GM-CSF reduces expression of chondroitin sulfate proteoglycan (CSPG) core proteins in TGF-β-treated primary astrocytes
GM-CSF reduces expression of chondroitin sulfate proteoglycan (CSPG) core proteins in TGF-β-treated primary astrocytes
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DOI：
10.5483/bmbrep.2014.47.12.018
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发表时间：
2014-12-31
期刊：
影响因子：
3.8
通讯作者：
Choi, Byung Hyune
中科院分区：
文献类型：
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作者：
Choi, Jung-Kyoung;Park, Sang-Yoon;Choi, Byung Hyune
GM-CSF在神经系统中起作用，特别是在损伤的情况下。已经报道了GM-CSF在各种中枢神经系统损伤的大鼠模型中的治疗效果。我们以前的研究表明，GM-CSF可以促进大鼠脊髓损伤模型的长期恢复，抑制胶质瘢痕形成，增加轴突结构的完整性。在此，我们研究了在体外系统中使用经TGF-β处理的原代星形胶质细胞的GM-CSF抑制胶质瘢痕形成的分子机制。GM-CSF抑制TGF-β处理的星形胶质细胞中硫酸软骨素蛋白聚糖（CSPG）核心蛋白的表达。GM-CSF还抑制TGF-β诱导的Rho-ROCK通路，这在CSPG表达中是重要的。最后，GM-CSF的抑制作用被JAK抑制剂阻断。这些结果可能为GM-CSF抑制胶质瘢痕的作用，并最终为它对神经细胞损伤的治疗作用提供了依据。
GM-CSF plays a role in the nervous system, particularly in cases of injury. A therapeutic effect of GM-CSF has been reported in rat models of various central nervous system injuries. We previously showed that GM-CSF could enhance long-term recovery in a rat spinal cord injury model, inhibiting glial scar formation and increasing the integrity of axonal structure. Here, we investigated molecular the mechanism(s) by which GM-CSF suppressed glial scar formation in an in vitro system using primary astrocytes treated with TGF-beta. GM-CSF repressed the expression of chondroitin sulfate proteoglycan (CSPG) core proteins in astrocytes treated with TGF-beta. GM-CSF also inhibited the TGF-beta-induced Rho-ROCK pathway, which is important in CSPG expression. Finally, the inhibitory effect of GM-CSF was blocked by a JAK inhibitor. These results may provide the basis for GM-CSF's effects in glial scar inhibition and ultimately for its therapeutic effect on neural cell injuries.