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Intracerebral hemorrhage (ICH) causes long term neurological abnormality or death. Oxidative stress is closely involved in ICH mediated brain damage. Steroid receptor cofactor 3 (SRC-3), a p160 family member, is widely expressed in the brain and regulates transactivation of Nrf2, a key component of antioxidant response. Our study aims to test if SRC-3 is implicated in ICH mediated brain injury. We first examined levels of SRC-3 and oxidative stress in the brain of mice following ICH and analyzed their correlation. Then ICH was induced in wild type (WT) and SRC-3 knock out mice and how SRC-3 deletion affected ICH induced brain damage, oxidative stress and behavioral outcome was assessed. We found that SRC-3 mRNA and protein expression levels were reduced gradually after ICH induction in WT mice along with an increase in oxidative stress levels. Correlation analysis revealed that SRC-3 mRNA levels negatively correlated with oxidative stress. Deletion of SRC-3 further increased ICH induced brain edema, neurological deficit score and oxidative stress and exacerbated ICH induced behavioral abnormality including motor dysfunction and cognitive impairment. Our findings suggest that SRC-3 is involved in ICH induced brain injury, probably through modulation of oxidative stress.
相似文献Long non-coding RNA (lncRNA) represents a new direction to identify expression profiles and regulatory mechanisms in various organisms. Here, we report the first dataset of lncRNAs of the golden snub-nosed monkey (GSM), including 12,557 putative lncRNAs identified from seven organs. Compared with mRNA, GSM lncRNA had fewer exons and isoforms, and longer length. LncRNA showed more obvious tissue-specific expression than mRNA. However, for the top ten most abundant genes in each organ, mRNAs expression was more tissue-specific than lncRNAs. By identification of specifically expressed lncRNAs and mRNAs in each organ, it indicates that the expression of SEG-lncRNA (specifically expressed lncRNA) and SEG-mRNA (specifically expressed mRNA) had high correlation. In particular, combined our lncRNA and mRNA data, we identified 92 heart SEG-lncRNAs targeted ten mRNA genes in the oxidative phosphorylation pathway and upregulated the expression of these target genes such as ND4, ATP6, and ATP8. These may contribute to GSM adaption to its high-elevation environment. We also identified 171 liver SEG-lncRNAs, which targeted 27 genes associated with the metabolism of xenobiotics and leaded to high expression of these target genes in liver. These lncRNAs may play important roles in GSM adaptation to a folivory diet.
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