Intermedin is upregulated and has protective roles in a mouse ischemia/reperfusion model
| Autor: | Wei Jiang, Jian-Ying Liu, Hong-Bo Xin, Chun-Lin Chen, De-Jia Huang, Heng-Yu Zhang, Yan Li |
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| Rok vydání: | 2009 |
| Předmět: |
Male
medicine.medical_specialty Physiology Molecular Sequence Data Myocardial Infarction Ischemia Blood Pressure Myocardial Reperfusion Injury RAMP1 Gene Mice Heart Rate Internal medicine Internal Medicine medicine Animals Amino Acid Sequence Creatine Kinase Receptor activity-modifying protein L-Lactate Dehydrogenase biology Reverse Transcriptase Polymerase Chain Reaction business.industry Neuropeptides CALCRL medicine.disease Immunohistochemistry Cytoprotection Up-Regulation Mice Inbred C57BL Endocrinology Neutrophil Infiltration RAMP2 Calcitonin biology.protein Creatine kinase Cardiology and Cardiovascular Medicine business |
| Zdroj: | Hypertension Research. 32:861-868 |
| ISSN: | 1348-4214 0916-9636 |
| DOI: | 10.1038/hr.2009.120 |
| Popis: | Intermedin (IMD), a new calcitonin/calcitonin gene-related peptide family peptide with vasodilatory and positive inotropic properties, has multiple functions in regulating cardiovascular homeostasis and is of particular interest in the pathophysiology of myocardial ischemia/reperfusion (MI/R). We created a mouse model of MI/R by ligating the cardiac left anterior descending artery to study the possible pathophysiological role of IMD and its receptor complexes in MI/R. Compared with the control, infarcted mice showed increased content, mRNA and protein expression of IMD in plasma and cardiac tissue. The mRNA expression of the receptor activity-modifying protein 3 (RAMP3) gene increased very early, and the calcitonin receptor-like receptor and RAMP2 mRNA levels increased later after reperfusion. However, the RAMP1 gene expression did not change. The tissue IMD content was positively correlated with the diastolic blood pressure and negatively correlated with pulse pressure. In addition, exogenous IMD treatment significantly ameliorated the MI/R injury by rescuing the pulse pressure, inhibiting neutrophil infiltration in the peri-infarction area, and decreasing the creatine kinase and lactate dehydrogenase activities in plasma. Our results indicated that IMD was upregulated in the ischemic myocardium and may induce important beneficial cytoprotection against cardiac ischemic injury. |
| Databáze: | OpenAIRE |
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