Injury Induced JAK/PKC-Dependent Phosphorylation of GAP-43 and STAT3 for Neurite Growth in Dorsal Root Ganglion

English | 正體中文 | 简体中文 | Items with full text/Total items : 45422/58598 (78%)
Visitors : 2515563 Online Users : 184

RC Version 7.0 © Powered By DSPACE, MIT. Enhanced by NTU Library IR team.

Home ‧ Login ‧ Upload ‧ Help ‧ About ‧ Administer

TMUIR > College of Medicine > Department of Medicine > Department of Physiology > Periodical Article > Item 987654321/3196

Please use this identifier to cite or link to this item: http://libir.tmu.edu.tw/handle/987654321/3196

Title:	Injury Induced JAK/PKC-Dependent Phosphorylation of GAP-43 and STAT3 for Neurite Growth in Dorsal Root Ganglion
Authors:	李怡萱;楊良友 Tsai SY;Yang LY;Wu CH;Chang SF;Hsu CY;Wei CP;Leu SJ;Liaw J;Lee YH;Tsai MD
Contributors:	醫學系生理學科
Date:	2007
Issue Date:	2009-08-24 10:44:49 (UTC+8)
Abstract:	Elevation of corticosteroids and excessive glutamate release are the two major stress responses that occur sequentially during traumatic CNS injury. We have previously reported that sequential application of corticosterone and kainic acid (CORT + KA) mimicking the nerve injury condition results in synergistic enhancement of neurite outgrowth and expression of growth-associated protein 43 (GAP-43) in cultured dorsal root ganglion (DRG). GAP-43 is known to promote neurite extension when phosphorylated by protein kinase C (PKC). In addition, PKC can phosphorylate the signal transducer and activator of transcription 3 (STAT3) at Ser727, which is phosphorylated primarily by Janus kinase (JAK) at Tyr705. In this study, we further examine the role of PKC in this stress-induced growth-promoting effect. In the cultured DRG neurons, the JAK inhibitor AG-490 and the PKC inhibitor Ro-318220 reduced the CORT + KA-enhanced neurite growth effect when applied prior to CORT and KA treatment, respectively. Both AG-490 and Ro-318220 diminished the CORT + KA-enhanced GAP-43 expression, phosphorylation, and axonal localization. Furthermore, CORT + KA treatment synergistically phosphorylated STAT3 at Ser727 but not at Tyr705. Similar phenomena were observed in an animal model of acute spinal cord injury (SCI), in which phosphorylation of GAP-43 and phospho-Ser727-STAT3 was elevated in the injured DRG 4 hr after the impact injury. Further treatment with the therapeutic glucocorticoid methylprednisolone enhanced the phosphorylation of GAP-43 in both the DRG and the spinal cord of SCI rats. These results suggest that elevated glucocorticoids and overexcitation following CNS injury contribute to nerve regeneration via induction of JAK/PKC-mediated GAP-43 and STAT3 activities.
Relation:	Journal of Neuroscience Research.(85):321-331.
Data Type:	article
Appears in Collections:	[Department of Physiology] Periodical Article

Files in This Item:

File	Description	Size	Format
13.pdf		785Kb	Adobe PDF	162	View/Open
摘要.pdf		39Kb	Adobe PDF	74	View/Open

著作權聲明 Copyright Notice

本平台之數位內容為臺北醫學大學所收錄之機構典藏，包含體系內各式學術著作及學術產出。秉持開放取用的精神，提供使用者進行資料檢索、下載與取用，惟仍請適度、合理地於合法範圍內使用本平台之內容，以尊重著作權人之權益。商業上之利用，請先取得著作權人之授權。
The digital content on this platform is part of the Taipei Medical University Institutional Repository, featuring various academic works and outputs from the institution. It offers free access to academic research and public education for non-commercial use. Please use the content appropriately and within legal boundaries to respect copyright owners' rights. For commercial use, please obtain prior authorization from the copyright owner.
瀏覽或使用本平台，視同使用者已完全接受並瞭解聲明中所有規範、中華民國相關法規、一切國際網路規定及使用慣例，並不得為任何不法目的使用TMUIR。
By utilising the platform, users are deemed to have fully accepted and understood all the regulations set out in the statement, relevant laws of the Republic of China, all international internet regulations, and usage conventions. Furthermore, users must not use TMUIR for any illegal purposes.
本平台盡力防止侵害著作權人之權益。若發現本平台之數位內容有侵害著作權人權益情事者，煩請權利人通知本平台維護人員([email protected])，將立即採取移除該數位著作等補救措施。
TMUIR is made to protect the interests of copyright owners. If you believe that any material on the website infringes copyright, please contact our staff([email protected]). We will remove the work from the repository.

Loading...