Role of PKCδ in Enhanced Expression of Gqα/PLCβ1 Proteins and VSMC Hypertrophy in Spontaneously Hypertensive Rats
Identifieur interne : 000208 ( Main/Exploration ); précédent : 000207; suivant : 000209Role of PKCδ in Enhanced Expression of Gqα/PLCβ1 Proteins and VSMC Hypertrophy in Spontaneously Hypertensive Rats
Auteurs : Mohammed Emehdi Atef ; Madhu B. Anand-SrivastavaSource :
- PLoS ONE [ 1932-6203 ] ; 2016.
Abstract
Gqα signaling has been implicated in cardiac hypertrophy. In addition, angiotensin II (Ang II) was also shown to induce its hypertrophic effect through Gqα and PKCδ activation. We recently showed the role of enhanced expression of Gqα/PLCβ1 proteins in vascular smooth muscle cell (VSMC) hypertrophy, however, the role of PKCδ in VSMC hypertrophy in animal model is still lacking. The present study was therefore undertaken to examine the role of PKCδ and the associated signaling mechanisms in VSMC hypertrophy using 16-week-old spontaneously hypertensive rats (SHR). VSMC from 16-week-old SHR exhibited enhanced phosphorylation of PKCδ-Tyr311 and increased protein synthesis, marker of hypertrophy, as compared to WKY rats which was attenuated by rottlerin, an inhibitor of PKCδ. In addition, knocking down of PKCδ by PKCδ-siRNA also attenuated enhanced protein synthesis in VSMC from SHR. Furthermore, rottlerin attenuated the increased production of superoxide anion, NAD(P)H oxidase activity, increased expression of Gqα, phospholipase C (PLC)β1, insulin like growth factor-1 receptor (IGF-1R) and epidermal growth factor receptor (EGFR) proteins in VSMC from SHR. In addition, the enhanced phosphorylation of c-Src, PKCδ-Tyr311, IGF-1R, EGFR and ERK1/2 exhibited by VSMC from SHR was also attenuated by rottlerin. These results suggest that VSMC from SHR exhibit enhanced activity of PKCδ and that PKCδ is the upstream molecule of reactive oxygen species (ROS) and contributes to the enhanced expression of Gqα and PLCβ1 proteins and resultant VSMC hypertrophy involving c-Src, growth factor receptor transactivation and MAP kinase signaling.
Url:
DOI: 10.1371/journal.pone.0157955
PubMed: 27379421
PubMed Central: 4933357
Affiliations:
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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Role of PKCδ in Enhanced Expression of Gqα/PLCβ1 Proteins and VSMC Hypertrophy in Spontaneously Hypertensive Rats</title><author><name sortKey="Atef, Mohammed Emehdi" sort="Atef, Mohammed Emehdi" uniqKey="Atef M" first="Mohammed Emehdi" last="Atef">Mohammed Emehdi Atef</name><affiliation><nlm:aff id="aff001"></nlm:aff></affiliation></author><author><name sortKey="Anand Srivastava, Madhu B" sort="Anand Srivastava, Madhu B" uniqKey="Anand Srivastava M" first="Madhu B." last="Anand-Srivastava">Madhu B. Anand-Srivastava</name><affiliation><nlm:aff id="aff001"></nlm:aff></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">27379421</idno><idno type="pmc">4933357</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4933357</idno><idno type="RBID">PMC:4933357</idno><idno type="doi">10.1371/journal.pone.0157955</idno><date when="2016">2016</date><idno type="wicri:Area/Pmc/Corpus">000159</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">000159</idno><idno type="wicri:Area/Pmc/Curation">000159</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Curation">000159</idno><idno type="wicri:Area/Pmc/Checkpoint">000063</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Checkpoint">000063</idno><idno type="wicri:Area/Ncbi/Merge">002019</idno><idno type="wicri:Area/Ncbi/Curation">002019</idno><idno type="wicri:Area/Ncbi/Checkpoint">002019</idno><idno type="wicri:Area/Main/Merge">000208</idno><idno type="wicri:Area/Main/Curation">000208</idno><idno type="wicri:Area/Main/Exploration">000208</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Role of PKCδ in Enhanced Expression of Gqα/PLCβ1 Proteins and VSMC Hypertrophy in Spontaneously Hypertensive Rats</title><author><name sortKey="Atef, Mohammed Emehdi" sort="Atef, Mohammed Emehdi" uniqKey="Atef M" first="Mohammed Emehdi" last="Atef">Mohammed Emehdi Atef</name><affiliation><nlm:aff id="aff001"></nlm:aff></affiliation></author><author><name sortKey="Anand Srivastava, Madhu B" sort="Anand Srivastava, Madhu B" uniqKey="Anand Srivastava M" first="Madhu B." last="Anand-Srivastava">Madhu B. Anand-Srivastava</name><affiliation><nlm:aff id="aff001"></nlm:aff></affiliation></author></analytic><series><title level="j">PLoS ONE</title><idno type="eISSN">1932-6203</idno><imprint><date when="2016">2016</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>Gqα signaling has been implicated in cardiac hypertrophy. In addition, angiotensin II (Ang II) was also shown to induce its hypertrophic effect through Gqα and PKCδ activation. We recently showed the role of enhanced expression of Gqα/PLCβ1 proteins in vascular smooth muscle cell (VSMC) hypertrophy, however, the role of PKCδ in VSMC hypertrophy in animal model is still lacking. The present study was therefore undertaken to examine the role of PKCδ and the associated signaling mechanisms in VSMC hypertrophy using 16-week-old spontaneously hypertensive rats (SHR). VSMC from 16-week-old SHR exhibited enhanced phosphorylation of PKCδ-Tyr<sup>311</sup> and increased protein synthesis, marker of hypertrophy, as compared to WKY rats which was attenuated by rottlerin, an inhibitor of PKCδ. In addition, knocking down of PKCδ by PKCδ-siRNA also attenuated enhanced protein synthesis in VSMC from SHR. Furthermore, rottlerin attenuated the increased production of superoxide anion, NAD(P)H oxidase activity, increased expression of Gqα, phospholipase C (PLC)β1, insulin like growth factor-1 receptor (IGF-1R) and epidermal growth factor receptor (EGFR) proteins in VSMC from SHR. In addition, the enhanced phosphorylation of c-Src, PKCδ-Tyr<sup>311</sup>, IGF-1R, EGFR and ERK1/2 exhibited by VSMC from SHR was also attenuated by rottlerin. These results suggest that VSMC from SHR exhibit enhanced activity of PKCδ and that PKCδ is the upstream molecule of reactive oxygen species (ROS) and contributes to the enhanced expression of Gqα and PLCβ1 proteins and resultant VSMC hypertrophy involving c-Src, growth factor receptor transactivation and MAP kinase signaling.</p></div></front><back><div1 type="bibliography"><listBibl><biblStruct><analytic><author><name sortKey="Korsgaard, N" uniqKey="Korsgaard N">N Korsgaard</name></author><author><name sortKey="Aalkjaer, C" uniqKey="Aalkjaer C">C Aalkjaer</name></author><author><name sortKey="Heagerty, Am" uniqKey="Heagerty A">AM Heagerty</name></author><author><name sortKey="Izzard, As" uniqKey="Izzard A">AS Izzard</name></author><author><name sortKey="Mulvany, Mj" uniqKey="Mulvany M">MJ Mulvany</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Atef, Me" uniqKey="Atef M">ME Atef</name></author><author><name sortKey="Anand Srivastava, Mb" 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Q">QW Chen</name></author><author><name sortKey="Edvinsson, L" uniqKey="Edvinsson L">L Edvinsson</name></author><author><name sortKey="Xu, Cb" uniqKey="Xu C">CB Xu</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Zhang, D" uniqKey="Zhang D">D Zhang</name></author><author><name sortKey="Anantharam, V" uniqKey="Anantharam V">V Anantharam</name></author><author><name sortKey="Kanthasamy, A" uniqKey="Kanthasamy A">A Kanthasamy</name></author><author><name sortKey="Kanthasamy, Ag" uniqKey="Kanthasamy A">AG Kanthasamy</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Maioli, E" uniqKey="Maioli E">E Maioli</name></author><author><name sortKey="Torricelli, C" uniqKey="Torricelli C">C Torricelli</name></author><author><name sortKey="Valacchi, G" uniqKey="Valacchi G">G Valacchi</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Ringshausen, I" uniqKey="Ringshausen I">I Ringshausen</name></author><author><name sortKey="Oelsner, M" uniqKey="Oelsner M">M Oelsner</name></author><author><name sortKey="Weick, K" uniqKey="Weick K">K Weick</name></author><author><name sortKey="Bogner, C" uniqKey="Bogner C">C Bogner</name></author><author><name sortKey="Peschel, C" uniqKey="Peschel C">C Peschel</name></author><author><name sortKey="Decker, T" uniqKey="Decker T">T Decker</name></author></analytic></biblStruct></listBibl></div1></back></TEI><affiliations><list></list><tree><noCountry><name sortKey="Anand Srivastava, Madhu B" sort="Anand Srivastava, Madhu B" uniqKey="Anand Srivastava M" first="Madhu B." last="Anand-Srivastava">Madhu B. Anand-Srivastava</name><name sortKey="Atef, Mohammed Emehdi" sort="Atef, Mohammed Emehdi" uniqKey="Atef M" first="Mohammed Emehdi" last="Atef">Mohammed Emehdi Atef</name></noCountry></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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