title: Ischemia/reperfusion in rat heart induces leptin and leptin receptor gene expression.
abstract: Concentrations of leptin, an adipocyte-derived hormone, are elevated in obesity. Recently, leptin has been shown to participate in multiple biological actions including inflammation, reproduction, and angiogenesis. Leptin has also been documented as a critical component in the process of wound healing; however, leptin involvement in cardiovascular disease is poorly understood. We examined the expression of leptin (ob) and leptin receptor (ob-R) genes in the rat heart following ischemia/reperfusion, which was induced by coronary artery ligation, and mRNA was obtained from hearts 0.5 to 36 h after initiating reperfusion. Expressions of ob and ob-R mRNA were examined by real-time quantitative RT-PCR and immunohistochemistry. The ob and ob-Ra mRNA and protein expressions were significantly increased (p<0.01) and ob-Rb mRNA was significantly decreased (p<0.01) in hearts after 8 h of reperfusion. Furthermore, ob and ob-R proteins were expressed in injured myocytes where inflammatory cells infiltrated. In contrast, those expressions were not influenced in hearts after 8 h of ischemia stress only. To determine the functional effects of leptin on the ischemic/reperfused heart, rats were treated with anti-leptin antibodies prior to ischemia/reperfusion; however, this treatment did not affect the elevation of mRNA expression levels of inflammatory markers such as TNF-alpha and IL-1beta in ischemic hearts. Our results demonstrated for the first time that ischemia/reperfusion induced leptin and leptin receptor gene expression in the rat heart. This study helps to elucidate the mechanisms behind the onset and development of ischemic heart disease concomitant with obesity.
authors.affiliation: Department of Laboratory Sciences, Gunma University School of Health Sciences, 3-39-22, Showa-machi, Maebashi, 371-8511, Japan.
authors.forename: Hiroki
authors.initials: H
authors.lastname: Matsui
authors.forename: Masahiko
authors.initials: M
authors.lastname: Motooka
authors.forename: Hiroto
authors.initials: H
authors.lastname: Koike
authors.forename: Masahiro
authors.initials: M
authors.lastname: Inoue
authors.forename: Tsutomu
authors.initials: T
authors.lastname: Iwasaki
authors.forename: Tadashi
authors.initials: T
authors.lastname: Suzuki
authors.forename: Masahiko
authors.initials: M
authors.lastname: Kurabayashi
authors.forename: Tomoyuki
authors.initials: T
authors.lastname: Yokoyama
mesh_terms: D000818:Animals; D019138:Antibodies, Blocking / Q000494:pharmacology; D004359:Drug Therapy, Combination; D005786:Gene Expression Regulation / Q000187:drug effects / Q000235:genetics*; D006321:Heart / Q000187:drug effects / Q000503:physiopathology; D007150:Immunohistochemistry; D053583:Interleukin-1beta / Q000235:genetics / Q000378:metabolism; D020738:Leptin / Q000235:genetics* / Q000276:immunology / Q000378:metabolism; D008297:Male; D015428:Myocardial Reperfusion Injury / Q000235:genetics* / Q000378:metabolism / Q000473:pathology; D009206:Myocardium / Q000378:metabolism / Q000473:pathology; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D011956:Receptors, Cell Surface / Q000235:genetics* / Q000378:metabolism; D054411:Receptors, Leptin; D020133:Reverse Transcriptase Polymerase Chain Reaction; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics / Q000378:metabolism
chemical_list: D019138:Antibodies, Blocking; D053583:Interleukin-1beta; D020738:Leptin; D012333:RNA, Messenger; D011956:Receptors, Cell Surface; D054411:Receptors, Leptin; D014409:Tumor Necrosis Factor-alpha