Kern Johanna, Schrage Kirsten, Koopmans Guido C, Joosten Elbert A, McCaffery Peter, Mey Jörg
Institute of Biology II, RWTH Aachen, Germany.
Int J Dev Neurosci. 2007 Feb;25(1):7-16. doi: 10.1016/j.ijdevneu.2006.11.006. Epub 2007 Jan 18.
The transcriptional activator retinoic acid (RA) supports axonal regeneration of several neuronal cell populations in vitro, and it has been suggested that its receptor RARbeta2 may be used to support axonal regeneration in the adult mammalian spinal cord. We have previously shown that spinal cord injury induces activity of the RA synthesizing enzyme retinaldehyde dehydrogenase (RALDH)2 in NG2-positive cells. This report quantifies the increase of RALDH2 protein in the injured spinal cord and characterizes the RALDH2/NG2 expressing cells probably as a unique RA synthesizing subpopulation of activated oligodendrocyte precursors or "polydendrocytes". In the uninjured spinal cord low levels of RALDH2 are present in oligodendrocytes as well as in the meninges and in blood vessels. Following injury there is a significant increase in RALDH2 in these latter two tissues and, given that the RALDH2/NG2 positive cells are clustered in the same area, this implies that these are specific foci of RA synthesis. It is presumed that these cells release RA in a paracrine fashion in the region of the wound; however, the RALDH2/NG2-immunoreactive cells expressed the retinoid receptors RARalpha, RARbeta, RXRalpha and RXRbeta, suggesting that RA also serves an autocrine function.
转录激活因子视黄酸（RA）在体外可支持多种神经元细胞群体的轴突再生，有人提出其受体RARβ2可用于支持成年哺乳动物脊髓的轴突再生。我们之前已经表明，脊髓损伤可诱导NG2阳性细胞中视黄酸合成酶视网膜醛脱氢酶（RALDH）2的活性。本报告量化了损伤脊髓中RALDH2蛋白的增加，并将表达RALDH2/NG2的细胞鉴定为可能是活化少突胶质前体细胞或“多突细胞”的独特视黄酸合成亚群。在未损伤的脊髓中，少突胶质细胞、脑膜和血管中存在低水平的RALDH2。损伤后，后两个组织中的RALDH2显著增加，鉴于RALDH2/NG2阳性细胞聚集在同一区域，这意味着这些是视黄酸合成的特定部位。据推测，这些细胞以旁分泌方式在伤口区域释放视黄酸；然而，RALDH2/NG2免疫反应性细胞表达了类视黄醇受体RARα、RARβ、RXRα和RXRβ，表明视黄酸也具有自分泌功能。
