TY - JOUR
T1 - Sp1 in Astrocyte Is Important for Neurite Outgrowth and Synaptogenesis
AU - Hung, Chia Yang
AU - Hsu, Tsung I.
AU - Chuang, Jian Ying
AU - Su, Tsung Ping
AU - Chang, Wen Chang
AU - Hung, Jan Jong
N1 - Funding Information:
We are grateful for the support of clinical specimens from the Human Biobank, Research Center of Clinical Medicine, and National Cheng Kung University Hospital.
Funding Information:
This work was supported by the grants (106-2320-B-006-065-MY3, 106-2320-B-006-020-MY3, and 104-2923-B-038-002-MY3) obtained from the Ministry of Science and Technology, Taiwan.
Publisher Copyright:
© 2019, Springer Science+Business Media, LLC, part of Springer Nature.
PY - 2020/1/1
Y1 - 2020/1/1
N2 - In this study, we found that Sp1 was highly expressed in astrocytes, implying that Sp1 might be important for the function of astrocytes. Sp1/GFAP-Cre-ERT2 conditional knockout mice were constructed to study the role of Sp1 in astrocytes. Knockout of Sp1 in astrocytes altered astrocytic morphology and decreased GFAP expression in the cortex and hippocampus but did not affect cell viability. Loss of Sp1 in astrocytes decreased the number of neurons in the cortex and hippocampus. Conditioned medium from primary astrocytes with Sp1 knockout disrupted neuronal dendritic outgrowth and synapse formation, resulting in abnormal learning, memory, and motor behavior. Sp1 knockout in astrocytes altered gene expression, including decreasing the expression of Toll-like receptor 2 and Cfb and increasing the expression of C1q and C4Bp, thereby affecting neurite outgrowth and synapse formation, resulting in disordered neuron function. Studying these gene regulations might be beneficial to understanding neuronal development and brain injury prevention.
AB - In this study, we found that Sp1 was highly expressed in astrocytes, implying that Sp1 might be important for the function of astrocytes. Sp1/GFAP-Cre-ERT2 conditional knockout mice were constructed to study the role of Sp1 in astrocytes. Knockout of Sp1 in astrocytes altered astrocytic morphology and decreased GFAP expression in the cortex and hippocampus but did not affect cell viability. Loss of Sp1 in astrocytes decreased the number of neurons in the cortex and hippocampus. Conditioned medium from primary astrocytes with Sp1 knockout disrupted neuronal dendritic outgrowth and synapse formation, resulting in abnormal learning, memory, and motor behavior. Sp1 knockout in astrocytes altered gene expression, including decreasing the expression of Toll-like receptor 2 and Cfb and increasing the expression of C1q and C4Bp, thereby affecting neurite outgrowth and synapse formation, resulting in disordered neuron function. Studying these gene regulations might be beneficial to understanding neuronal development and brain injury prevention.
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U2 - 10.1007/s12035-019-01694-7
DO - 10.1007/s12035-019-01694-7
M3 - Article
C2 - 31317491
AN - SCOPUS:85069214936
SN - 0893-7648
VL - 57
SP - 261
EP - 277
JO - Molecular Neurobiology
JF - Molecular Neurobiology
IS - 1
ER -