【摘 要】
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Astrogliosis is a hallmark of many neurological disorders,yet its regulatory molecular mechanisms remain elusive.Here we used genetically engineered animal models to change ErbB signaling in adult res
【机 构】
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Institute of Developmental and Regenerative Biology,School of Life Science,Hangzhou Normal Universit
【出 处】
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第九届海内外华人神经科学家研讨会(The 9th Symposium for Chinese Neuroscientis
论文部分内容阅读
Astrogliosis is a hallmark of many neurological disorders,yet its regulatory molecular mechanisms remain elusive.Here we used genetically engineered animal models to change ErbB signaling in adult resident astrocytes.Mice overexpressing constitutive active ErbB2 specifically in astrocytes exhibited activated ErbB downstream signaling such as Akt,Erk and STAT3 and astrocytosis in the intact brain,which demonstrates that the active ErbB signaling is sufficient to initiate reactive responses of astrocytes.On the contrary,mice overexpressing dominant negative EGFR(ErbB1)showed suppressed expression and phosphorylation of native ErbB3 and inhibited ErbB downstream signaling – FAK-Src.The compromised ErbB signaling did not influence the development of astrocyte,however it suppressed the hypertrophic morphological remodeling of reactive astrocytes in injured cortex.Therefore,this work identified ErbB signaling as the positive regulator for astrocyte reactivity,and provided novel animal models with inducible or suppressible astrogliosis for further investigation of diverse neurological disorders.
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