期刊
AMERICAN JOURNAL OF OBSTETRICS AND GYNECOLOGY
卷 199, 期 1, 页码 -出版社
MOSBY-ELSEVIER
DOI: 10.1016/j.ajog.2007.12.004
关键词
cytokines; fetal guinea pig heart; intrauterine hypoxia; MMP
资金
- NHLBI NIH HHS [R01 HL49999, R01 HL049999] Funding Source: Medline
OBJECTIVE: Intrauterine infection increases proinflammatory cytokines in the fetus. We hypothesize that proinflammatory cytokines and matrix metalloproteinases (MMPs) are upregulated in fetal hearts in response to hypoxic stress. STUDY DESIGN: Timed-pregnant guinea pigs were exposed to either hypoxia (10.5% O-2, 14 day) or normoxia (room air). Left ventricles of fetal hearts were excised from anesthetized age-matched fetuses and frozen until ready for study. Messenger RNA of pro- (TNF-alpha, IL-6, IL-1 beta) and anti- (IL-4, TGF, IFN-gamma) inflammatory cytokines and MMP2 and 9 was quantified by real-time PCR, MMP proteins by Western analysis, and MMP activity by gel zymography. RESULTS: Chronic hypoxia increased (P < .05) TNF-alpha, IL-6, MMP2, and MMP9 mRNA levels but not IL-4, TGF, or IFN-gamma. Hypoxia increased protein levels of MMP9 but not MMP2, despite a hypoxia-induced increase in MMP2 activity. CONCLUSION: Intrauterine hypoxia may be an important stimulus in local generation of selected proinflammatory cytokines and MMPs in fetal hearts.
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