The Role of Homer1b/c in Neuronal Apoptosis Following LPS-Induced Neuroinflammation
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- 作者：Zhiming Cui (1)
Li Zhou (2)
Chun Liu (3)
Guanghui Zhu (1)
Xinmin Wu (1)
Yaohua Yan (1)
Xiaopeng Xia (1)
Zhiyun Ben (4)
Yan Song (4)
Ying Zhou (4)
Haiyan Zhang (4)
Dongmei Zhang (5)
1. Department of Orthopaedics ; The Second Affiliated Hospital of Nantong University ; Jiangsu Province Key Laboratory for Inflammation and Molecular Drug Target ; Nantong University ; Nantong ; 226002 ; Jiangsu ; People鈥檚 Republic of China
2. Department of Pharmacology ; Pharmacy College ; Nantong University ; Nantong ; 226001 ; Jiangsu ; People鈥檚 Republic of China
3. Laboratory animal center ; Nantong University ; Nantong ; 226001 ; Jiangsu ; People鈥檚 Republic of China
4. Department of Immunology ; Medical College ; Nantong University ; Nantong ; 226001 ; Jiangsu ; People鈥檚 Republic of China
5. Department of Pathogen Biology ; Medical College ; Nantong University ; Nantong ; 226001 ; Jiangsu ; People鈥檚 Republic of China - 关键词：Homer1b/c ; Neuroinflammation ; Neuronal apoptosis ; Lipopolysaccharide ; Rat
- 刊名：Neurochemical Research
- 出版年：2015
- 出版时间：January 2015
- 年：2015
- 卷：40
- 期：1
- 页码：204-215
- 全文大小：1,833 KB
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- 刊物主题：Biomedicine
Neurosciences
Biochemistry
Neurology - 出版者：Springer Netherlands
- ISSN：1573-6903
文摘
Homer, also designated Vesl, is one member of the newly found postsynaptic density scaffold proteins, playing a vital role in maintaining synaptic integrity, regulating intracellular calcium mobilization, and being critical for the regulation of cellular apoptosis. However, its function in the inflamed central nervous system (CNS) is not fully elucidated. Here, we investigated the role of Homer1b/c, a long form of Homer1, in lipopolysaccharide (LPS) induced neuroinflammation in CNS. Western blot analysis indicated that LPS administration significantly increased the expression of Homer1b/c in rat brain. Moreover, double immunofluorescent staining suggested Homer1b/c was mainly distributed in the cytoplasm of neurons and had a close association with cleaved caspase-3 level in neurons in rat brain after LPS injection. In vitro studies indicated that up-regulation of Homer1b/c might be related to the subsequent apoptosis in neurons treated by conditioned media (CM), collected from LPS-stimulated mixed glial cultures (MGC). We also found down-regulation of Homer1b/c partly blocked the increase of cleaved caspase-3 and the proportion of Bax/Bcl-2 in neurons induced by MGC-CM. Taken together, these findings suggested that Homer1b/c might promote neuronal apoptosis via the Bax/Bcl-2 dependent pathway during neuroinflammation in CNS, and inhibiting Homer1b/c expression might provide a novel neuroprotective strategy against the inflammation-related neuronal apoptosis.