Changes in Cellular Localization of Inter-Alpha Inhibitor Proteins after Cerebral Ischemia in the Near-Term Ovine Fetus.
Changes in Cellular Localization of Inter-Alpha Inhibitor Proteins after Cerebral Ischemia in the Near-Term Ovine Fetus.
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DOI：
10.3390/ijms221910751
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发表时间：
2021-10-04
影响因子：
5.6
通讯作者：
Stonestreet BS
中科院分区：
文献类型：
--
作者：
Hatayama K;Kim B;Chen X;Lim YP;Davidson JO;Bennet L;Gunn AJ;Stonestreet BS
α-间抑制蛋白（IAIP）是关键的免疫调节分子。内源性IAIP存在于人类、啮齿动物和绵羊的脑中，并且在多个发育阶段不稳定地定位于细胞质和细胞核。我们以前曾报道，缺血再灌注（I/R）降低IAIP浓度在胎羊脑。在这项研究中，我们研究了I/R对神经元（NeuN+），小胶质细胞（Iba 1+），少突胶质细胞（Olig 2+）和增殖细胞（Ki 67+）中IAIP的总，胞质和核表达的影响，以及它们与组蛋白和内质网在胎儿脑细胞中的共定位。孕128天的胎羊分别暴露于假手术组（n = 6）和缺血再灌注组（n = 5）。虽然I/R没有改变大脑皮层或白色物质中IAIP+细胞的总数，但皮质中IAIP+细胞质的细胞减少，而IAIP+细胞核的细胞增加。I/R减少总神经元数量，但不改变IAIP+神经元数量。细胞质IAIP+神经元的比例减少，但核IAIP+神经元的数量没有变化。I/R增加了小胶质细胞的数量，减少了IAIP+小胶质细胞和核IAIP+小胶质细胞的总数，但不减少胞质IAIP+小胶质细胞的数量。I/R与少突胶质细胞数量减少和增殖细胞增加有关，而亚细胞IAIP定位没有变化。IAIP与内质网和组蛋白共定位。总之，I/R改变了皮质神经元和小胶质细胞中IAIP的亚细胞定位，但在少突胶质细胞或增殖细胞中没有。结合已知的外源性IAIP的神经保护作用，我们推测内源性IAIP可能在I/R恢复过程中发挥作用。
Inter-alpha Inhibitor Proteins (IAIPs) are key immunomodulatory molecules. Endogenous IAIPs are present in human, rodent, and sheep brains, and are variably localized to the cytoplasm and nuclei at multiple developmental stages. We have previously reported that ischemia-reperfusion (I/R) reduces IAIP concentrations in the fetal sheep brain. In this study, we examined the effect of I/R on total, cytoplasmic, and nuclear expression of IAIPs in neurons (NeuN+), microglia (Iba1+), oligodendrocytes (Olig2+) and proliferating cells (Ki67+), and their co-localization with histones and the endoplasmic reticulum in fetal brain cells. At 128 days of gestation, fetal sheep were exposed to Sham (n = 6) or I/R induced by cerebral ischemia for 30 min with reperfusion for 7 days (n = 5). Although I/R did not change the total number of IAIP+ cells in the cerebral cortex or white matter, cells with IAIP+ cytoplasm decreased, whereas cells with IAIP+ nuclei increased in the cortex. I/R reduced total neuronal number but did not change the IAIP+ neuronal number. The proportion of cytoplasmic IAIP+ neurons was reduced, but there was no change in the number of nuclear IAIP+ neurons. I/R increased the number of microglia and decreased the total numbers of IAIP+ microglia and nuclear IAIP+ microglia, but not the number of cytoplasmic IAIP+ microglia. I/R was associated with reduced numbers of oligodendrocytes and increased proliferating cells, without changes in the subcellular IAIP localization. IAIPs co-localized with the endoplasmic reticulum and histones. In conclusion, I/R alters the subcellular localization of IAIPs in cortical neurons and microglia but not in oligodendrocytes or proliferating cells. Taken together with the known neuroprotective effects of exogenous IAIPs, we speculate that endogenous IAIPs may play a role during recovery from I/R.
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