Graduate School of Humanities and Sciences, Ochanomizu University, Ohtsuka, Bunkyo-ku, Tokyo, Japan; Institute for Human Life Innovation, Ochanomizu University, Ohtsuka, Bunkyo-ku, Tokyo, Japan.
Institute for Human Life Innovation, Ochanomizu University, Ohtsuka, Bunkyo-ku, Tokyo, Japan; Research division of human welfare science, Ochanomizu University, Ohtsuka, Bunkyo-ku, Tokyo, Japan.
J Neuroimmunol. 2021 Dec 15;361:577749. doi: 10.1016/j.jneuroim.2021.577749. Epub 2021 Oct 9.
We examined the mechanism how 2-carba-cyclic phosphatidic acid (2ccPA), a lipid mediator, regulates neuronal apoptosis in traumatic brain injury (TBI). First, we found 2ccPA suppressed neuronal apoptosis after the injury, and increased the immunoreactivity of tenascin-C (TN-C), an extracellular matrix protein by 2ccPA in the vicinity of the wound region. 2ccPA increased the mRNA expression levels of Tnc in primary cultured astrocytes, and the conditioned medium of 2ccPA-treated astrocytes suppressed the apoptosis of cortical neurons. The neuroprotective effect of TN-C was abolished by knockdown of TN-C. These results indicate that 2ccPA contributes to neuroprotection via TN-C from astrocytes in TBI.
我们研究了脂质介质 2- carbacylic 磷酸脂酸(2ccPA)调节创伤性脑损伤(TBI)中神经元凋亡的机制。首先,我们发现 2ccPA 在损伤后抑制神经元凋亡,并增加了创伤区域附近细胞外基质蛋白 tenascin-C(TN-C)的免疫反应性。2ccPA 增加了原代培养星形胶质细胞中 Tnc 的 mRNA 表达水平,2ccPA 处理的星形胶质细胞条件培养基抑制了皮质神经元的凋亡。TN-C 的神经保护作用被 TN-C 的敲低所消除。这些结果表明,2ccPA 通过星形胶质细胞中的 TN-C 参与 TBI 的神经保护。