Abstract:
:It has been reported that haem oxygenase-1 (Hmox1) induction attenuates neointimal thickening. Here we further investigated the potential mechanisms regulating this important pathological process. We revealed that histone deacetylase 2 (HDAC2) was induced following Hmox1 induction under 1% oxygen treatment and this induction was attenuated after the treatment of siRNA against Hmox1. Interestingly, this HDAC2 induction was dependent on Hmox1 protein as well as its enzymatic activity, and was regulated by carbon monoxide released from haem degradation. Furthermore, histone deacetylase inhibitor, trichostatin A, successfully abrogated the inhibitory effects of vascular smooth muscle migration and proliferation by Hmox1 induction in vitro. In a rat carotid balloon injury model, similar results were observed by measuring neointimal thickening. As such, we concluded that Hmox1 inhibits neointimal hyperplasia via HDAC2 in rats.
journal_name
Free Radic Resjournal_title
Free radical researchauthors
Ni J,Yang W,Shen W,Zhang Rdoi
10.1080/10715762.2018.1524578subject
Has Abstractpub_date
2018-10-01 00:00:00pages
1110-1117issue
10eissn
1071-5762issn
1029-2470journal_volume
52pub_type
杂志文章abstract::We have reported previously that the apparent rate of peroxynitrite (ONOO(-) ) decay, as followed from its absorbance at 302 nm, decreases in the presence of hydrogen peroxide, mannitol and ethanol (Alvarez et al., 1995, Chem. Res. Toxicol. 8:859-864; Alvarez et al., 1998, Free Radic. Biol. Med. 24:1331-1337). Recentl...
journal_title:Free radical research
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journal_title:Free radical research
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journal_title:Free radical research
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journal_title:Free radical research
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pub_type: 杂志文章,评审
doi:10.3109/10715762.2011.574290
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