Background: Brain astroglia are activated preceding the onset of experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis (MS). We characterized the effects of brain astroglia on spinal cord inflammation, focusing on astroglial connexin (Cx)43, because we recently reported that Cx43 has a critical role in regulating neuroinflammation.
Methods: Because glutamate aspartate transporter (GLAST) astroglia are enriched in the brain gray matter, we generated Cx43;GLAST-CreER mice that were brain gray matter astroglia-specific Cx43 conditional knockouts (Cx43 icKO).
Microglia play key roles in synaptic pruning, which primarily occurs from the postnatal period to adolescence. Synaptic pruning is essential for normal brain development and its impairment is implicated in neuropsychiatric developmental diseases such as autism spectrum disorders (ASD). Recent epidemiological surveys reported a strong link between ASD and atopic/allergic diseases.
View Article and Find Full Text PDFIn multiple sclerosis plaques, oligodendroglial connexin (Cx) 47 constituting main gap junction channels with astroglial Cx43 is persistently lost. As mice with Cx47 single knockout exhibit no demyelination, the roles of Cx47 remain undefined. We aimed to clarify the effects of oligodendroglia-specific Cx47 inducible conditional knockout (icKO) on experimental autoimmune encephalomyelitis (EAE) induced by myelin oligodendrocyte glycoprotein peptide (MOG35-55) in PLP/CreERT;Cx47fl/fl mice at 14 d after tamoxifen injection.
View Article and Find Full Text PDFMesenchymal stem cells (MSCs) has been used as one of the new cell sources in osteochondral tissue engineering. It has been well known that control of their differentiation into chondrocytes plays a key role in developing engineered cartilages. Therefore, this study aims to develop a fundamental protocol to control the differentiation and proliferation of MSCs to construct an engineered cartilage.
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