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首页> 外文期刊>Journal of cellular physiology. >MicroRNA-26b inhibits oligodendrocyte precursor cell differentiation by targeting adrenomedullin in spinal cord injury
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MicroRNA-26b inhibits oligodendrocyte precursor cell differentiation by targeting adrenomedullin in spinal cord injury

机译：MicroRNA-26b抑制少突细胞前体通过针对adrenomedullin细胞分化在脊髓损伤

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摘要

Oligodendrocyte precursor cells (OPCs) serve as a reservoir of newborn oligoden-drocytes (OLs) in pathological and homeostatic conditions. After spinal cord injury (SCI), OPCs are activated to generate myelinating OLs, contributing to remyelination and functional recovery; however, the underlying molecular mechanisms remain unclear. Here, microRNA-26b (miR-26b) expression in the spinal cord tissues of SCI rats was examined by real-time polymerase chain reaction analysis. The influences of miR-26b on locomotor recovery following SCI were assessed utilizing Basso, Beattie, and Bresnahan (BBB) scores. The effects of miR-26b on OPC differentiation were explored using immunofluorescence and western blot analyses in vitro and in vivo. The potential targets that are modulated by miR-26b were identified by bioinfor-matics, luciferase reporter assays, and western blot analyses. The effects of adrenomedullin (ADM) on OPC differentiation were explored in vitro using immunofluorescence and western blot analyses. We demonstrated that miR-26b was significantly downregulated after SCI. BBB scores showed that miR-26b exacerbated the locomotor function deficits induced by SCI. In vitro, miR-26b inhibited the differentiation of primary rat OPCs. In vivo, miR-26b suppressed OPC differentiation in SCI rats. Bioinformatics analyses and experimental detection revealed that miR-26b directly targeted ADM in OPCs. In addition, knockdown of ADM suppressed the differentiation of primary rat OPCs. Our study provides evidence that ADM may mediate miR-26b-inhibited OPC differentiation in SCI.
机译：少突细胞前体细胞(信息公开化)作为水库的新生儿oligoden-drocytes (OLs)病理和自我平衡的条件。脊髓损伤(SCI),信息公开化被激活生成髓鞘OLs,导致remyelination和功能恢复;潜在的分子机制仍然存在不清楚。SCI大鼠脊髓组织的检查实时聚合酶链反应分析。复苏后科学评估利用低音部,比蒂和Bresnahan (BBB)分数。miR-26b对OPC分化的影响探索使用免疫荧光和西方污点分析体外和体内。目标由miR-26b调制被bioinfor-matics,荧光素酶记者分析,免疫印迹分析。影响adrenomedullin OPC (ADM)使用体外分化进行了探讨免疫荧光和免疫印迹分析。证明miR-26b明显SCI后表达下调。miR-26b加剧了运动功能赤字SCI引起的。抑制主要鼠的分化信息公开化。在SCI大鼠分化。分析和实验检测显示miR-26b直接针对ADM公开化。此外,击倒ADM镇压了分化的主要鼠信息公开化。提供了证据表明,ADM可调解miR-26b-inhibited OPC在SCI分化。

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