ArticleBrazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica2025
lncRNA ENSRNOT00000087717 mediated differentiation of satellite glial cells derived from dorsal root ganglion via AKT1.
Article in Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Satellite glial cells (SGCs) within the dorsal root ganglion (DRG) possess the potential for transdifferentiation. Our previous study (doi: 10.1007/s12257-019-0317-x) has identified lncRNA ENSRNOT00000087717 (lnc87717) and its target AKT1 as potential regulators in the differentiation process of DRG-SGCs. In this study, the cell morphology of SGCs was assessed using immunofluorescence cytochemistry during the differentiation following knockdown of lnc87717, as well as downregulation or upregulation AKT1. The subcellular localization of lnc87717 was visualized by fluorescence in situ hybridization (FISH). The mRNA expression levels of lnc87717, AKT1, BDNF, TrkB, proBDNF, and p75NTR were assessed using qRT-PCR. For the in vivo study, 27 male Sprague-Dawley rats aged 6-9 weeks were used to establish the sciatic nerve injury model. The number of apoptotic cells in DRGs was subsequently detected in the AKT1 inhibitor, activator, and control group after the administration of proBDNF antiserum. In vitro, following knockdown of lnc87717, there was a significant decrease in the expression levels of proBDNF, BDNF, TrkB, and p75NTR (P<0.05). Furthermore, the number of nestin-positive SGCs and the expression of lnc87717 and AKT1 were increased in the AKT1-activated group (P<0.05). In vivo, compared to the control group, the number of apoptotic cells in the DRG was increased in the AKT1-inhibited group. Additionally, the expressions of lnc87717 and AKT1 were significantly upregulated (P<0.05), whereas the expression levels of PI3K, NF-κB, and Bad were significantly downregulated (P<0.05) in DRGs following AKT1 up-regulation compared to those in the control group. The differentiation of DRG-SGCs is suggested to be mediated through the activation of AKT1, while lnc87717 downregulates AKT1.
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