@article{TEXTUAL,
      recid = {8833},
      author = {Maruhashi, Tatsuya and Noma, Kensuke and Iwamoto, Yumiko  and Iwamoto, Akimichi and Oda, Nozomu and Kajikawa, Masato  and Matsumoto, Takeshi and Hidaka, Takayuki and Kihara,  Yasuki and Chayama, Kazuaki and Nakashima, Ayumu and Goto,  Chikara and Liao, James K. and Higashi, Yukihito},
      title = {Critical Role of Exogenous Nitric Oxide in ROCK Activity  in Vascular Smooth Muscle Cells},
      journal = {PLOS ONE},
      address = {2014-10-03},
      number = {TEXTUAL},
      abstract = {&lt;p&gt;Objective: Rho-associated kinase (ROCK) signaling  pathway has been shown to mediate various cellular  functions including cell proliferation, migration,  adhesion, apoptosis, and contraction, all of which may be  involved in pathogenesis of atherosclerosis. Endogenous  nitric oxide (NO) is well known to have an  anti-atherosclerotic effect, whereas the exogenous  NO-mediated cardiovascular effect still remains  controversial. The purpose of this study was to evaluate  the effect of exogenous NO on ROCK activity in vascular  smooth muscle cells (VSMCs) in vitro and in  vivo.&lt;/p&gt;&lt;p&gt;Methods: VSMCs migration was evaluated using a  modified Boyden chamber assay. ROCK activities were  measured by Western blot analysis in murine and human VSMCs  and aorta of mice treated with or without angiotensin II  (Ang II) and/or sodium nitroprusside (SNP), an NO  donor.&lt;/p&gt;&lt;p&gt;Results: Co-treatment with SNP inhibited the  Ang II-induced cell migration and increases in ROCK  activity in murine and human VSMCs. Similarly, the  increased ROCK activity 2 weeks after Ang II infusion in  the mouse aorta was substantially inhibited by subcutaneous  injection of SNP.&lt;/p&gt;&lt;p&gt;Conclusions: These findings suggest  that administration of exogenous NO can inhibit ROCK  activity in VSMCs in vitro and in vivo.&lt;/p&gt;},
      url = {http://knowledge.uchicago.edu/record/8833},
}