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首页> 外文期刊>Journal of Neurochemistry: Offical Journal of the International Society for Neurochemistry >Endogenous and exogenous fibroblast growth factor 2 support survival of chick retinal neurons by control of neuronal neuronal bcl-x(L) and bcl-2 expression through a fibroblast berowth factor receptor 1- and ERK-dependent pathway.
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Endogenous and exogenous fibroblast growth factor 2 support survival of chick retinal neurons by control of neuronal neuronal bcl-x(L) and bcl-2 expression through a fibroblast berowth factor receptor 1- and ERK-dependent pathway.

机译：内源性和外源性成纤维细胞生长因子2通过成纤维细胞生成因子受体1和ERK依赖性途径控制神经元神经元bcl-x（L）和bcl-2表达，从而支持小鸡视网膜神经元的存活。

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Fibroblast growth factor (FGF) 2 is a survival factor for various cell types, including retinal neurons. However, little is understood about the molecular bases of the neuroprotective role of FGF2 in the retina. In this report, FGF2 survival activity was studied in chick retinal neurons subjected to apoptosis by serum deprivation. Exogenous FGF2 supported neuronal survival after serum deprivation and increased neuronal bcl-x(L) and bcl-2 expression, through binding to its receptor R1 (FGF-R1), and subsequent extracellular signal-regulated kinase (ERK) activation. Endogenous FGF2 was transiently overexpressed after serum deprivation. Its down-regulation by antisense oligonucleotides and blockade of its signaling pathway (binding to FGF-R1, tyrosine phosphorylation, and ERK inhibition) decreased bcl-x(L) and bcl-2 levels and and enhanced apoptosis, suggesting that endogenous FGF2 supported neuronal survival through a pathway similar to that of exogenous FGF2. This pathway may serve to up-regulate, or maintain, bcl-x(L) and bcl-2 levels that normally decrease during the onset of apoptosis. Indeed, long-term ERK activation and high bcl-x(L) levels are necessary for the survival activity of both exogenous and endogenous FGF2. Because FGF2 is upregulated following retinal injury in vivo, we suggest that an injury-stimulated autocrine/paracrine FGF2 loop may serve to maintain high levels of survival proteins, such as Bcl-x(L), through ERK activation in retinal neurons.
机译：成纤维细胞生长因子（FGF）2是多种细胞类型（包括视网膜神经元）的存活因子。然而，对于FGF2在视网膜中的神经保护作用的分子基础知之甚少。在该报告中，通过血清剥夺研究了在经历凋亡的鸡视网膜神经元中FGF2的存活活性。外源FGF2通过与受体R1（FGF-R1）结合以及随后的细胞外信号调节激酶（ERK）激活，支持血清剥夺后的神经元存活并增加神经元bcl-x（L）和bcl-2的表达。血清剥夺后内源性FGF2瞬时过表达。它被反义寡核苷酸下调并阻断其信号传导途径（与FGF-R1，酪氨酸磷酸化和ERK抑制结合）降低bcl-x（L）和bcl-2水平，并增强细胞凋亡，表明内源性FGF2支持神经元。通过类似于外源性FGF2的途径存活。该途径可用于上调或维持通常在凋亡开始期间降低的bcl-x（L）和bcl-2水平。实际上，长期的ERK激活和高bcl-x（L）水平对于外源性和内源性FGF2的存活活动都是必需的。由于体内视网膜损伤后FGF2上调，因此我们建议损伤刺激的自分泌/旁分泌FGF2环可通过视网膜神经元中的ERK激活来维持高水平的生存蛋白，例如Bcl-x（L）。

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