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	Interleukin-1 beta downregulates the l-type ca2+ channel activity by depressing the expression of channel protein in cortical neurons
	Zhou, C; Tai, C; Ye, HH; Ren, X; Chen, JG; Wang, SQ; Chai, Z
刊名	Journal of cellular physiology
	2006-03-01
卷号	206期号:3页码:799-806
ISSN号	0021-9541
DOI	10.1002/jcp.20518
通讯作者	Wang, sq()
英文摘要	Interleukin-1 beta (il-1 beta), a proinflammatory cytokine, has been involved in various diseases of the central nervous system (cns). due to the diverse, "contradictory" effects of il-1 beta on neurons during insults to the brain, the mechanisms underlying these effects have not been elucidated. calcium influx through the l-type ca2+ channels (lccs) is believed to play a critical role in the cascade of biochemical events leading to neuron death in these pathophysiological conditions. so far, the mechanism of the interaction of il-1 beta and lccs in the initiation and progression of these diseases is unclear. in this study, we investigate systemically the effects of il-1 beta on the lccs current, which are believed to be implicated in the cascade of biochemical events leading to neuron death in neuropathological conditions. using patch clamp, we observe that il-1 beta treatment (10 ng/ml, 24 h) suppresses lcc currents by similar to 38%, which made up half of the whole-cell ca2+ current determined by nifedipine. il-1 beta does not alter the characteristics of single lcc including current amplitude, open probability, and conductance, but decreases the number of the functioning channel by 40%. moreover, immunoblot assay exhibits that il-1 beta reduces the expression of lcc proteins by 38 similar to 42% in both whole neuron and plasma membrane fraction, and demonstrates that il-1 beta down regulates the lcc activity via the reduction of lcc density. according to early research pretreatments longer than 12 h may play a crucial role in the neuroprotective effects of il-1 beta, our findings may establish an explanation for the protective effects of this interleukin on neurons in the late stage of injury, and could raise a new issue to clinical treatment for insults to brain. (c) 2005 wiley-liss, inc.
WOS关键词	MESSENGER-RNA EXPRESSION ; NEUROTRANSMITTER RELEASE ; HIPPOCAMPAL-NEURONS ; CALCIUM-CHANNELS ; CELL-DEATH ; IN-VITRO ; RAT ; BRAIN ; MECHANISMS ; NEURODEGENERATION
WOS研究方向	Cell Biology ; Physiology
WOS类目	Cell Biology ; Physiology
语种	英语
出版者	WILEY-LISS
WOS记录号	WOS:000235152400027
内容类型	期刊论文
URI标识	http://www.corc.org.cn/handle/1471x/2379465
专题	中国科学院大学
通讯作者	Wang, SQ
作者单位	1.Peking Univ, Coll Life Sci, Dept Physiol & Biophys, State Key Lab Biomembrane & Membrane Biotechnol, Beijing 100871, Peoples R China 2.Tsing Hua Univ, Dept Biol Sci & Biotechnol, Beijing 100084, Peoples R China
推荐引用方式 GB/T 7714	Zhou, C,Tai, C,Ye, HH,et al. Interleukin-1 beta downregulates the l-type ca2+ channel activity by depressing the expression of channel protein in cortical neurons[J]. Journal of cellular physiology,2006,206(3):799-806.
APA	Zhou, C.,Tai, C.,Ye, HH.,Ren, X.,Chen, JG.,...&Chai, Z.(2006).Interleukin-1 beta downregulates the l-type ca2+ channel activity by depressing the expression of channel protein in cortical neurons.Journal of cellular physiology,206(3),799-806.
MLA	Zhou, C,et al."Interleukin-1 beta downregulates the l-type ca2+ channel activity by depressing the expression of channel protein in cortical neurons".Journal of cellular physiology 206.3(2006):799-806.

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