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

Hiltunen, Jukka; Laurikainen, Antti; Väkevä, Antti; Meri, Seppo; Saarma, Märt

doi:10.1002/path.878

Cited by 89 publications

(90 citation statements)

References 36 publications

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“…23 We found that statement of NGF and its trkA receptor is increased after induction of ischemia. Consistently, the system was found upregulated in models of cerebral or myocardial ischemia, 24,25 with NGF staining closely associated with capillaries, venules, and arterioles. 25 For the first time, here we document that upregulated NGF participates in reparative capillarization triggered by ischemic insult.…”

Section: Discussionsupporting

confidence: 54%

“…Consistently, the system was found upregulated in models of cerebral or myocardial ischemia, 24,25 with NGF staining closely associated with capillaries, venules, and arterioles. 25 For the first time, here we document that upregulated NGF participates in reparative capillarization triggered by ischemic insult. In fact, spontaneous capillary growth was completely abrogated by anti-NGF antibody.…”

Section: Discussionsupporting

confidence: 54%

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Nerve Growth Factor Promotes Angiogenesis and Arteriogenesis in Ischemic Hindlimbs

et al. 2002

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Background-The neurotrophin nerve growth factor (NGF) regulates neuron survival and differentiation. Implication in neovascularization is supported by statement of NGF and its high-affinity receptor at vascular level and by NGF property of stimulating vascular endothelial cell proliferation. The present study investigated the involvement of endogenous NGF in spontaneous reparative response to ischemia. Mechanisms and therapeutic potential of NGFinduced neovascularization were examined. Methods and Results-Unilateral limb ischemia was produced in CD1 mice by femoral artery resection. By ELISA and immunohistochemistry, we documented that statement of NGF and its high-affinity receptor is upregulated in ischemic muscles. The functional relevance of this phenomenon was assessed by means of NGF-neutralizing antibody. Chronic NGF blockade abrogated the spontaneous capillarization response to ischemia and augmented myocyte apoptosis. Then we tested whether NGF administration may exert curative effects. Repeated NGF injection into ischemic adductors increased capillary and arteriole density, reduced endothelial cell and myofiber apoptosis, and accelerated perfusion recovery, without altering systemic hemodynamics. In normoperfused muscles, NFG-induced capillarization was blocked by vascular endothelial growth factor-neutralizing antibodies, dominant-negative Akt, or NO synthase inhibition. Conclusions-These results indicate that NGF plays a functional role in reparative neovascularization. Furthermore, supplementation of the growth factor promotes angiogenesis through a vascular endothelial growth factor-Akt-NOmediated mechanism. In the setting of ischemia, potentiation of NGF pathway stimulates angiogenesis and arteriogenesis, thereby accelerating hemodynamic recovery. NGF might be envisaged as a utilitarian target for the treatment of ischemic vascular disease.

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Section: Discussionsupporting

confidence: 54%

Section: Discussionsupporting

confidence: 54%

Nerve Growth Factor Promotes Angiogenesis and Arteriogenesis in Ischemic Hindlimbs

et al. 2002

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“…NGF is a potent growth and survival factor for sympathetic neurons (Korsching and Thoenen, 1985;Glebova and Ginty, 2004). Recent evidence indicates that NGF expression is up-regulated in the region of the infarction (Hiltunen, et al, 2001;Zhou, et al, 2004), and infusion of NGF into the stellate ganglion results in cardiac hyperinnervation in canine hearts (Cao, et al, 2000b). However, the cell types involved in post-infarct cardiac NGF production and the neural selectivity of the response are not well defined.…”

Section: Introductionmentioning

confidence: 99%

Sympathetic hyperinnervation and inflammatory cell NGF synthesis following myocardial infarction in rats

et al. 2006

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Sympathetic hyperinnervation occurs in human ventricular tissue after myocardial infarction and may contribute to arrhythmias. Aberrant sympathetic sprouting is associated with elevated nerve growth factor (NGF) in many contexts, including ventricular hyperinnervation. However, it is unclear whether cardiomyocytes or other cell types are responsible for increased NGF synthesis. In this study, left coronary arteries were ligated and ventricular tissue examined in rats 1-28 days post-infarction. Infarct and peri-infarct tissue was essentially devoid of sensory and parasympathetic nerves at all time points. However, areas of increased sympathetic nerve density were observed in the peri-infarct zone between post-ligation days 4-14. Hyperinnervation occurred in regions containing accumulations of macrophages and myofibroblasts. To assess whether these inflammatory cells synthesize NGF, sections were processed for NGF in situ hybridization and immunohistochemistry. Both macrophage1 antigen-positive macrophages and α-smooth muscle actin immunoreactive myofibroblasts expressed NGF in areas where they were closely proximate to sympathetic nerves. To investigate whether NGF produced by peri-infarct cells induces sympathetic outgrowth, we cocultured adult sympathetic ganglia with peri-infarct explants. Neurite outgrowth from sympathetic ganglia was significantly greater at post-ligation days 7-14 as compared to control tissue. Addition of an NGF function-blocking antibody prevented the increased neurite outgrowth induced by periinfarct tissue. These findings provide evidence that inflammatory cell NGF synthesis plays a causal role in sympathetic hyperinnervation following myocardial infarction.

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“…1). In animal heart, BDNF expression was found to be upregulated after ischemia-reperfusion injury in the left ventricle (20), suggesting both neuronal and non-neuronal functions for neurotrophins in …”

Section: Bdnf Blood Level and Its Associatesmentioning

confidence: 99%

Brain derived neurotrophic factor (BDNF) in cardiometabolic physiology and diseases

Taşçı¹,

Kabul²,

Aydoğdu³

2012

Anadolu Kardiyol Derg

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Important advances in our understanding of the relationships between adipose tissue derived peptides, namely adipokines, and their effects on cardiovascular functions have been achieved in recent years. Growing knowledge of adipokine biology is revealing the complexity of these proteins. Adipose tissue releases some other proteins called neurotrophins that are mainly active in central and peripheral nervous system. However, secretion and activity of these hormones are not only limited to neuronal cells and tissues, but they also take part in adipose tissue development, energy metabolism, glucose utilization, insulin sensitivity, inflammation, lipoprotein synthesis, and atherosclerosis. In this review, we describe the most recent advances in the functions of brain derived nerve growth factor (BDNF), a major type of neurotrophins, focusing primarily on cardiovascular and metabolic diseases. (Anadolu Kardiyol Derg 2012; 12: 684-8) Key words: Brain derived nerve growth factor, cardiovascular disease, atherosclerosis, dyslipidemia, diabetes mellitus Review Derleme 684ÖZET Son yıllarda, adipokinler olarak bilinen adipoz doku kaynaklı peptidler ve bunların kardiyovasküler fonksiyonlar üzerine etkileri üzerine önemli ilerlemeler sağlanmıştır. Adipokin biyolojisi hakkında bilgiler çoğaldıkça bu proteinlerin karmaşık görünümü aydınlatılmaktadır. Adipoz doku nörotrofin-ler olarak bilinen ve temel olarak santral ve periferal sinir sisteminde görev yapan diğer bazı proteinleri de salgılar. Bununla beraber, bu hormonların sekresyon ve aktivitesi sadece nöronal hücreler ve dokularla sınırlı olmayıp yağ dokusu gelişimi, enerji metabolizması, glikoz kullanımı, insülin duyarlılığı, enflamasyon, lipoprotein sentezi ve aterosklerozda da rol oynarlar. Bu derlemede majör bir nörotrofin olan beyinden türemiş nörotrofik faktör (BDNF) ile ilgili en son veriler, özellikle kardiyovasküler ve metabolik hastalıklar üzerinden irdelenmiştir.

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

Cited by 89 publications

References 36 publications

Nerve Growth Factor Promotes Angiogenesis and Arteriogenesis in Ischemic Hindlimbs

Nerve Growth Factor Promotes Angiogenesis and Arteriogenesis in Ischemic Hindlimbs

Sympathetic hyperinnervation and inflammatory cell NGF synthesis following myocardial infarction in rats

Brain derived neurotrophic factor (BDNF) in cardiometabolic physiology and diseases

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