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Titolo:
NHE and ICAM-1 expression in hypoxic/reoxygenated coronary microvascular endothelial cells
Autore:
Hattori, R; Otani, H; Moriguchi, Y; Matsubara, H; Yamamura, T; Nakao, Y; Omiya, H; Osako, M; Imamura, H;
Indirizzi:
Kansai Med Univ, Dept Thorac & Cardiovasc Surg, Moriguchi, Osaka 5708507, Japan Kansai Med Univ Moriguchi Osaka Japan 5708507 guchi, Osaka 5708507, Japan Kansai Med Univ, Dept Internal Med, Moriguchi, Osaka 5708507, Japan KansaiMed Univ Moriguchi Osaka Japan 5708507 guchi, Osaka 5708507, Japan
Titolo Testata:
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY
fascicolo: 6, volume: 280, anno: 2001,
pagine: H2796 - H2803
SICI:
0363-6135(200106)280:6<H2796:NAIEIH>2.0.ZU;2-M
Fonte:
ISI
Lingua:
ENG
Soggetto:
INTERCELLULAR-ADHESION MOLECULE-1; VASCULAR SMOOTH-MUSCLE; MYOCARDIAL-ISCHEMIA; ANGIOTENSIN-II; E-SELECTIN; EXCHANGE; INHIBITION; HEART; REPERFUSION; CALCIUM;
Keywords:
myocardial ischemia-reperfusion; intracellular pH; intracellular Ca2+; intercellular adhesion molecule-1;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
29
Recensione:
Indirizzi per estratti:
Indirizzo: Otani, H Kansai Med Univ, Dept Thorac & Cardiovasc Surg, 10-15 Fumizono Cho, Moriguchi, Osaka 5708507, Japan Kansai Med Univ 10-15 Fumizono Cho Moriguchi Osaka Japan 5708507
Citazione:
R. Hattori et al., "NHE and ICAM-1 expression in hypoxic/reoxygenated coronary microvascular endothelial cells", AM J P-HEAR, 280(6), 2001, pp. H2796-H2803

Abstract

Although Na+/H+ exchange (NHE) has been implicated in myocardial reperfusion injury, participation of coronary microvascular endothelial cells (CMECs) in this pathogenesis has been poorly understood. NHE-induced intracellular Ca2+ concentration ([Ca2+](i)) overload in CMECs may increase the synthesis of intercellular adhesion molecules (ICAM), which is potentially involved in myocardial reperfusion injury. The present study tested the hypothesisthat NHE plays a crucial role in [Ca2+](i) overload and ICAM-1 synthesis in CMECs. Primary cultures of CMECs isolated from adult rat hearts were subjected to acidic hypoxia for 30 min followed by reoxygenation. Two structurally distinct NHE inhibitors, cariporide and 5-(N-N-dimethyl)-amiloride (DMA), had no significant effect on the acidic hypoxia-induced decrease in intracellular pH (pH(i)) of CMECs but significantly retarded pH(i) recovery after reoxygenation. These NHE inhibitors abolished the hypoxia- and reoxygenation-induced increase in [Ca2+](i). Expression of ICAM-1 mRNA was markedly increased in the vehicle-treated CMECs 3 h after reoxygenation, and this was significantly inhibited by treatment with cariporide, DMA, or Ca2+-free buffer. In addition, enhanced ICAM-I protein expression on the cell surface of CMECs 8 h after reoxygenation was attenuated by treatment with cariporide, DMA, or Ca2+-free buffer. These results suggest that NHE plays a crucialrole in the rise of [Ca2+](i) and ICAM-1 expression during acidic hypoxia/reoxygenation in CMECs. We propose that inhibition of ICAM-1 expression in CMECs may represent a novel mechanism of action of NHE inhibitors against ischemia-reperfusion injury.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 02/06/20 alle ore 23:07:02