Primary cilia are small microtubule‐based organelles capable of transducing signals from growth factor receptors embedded in the cilia membrane. Developmentally, oligodendrocyte progenitor cells (OPCs) express genes associated with primary cilia assembly, disassembly, and signaling, however, the importance of primary cilia for adult myelination has not been explored. We show that OPCs are ciliated in vitro and in vivo, and that they disassemble their primary cilia as they progress through the cell cycle. OPC primary cilia are also disassembled as OPCs differentiate into oligodendrocytes. When kinesin family member 3a (Kif3a), a gene critical for primary cilium assembly, was conditionally deleted from adult OPCs in vivo (Pdgfrα‐CreER™:: Kif3a fl/fl transgenic mice), OPCs failed to assemble primary cilia. Kif3a‐deletion was also associated with reduced OPC proliferation and oligodendrogenesis in the corpus callosum and motor cortex and a progressive impairment of fine motor coordination.
This study was conducted to demonstrate myocardial protective effects and possible underlying mechanisms of vitexin on myocardial ischemia/reperfusion (I/R) injury in rats. Occluding the anterior descending artery for 30 min and restoring blood perfusion for 60 min in rat established a model of myocardial I/R. The elevation of the ST segment of Electrocardiograph (ECG) was observed. The infarct size of the rat heart was assessed by triphenyltetrazolium chloride staining (TTC). LDH, CK, SOD activities and MDA content were determined. An immunohistochemical analysis was applied to measure the expression of myocardial NF-κBp65 and TNF-α. ERK/phospho-ERKand c-Jun/phospho-c-Jun protein expression was examined via Western Blot. Vitexin significantly reduced the elevation of the ST segment of ECG and myocardial infarct size. LDH and CK activities and MDA content were attenuated in serum, while SOD activity was markedly enhanced. Vitexin significantly attenuated I/R-induced increases of myocardial NF-κB and TNF-α. Moreover, Western Blot analysis presented that vitexin markedly enhanced the expression of phospho-ERK and weakened the expression of phospho-c-Jun compared to I/R group. The significant protective effect against myocardial ischemical/reperfusion injury in rat, which is exhibited by vitexin, may be related to its antioxidative and anti-inflammatory effects by regulating inflammatory cytokines and the MAPK pathway.
Oligodendrocyte progenitor cells (OPCs) express protocadherin 15 (Pcdh15), a member of the cadherin superfamily of transmembrane proteins. Little is known about the function of Pcdh15 in the central nervous system (CNS), however, Pcdh15 expression can predict glioma aggression and promote the separation of embryonic human OPCs immediately following a cell division. Herein, we show that Pcdh15 knockdown significantly increases extracellular signal-related kinase (ERK) phosphorylation and activation to enhance OPC proliferation in vitro. Furthermore, Pcdh15 knockdown elevates Cdc42-Arp2/3 signalling and impairs actin kinetics, reducing the frequency of lamellipodial extrusion and slowing filopodial withdrawal. Pcdh15 knockdown also reduces the number of processes supported by each OPC and new process generation. Our data indicate that Pcdh15 is a critical regulator of OPC proliferation and process motility, behaviours that characterise the function of these cells in the healthy CNS, and provide mechanistic insight into the role that Pcdh15 might play in glioma progression.
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