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Expression of Mipu1 in response to myocardial infarction in rats.

ABSTRACT: Myocardial ischemic preconditioning up-regulated protein 1 (Mipu1) was cloned in our laboratory. Male Wistar rats were subjected to left anterior coronary artery ligation and sham-operation and sacrificed at 1 h, 3 h, 6 h, 12 h, 24 h, 3 d or 5 d after ligation. Expression of Mipu1 mRNA and protein were assessed by Northern blotting, real-time quantitative RT-PCR, In Situ hybridization and Western blotting. Expression of Mipu1 was up-regulated at 3 h and lasted to 12 h with a peak at 6 h. Mipu1 mRNA and protein signals express in the endothelium and myocardium in normal and infarcted heart, mainly in infarcted zone. Fluorescent immunocytochemistry showed that Mipu1 protein was localized to the nuclei of H9c2 myogenic cells and was upregulated after the cells being exposed to H(2)O(2). These observations indicates that Mipu1 may play a role in maintaining vascular homeostasis and protecting the myogenic cells from being injured by ischemia-reperfusion or oxidation stress.

SUBMITTER: Wang G

PROVIDER: S-EPMC2660662 | biostudies-literature | 2009 Feb

REPOSITORIES: biostudies-literature

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Expression of Mipu1 in response to myocardial infarction in rats.

Wang Guiliang G Zuo Xiaoxia X Liu Junwen J Jiang Lei L Liu Ying Y Zheng Yazhu Y Zhang Bin B Xiao Xianzhong X

International journal of molecular sciences 20090203 2

Myocardial ischemic preconditioning up-regulated protein 1 (Mipu1) was cloned in our laboratory. Male Wistar rats were subjected to left anterior coronary artery ligation and sham-operation and sacrificed at 1 h, 3 h, 6 h, 12 h, 24 h, 3 d or 5 d after ligation. Expression of Mipu1 mRNA and protein were assessed by Northern blotting, real-time quantitative RT-PCR, In Situ hybridization and Western blotting. Expression of Mipu1 was up-regulated at 3 h and lasted to 12 h with a peak at 6 h. Mipu1 m ...[more]

PMID: 19333417

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Project description:Inflammation is associated with increased sympathetic drive in cardiovascular diseases. Blood-borne proinflammatory cytokines, markers of inflammation, induce cyclooxygenase 2 (COX-2) activity in perivascular macrophages of the blood-brain barrier. COX-2 generates prostaglandin E(2), which may enter the brain and increase sympathetic nerve activity. We examined the contribution of this mechanism to augmented sympathetic drive in rats after myocardial infarction (MI). Approximately 24 hours after acute MI, rats received an intracerebroventricular injection (1 microL/min over 40 minutes) of clodronate liposomes (MI+CLOD) to eliminate brain perivascular macrophages, liposomes alone, or artificial cerebrospinal fluid. A week later, COX-2 immunoreactivity in perivascular macrophages and COX-2 mRNA and protein had increased in hypothalamic paraventricular nucleus of MI rats treated with artificial cerebrospinal fluid or liposomes alone compared with sham-operated rats. In MI+CLOD rats, neither perivascular macrophages nor COX-2 immunoreactivity was seen in the paraventricular nucleus, and COX-2 mRNA and protein levels were similar to those in sham-operated rats. Prostaglandin E(2) in cerebrospinal fluid, paraventricular nucleus neuronal excitation, and plasma norepinephrine were less in MI+CLOD rats than in MI rats treated with artificial cerebrospinal fluid or liposomes alone but more than in sham-operated rats. Intracerebroventricular CLOD had no effect on interleukin 1beta and tumor necrosis factor-alpha mRNA and protein in the paraventricular nucleus or plasma interleukin-1beta and tumor necrosis factor-alpha, which were increased in MI compared with sham-operated rats. In normal rats, pretreatment with intracerebroventricular CLOD reduced (P<0.05) the renal sympathetic, blood pressure, and heart rate responses to intracarotid artery injection of tumor necrosis factor-alpha (0.5 microg/kg); intracerebroventricular liposomes had no effect. The results suggest that proinflammatory cytokines stimulate sympathetic excitation after MI by inducing COX-2 activity and prostaglandin E(2) production in perivascular macrophages of the blood-brain barrier.

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Expression of Mipu1 in response to myocardial infarction in rats.

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Expression of Mipu1 in response to myocardial infarction in rats.

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