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IL-10 promotes survival of microglia without activating Akt.

机译:IL-10在不激活Akt的情况下促进小胶质细胞的存活。

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摘要

IL-10 is an anti-inflammatory cytokine that has recently been shown to promote survival of neurons and glia. Here we establish that IL-10 induces phosphorylation of Stat3 on Tyr(705) and serves as a survival factor for N13 microglial cells. Recombinant IL-10 (10 ng/ml) decreases growth factor withdrawal-induced apoptosis by 50%, as assessed by TUNEL. In contrast to IL-10, IGF-I increases enzymatic activity of PI 3-kinase and causes phosphorylation on serine(473) of Akt but does not prevent microglial apoptosis. These data establish that IL-10 activates Stat3 and inhibits the mitochondrial pathway of cell death without activating the Akt cell survival pathway.
机译:IL-10是一种抗炎细胞因子,最近已被证明可以促进神经元和神经胶质细胞的存活。在这里我们建立IL-10诱导Tyr(705)上Stat3的磷酸化,并作为N13小胶质细胞的存活因子。 TUNEL评估,重组IL-10(10 ng / ml)将生长因子戒断诱导的细胞凋亡降低了50%。与IL-10相比,IGF-I增加了PI 3-激酶的酶促活性,并在Akt的丝氨酸(473)上引起磷酸化,但不能阻止小胶质细胞凋亡。这些数据确定IL-10激活Stat3并抑制细胞死亡的线粒体途径,而不激活Akt细胞存活途径。

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