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首页> 外文期刊>BMC Neuroscience >Neurotrophin and Trk expression by cells of the human lamina cribrosa following oxygen-glucose deprivation
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Neurotrophin and Trk expression by cells of the human lamina cribrosa following oxygen-glucose deprivation

机译：氧葡萄糖剥夺后人筛板细胞的神经营养蛋白和Trk表达

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Background Ischemia within the optic nerve head (ONH) may contribute to retinal ganglion cell (RGC) loss in primary open angle glaucoma (POAG). Ischemia has been reported to increase neurotrophin and high affinity Trk receptor expression by CNS neurons and glial cells. We have previously demonstrated neurotrophin and Trk expression within the lamina cribrosa (LC) region of the ONH. To determine if ischemia alters neurotrophin and Trk protein expression in cells from the human LC, cultured LC cells and ONH astrocytes were exposed to 48 hours of oxygen-glucose deprivation (OGD). Also cells were exposed to 48 hours of OGD followed by 24 hours of recovery in normal growth conditions. Cell number, neurotrophin and Trk receptor protein expression, neurotrophin secretion, and Trk receptor activation were examined. Results Cell number was estimated using an assay for cell metabolism following 24, 48 and 72 hours of OGD. A statistically significant decrease in LC and ONH astrocyte cell number did not occur until 72 hours of OGD, therefore cellular protein and conditioned media were collected at 48 hours OGD. Protein expression of NGF, BDNF and NT-3 by LC cells and ONH astrocytes increased following OGD, as did NGF secretion. Recovery from OGD increased BDNF protein expression in LC cells. In ONH astrocytes, recovery from OGD increased NGF protein expression, and decreased BDNF secretion. Trk A expression and activation in LC cells was increased following OGD while expression and activation of all other Trk receptors was decreased. A similar increase in Trk A expression and activation was observed in ONH astrocytes following recovery from OGD. Conclusions In vitro conditions that mimic ischemia increase the expression and secretion of neurotrophins by cells from the ONH. Increased Trk A expression and activation in LC cells following OGD and in ONH astrocytes following recovery from OGD suggest autocrine/paracrine neurotrophin signaling could be a response to ONH ischemia in POAG. Also, the increase in NGF, BDNF and NT-3 protein expression and NGF secretion following OGD also suggest LC cells and ONH astrocytes may be a paracrine source of neurotrophins for RGCs.
机译：背景视神经乳头（ONH）局部缺血可能导致原发性开角型青光眼（POAG）视网膜神经节细胞（RGC）丢失。据报道，缺血会增加CNS神经元和神经胶质细胞的神经营养蛋白和高亲和力Trk受体表达。我们以前已经证明了神经营养蛋白和Trk在ONH的筛板（LC）区域内表达。为了确定局部缺血是否改变人LC细胞中神经营养蛋白和Trk蛋白的表达，将培养的LC细胞和ONH星形胶质细胞暴露于48小时的氧-葡萄糖剥夺（OGD）。同样，将细胞暴露于48小时的OGD，然后在正常生长条件下恢复24小时。检查细胞数，神经营养蛋白和Trk受体蛋白表达，神经营养蛋白分泌和Trk受体激活。结果在OGD 24、48和72小时后，使用细胞代谢测定法估计细胞数。直到OGD 72小时，LC和ONH星形胶质细胞的数量才出现统计上的显着下降，因此在OGD 48小时时收集了细胞蛋白和条件培养基。 OGD后，LC细胞和ONH星形胶质细胞的NGF，BDNF和NT-3蛋白表达增加，NGF分泌也增加。从OGD中恢复可增加LC细胞中BDNF蛋白的表达。在ONH星形胶质细胞中，从OGD中恢复可增加NGF蛋白表达，并减少BDNF分泌。 OGD后，LC细胞中Trk A的表达和激活增加，而所有其他Trk受体的表达和激活降低。从OGD恢复后，在ONH星形胶质细胞中观察到了类似的Trk A表达和激活增加。结论模拟缺血的体外条件增加了ONH细胞表达和分泌神经营养蛋白的能力。 OGD后LC细胞中的Trk A表达和激活增加以及OGD恢复后ONH星形胶质细胞中Trk A表达增加，这表明自分泌/旁分泌神经营养蛋白信号可能是POAG中对ONH缺血的反应。另外，OGD后NGF，BDNF和NT-3蛋白表达的增加以及NGF的分泌也表明LC细胞和ONH星形胶质细胞可能是RGC的神经营养蛋白的旁分泌来源。

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