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http://purl.uniprot.org/citations/18567639http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/18567639http://www.w3.org/2000/01/rdf-schema#comment"

Aims

We showed previously that insulin-like growth factor-I (IGF-I)-induced vascular smooth muscle cells (VSMCs) proliferation through the production of reactive oxygen species (ROS). However, how IGF-I-induced ROS was unknown. The aim of this study is to investigate the mechanisms by which IGF-I induces ROS production in VSMCs. Methods results Reverse transcription-PCR, real-time PCR, immunoblotting, and confocal microscopic image analysis were employed to determine protein expression, small Rho-GTPase Rac1 activation, and ROS production. Inhibition of NADPH oxidase 4 (Nox4) or Rac1 was performed by means of siRNA technology. Inhibition of Rac1 activity was accomplished using dominant-negative form of Rac1 (N17Rac1) plasmid. VSMCs from Sprague-Dawley rat thoracic aortas were used in this work.IGF-I enhanced ROS production in rat VSMCs. IGF-I increased the protein level of Nox4 but had little effect on its mRNA level. IGF-I induced the activation of Rac1. Either knockdown of Nox4 or inactivation of Rac1 impaired IGF-I-induced ROS. Over-expression of Nox4 increased NADPH oxidase activity, which was not influenced by inactivation of Rac1. Neither over-expression nor knockdown of Rac1 influenced Nox4 expression. Knockdown of Nox4 did not affect IGF-I-induced activation of Rac1. IGF-I increased matrix metalloproteinase (MMP)-2 and 9 activity and promoted VSMC migration, which was inhibited by knockdown of Nox4 and inactivation of Rac1.

Conclusion

Our results suggest that Nox4 and Rac1 mediate IGF-I-induced ROS production and cell migration in VSMCs and that Nox4 is not regulated by Rac1."xsd:string
http://purl.uniprot.org/citations/18567639http://purl.org/dc/terms/identifier"doi:10.1093/cvr/cvn173"xsd:string
http://purl.uniprot.org/citations/18567639http://purl.uniprot.org/core/author"Fang J."xsd:string
http://purl.uniprot.org/citations/18567639http://purl.uniprot.org/core/author"Meng D."xsd:string
http://purl.uniprot.org/citations/18567639http://purl.uniprot.org/core/author"Lv D.D."xsd:string
http://purl.uniprot.org/citations/18567639http://purl.uniprot.org/core/date"2008"xsd:gYear
http://purl.uniprot.org/citations/18567639http://purl.uniprot.org/core/name"Cardiovasc Res"xsd:string
http://purl.uniprot.org/citations/18567639http://purl.uniprot.org/core/pages"299-308"xsd:string
http://purl.uniprot.org/citations/18567639http://purl.uniprot.org/core/title"Insulin-like growth factor-I induces reactive oxygen species production and cell migration through Nox4 and Rac1 in vascular smooth muscle cells."xsd:string
http://purl.uniprot.org/citations/18567639http://purl.uniprot.org/core/volume"80"xsd:string
http://purl.uniprot.org/citations/18567639http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/18567639
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