v rámci svazku

Jul

Stát vydavatele periodika

US - Spojené státy americké

Počet stran výsledku

8

Strana od-do

44-51

Kód UT WoS článku

000433643600005

EID výsledku v databázi Scopus

2-s2.0-85044588949