Nerve growth factor and brain-derived neurotrophic factor mRNAs are regulated in distinct cell populations of rat heart after ischaemia and reperfusion

Citation
Jo. Hiltunen et al., Nerve growth factor and brain-derived neurotrophic factor mRNAs are regulated in distinct cell populations of rat heart after ischaemia and reperfusion, J PATHOLOGY, 194(2), 2001, pp. 247-253
Citations number
38
Categorie Soggetti
Research/Laboratory Medicine & Medical Tecnology","Medical Research Diagnosis & Treatment
Journal title
JOURNAL OF PATHOLOGY
ISSN journal
00223417 → ACNP
Volume
194
Issue
2
Year of publication
2001
Pages
247 - 253
Database
ISI
SICI code
0022-3417(200106)194:2<247:NGFABN>2.0.ZU;2-H
Abstract
Neurotrophins play a crucial role in the development of the peripheral nerv ous system and their mRNAs are often regulated after several types of tissu e injury. This study has investigated the regulation of nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF), and neurotrophin-3 (NT-3) mRNAs 30 min after myocardial ischaemia followed by reperfusion, by northe rn blotting, and in situ hybridization in a rat model. Between 2 and 120 h of reperfusion, Ngf. mRNA levels showed two- to four-fold up-regulation com pared with sham-operated hearts. Scattered;Ngf-expressing cells, probably p ericytes, were detected in the viable border zone of the myocardium in clos e association with capillaries, venules, and arterioles, In addition, diffu se;Ngf expression was seen in the infarct area after 120 h of reperfusion, Bdnf mRNA showed transient up-regulation after 2 and 5 h of reperfusion and remained at control levels thereafter. Bdnf was expressed in the myocytes of the viable border zone. Nt-3 expression showed no significant changes co mpared with sham-operated hearts. These results suggest a role for NGF and/ or BDNF in the pathogenesis of reperfusion injury or in the alterations of cardiac sensory and sympathetic neuronal function after myocardial ischaemi a and reperfusion. Copyright (C) 2001 John Wiley & Sons, Ltd.