Growth hormone pathways signaling for cell proliferation and survival in hippocampal neural precursors from postnatal mice

Devesa, Pablo; Agasse, Fabienne; Xapelli, Sara; Almengló, Cristina; Devesa, Jesús; Malva, João O.; Arce, V.

doi:10.1186/1471-2202-15-100

Cited by 48 publications

(41 citation statements)

References 58 publications

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“…In keeping with previous reports in hippocampal neural precursors [24], GH elicited the activation of both PI3K-Akt and ERK signaling pathways (Figure 4B) that was prevented using selective inhibitors (Figure 4D,E). As also occurred when we investigated the effect of combined administration of GPE and GH on cell proliferation and migration, no differences were observed on either Akt or ERK phosphorylation when both drugs were given simultaneously, as compared with their independent effects (Figure 4C).…”

Section: Resultssupporting

confidence: 92%

GPE Promotes the Proliferation and Migration of Mouse Embryonic Neural Stem Cells and Their Progeny In Vitro

Almengló

Devesa²,

Devesa³

et al. 2017

IJMS

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This study was designed to investigate a possible role of the N-terminal tripeptide of insulin-like growth factor-1 (IGF-I), Gly-Pro-Glu (GPE), physiologically generated in neurons following IGF-I-specific cleavage, in promoting neural regeneration after an injury. Primary cultures of mouse neural stem cells (NSCs), obtained from 13.5 Days post-conception (dpc) mouse embryos, were challenged with either GPE, growth hormone (GH), or GPE + GH and the effects on cell proliferation, migration, and survival were evaluated both under basal conditions and in response to a wound healing assay. The cellular pathways activated by GPE were also investigated by using specific chemical inhibitors. The results of the study indicate that GPE treatment promotes the proliferation and the migration of neural stem cells in vitro through a mechanism that involves the activation of extracellular signal-regulated kinase (ERK) and phosphoinositide 3-kinase PI3K-Akt pathways. Intriguingly, both GPE effects and the signaling pathways activated were similar to those observed after GH treatment. Based upon the results obtained from this study, GPE, as well as GH, may be useful in promoting neural protection and/or regeneration after an injury.

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Section: Resultssupporting

confidence: 92%

GPE Promotes the Proliferation and Migration of Mouse Embryonic Neural Stem Cells and Their Progeny In Vitro

Almengló

Devesa²,

Devesa³

et al. 2017

IJMS

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“…Blackmore and his colleagues showed that a seven-day intracerebroventricular infusion of GH increases neural stem cell numbers and augments neurogenesis activity in vitro 35 . Furthermore, GH treatment promotes the proliferation and survival of hippocampal progenitors 21 . Lynch and his colleagues determined that IGF-1 infusion in the right lateral ventricle for 14 days ameliorates age deficits in local cerebral glucose utilization, a function believed to be correlated with neuronal activity 36 and cerebral blood flow 13,37 .…”

Section: Discussionmentioning

confidence: 99%

“…Molecular mechanisms of improved cognitive functions after GH treatment are not known but may be due to the direct impact of the hormone on the brain. Observations have indicated that hormones may cross the blood-brain barrier and have confirmed the existence of GH receptors on neural stem and progenitor cells through immunoreactivity studies of GH and its receptors in the various brain areas (especially regions involved in postnatal neurogenesis such as neurospheres derived from the hippocampus) 16,17,18,19,20,21 . Growth hormone treatment has been shown to promote proliferation, differentiation and survival of these neural stem cells 21 .…”

mentioning

confidence: 91%

Effect of intra-hippocampal injection of human recombinant growth hormone on synaptic plasticity in the nucleus basalis magnocellularis-lesioned aged rats

Malek

Sarkaki

Zahediasl

et al. 2017

Arq. Neuro-Psiquiatr.

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REVIEW Effect of intra-hippocampal injection of human recombinant growth hormone on synaptic plasticity in the nucleus basalis magnocellularis-lesioned aged ratsEfeito da injeção intrahipocampal de hormônio do crescimento humano recombinante sobre a plasticidade sináptica em ratos envelhecidos lesados do núcleo basalis magnocellularis Many common age-related problems are due to neuroendocrine phenomena including memory impairment and Alzheimer's disease (AD) 1 . Alzheimer's disease is a senile neurodegenerative disorder with specific pathological changes in the brain that can cause progressive dementia 2 and is characterized by serious memory problems 3 . The causes and mechanisms of AD are still under intensive investigation 4 . According to the cholinergic hypothesis, high destruction of basal forebrain cholinergic neurons, particularly the nucleus basalis magnocellularis (NBM), have been seen in ABSTRACTIn this study, we proposed that administration of hippocampal growth hormone in ageing animals with growth hormone deficiency can compensate long-term potentiation and synaptic plasticity in nucleus basalis magnocellularis (NBM)-lesioned rats. Aged male Wistar rats were randomly divided into six groups (seven in each) of sham-operated healthy rats (Cont); NBM-lesioned rats (L); NBM-lesioned rats and intrahippocampal injection of growth hormone vehicle (L + Veh); NBM-lesioned and intrahippocampal injection of growth hormone (10, 20 and 40 µg.2 µl-1) (L + GH). In vivo electrophysiological recording techniques were used to characterize maintenance of long-term potentiation at distinct times (1, 2, 3, 24 and 48 hours) after high-frequency stimulation. The population spike was enhanced significantly for about 48 hours following tetanic stimulation in rats treated with a dose-dependent growth hormone compared to the vehicle group (p < 0.05), possibly through neuronal plasticity and neurogenesis in affected areas.Keywords: growth hormone; hippocampus; basal nucleus of Meynert; long-term potentiation; Alzheimer disease; cognition disorders. RESUMONeste estudo, propusemos que a administração de hormônio hipocampal do crescimento em animais envelhecidos com deficiência de hormônio do crescimento pode compensar a potencialização em longo prazo e a plasticidade sináptica em ratos lesados do núcleo basalis magnocellularis (NBM). Ratos machos Wistar foram divididos aleatoriamente em seis grupos (sete ratos em cada grupo) de ratos falso-operados saudáveis (Cont); ratos lesados do NBM (L); ratos lesados do NBM e injeção intrahipocampal de veículo de hormônio do crescimento (L + Veh); ratos lesados do NBM e injeção de hormônio do crescimento (10, 20 e 40 μg.2 μl-1) (L + GH). Técnicas de registro eletrofisiológico in vivo foram utilizadas para caracterizar a manutenção da potencialização em longo prazo em momentos distintos (1, 2, 3, 24 e 48 horas) após estimulação de alta frequência. O pico populacional aumentou significativamente cerca de 48 horas após a estimulação tetânica em ratos tratados com um hormônio do crescimento...

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“…Three themes arise from our genomic data that surgery induces an alteration in endothelial function (thrombin, aldosterone, ERK-5 and eNOS signalling) [24, 30, 37–43], inflammation (B-cell receptor, GABA-A and iCOS-iCOSL T-helper cell signalling) [35, 36, 44] and neural plasticity (axonal, GABA A and growth hormone signalling) [31, 34, 45, 46, 48, 50]. Developmentally inappropriate perturbations to any of these processes have the potential to contribute to the development of adverse neural and cognitive development.…”

Section: Discussionmentioning

confidence: 99%

Surgery increases cell death and induces changes in gene expression compared with anesthesia alone in the developing piglet brain

et al. 2017

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In a range of animal species, exposure of the brain to general anaesthesia without surgery during early infancy may adversely affect its neural and cognitive development. The mechanisms mediating this are complex but include an increase in brain cell death. In humans, attempts to link adverse cognitive development to infantile anaesthesia exposure have yielded ambiguous results. One caveat that may influence the interpretation of human studies is that infants are not exposed to general anaesthesia without surgery, raising the possibility that surgery itself, may contribute to adverse cognitive development. Using piglets, we investigated whether a minor surgical procedure increases cell death and disrupts neuro-developmental and cognitively salient gene transcription in the neonatal brain. We randomly assigned neonatal male piglets to a group who received 6h of 2% isoflurane anaesthesia or a group who received an identical anaesthesia plus 15 mins of surgery designed to replicate an inguinal hernia repair. Compared to anesthesia alone, surgery-induced significant increases in cell death in eight areas of the brain. Using RNAseq data derived from all 12 piglets per group we also identified significant changes in the expression of 181 gene transcripts induced by surgery in the cingulate cortex, pathway analysis of these changes suggests that surgery influences the thrombin, aldosterone, axonal guidance, B cell, ERK-5, eNOS and GABAA signalling pathways. This suggests a number of novel mechanisms by which surgery may influence neural and cognitive development independently or synergistically with the effects of anaesthesia.

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Growth hormone pathways signaling for cell proliferation and survival in hippocampal neural precursors from postnatal mice

Cited by 48 publications

References 58 publications

GPE Promotes the Proliferation and Migration of Mouse Embryonic Neural Stem Cells and Their Progeny In Vitro

GPE Promotes the Proliferation and Migration of Mouse Embryonic Neural Stem Cells and Their Progeny In Vitro

Effect of intra-hippocampal injection of human recombinant growth hormone on synaptic plasticity in the nucleus basalis magnocellularis-lesioned aged rats

Surgery increases cell death and induces changes in gene expression compared with anesthesia alone in the developing piglet brain

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