IR@PKUHSC  > 北京大学基础医学院  > 药理学系
学科主题基础医学
Endothelium-specific GTP cyclohydrolase I overexpression accelerates refractory wound healing by suppressing oxidative stress in diabetes
Tie, Lu1,2; Li, Xue-Jun2; Wang, Xian3; Channon, Keith M.4; Chen, Alex F.1
关键词tetrahydrobiopterin
刊名AMERICAN JOURNAL OF PHYSIOLOGY-ENDOCRINOLOGY AND METABOLISM
2009-06-01
DOI10.1152/ajpendo.00150.2009
296期:6页:E1423-E1429
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Endocrinology & Metabolism ; Physiology
研究领域[WOS]Endocrinology & Metabolism ; Physiology
关键词[WOS]NITRIC-OXIDE SYNTHASE ; LOW-RENIN HYPERTENSION ; IMPAIRED SKIN REPAIR ; GENE-TRANSFER ; TETRAHYDROBIOPTERIN DEFICIENCY ; DEPENDENT RELAXATION ; MICE ; ENOS ; DYSFUNCTION ; EXPRESSION
英文摘要

Tie L, Li XJ, Wang X, Channon KM, Chen AF. Endothelium-specific GTP cyclohydrolase I overexpression accelerates refractory wound healing by suppressing oxidative stress in diabetes. Am J Physiol Endocrinol Metab 296: E1423-E1429, 2009. First published March 31, 2009; doi: 10.1152/ajpendo.00150.2009.-Refractory wound is a severe complication that leads to limb amputation in diabetes. Endothelial nitric oxide synthase (eNOS) plays a key role in normal wound repair but is uncoupled in streptozotocin (STZ)-induced type 1 diabetes because of reduced cofactor tetrahydrobiopterin (BH4). We tested the hypothesis that overexpression of GTP cyclohydrolase I (GTPCH I), the rate-limiting enzyme for de novo BH4 synthesis, retards NOS uncoupling and accelerates wound healing in STZ mice. Blood glucose levels were significantly increased in both male endothelium-specific GTPCH I transgenic mice (Tg-GCH; via a tie-2 promoter) and wild-type (WT) littermates 5 days after STZ regimen. A full-thickness excisional wound was created on mouse dorsal skin by a 4-mm punch biopsy. Wound closure was delayed in STZ mice, which was rescued in STZ Tg-GCH mice. Cutaneous BH4 level was significantly reduced in STZ mice vs. WT mice, which was maintained in STZ Tg-GCH mice. In STZ mice, constitutive NOS (cNOS) activity and nitrite levels were decreased compared with WT mice, paralleled by increased superoxide anion (O-2(-)) level and inducible NOS (iNOS) activity. In STZ Tg-GCH mice, nitrite level and cNOS activity were potentiated and O-2(-) level and iNOS activity were suppressed compared with STZ mice. Thus endothelium-specific BH4 overexpression accelerates wound healing in type 1 diabetic mice by enhancing cNOS activity and suppressing oxidative stress.

语种英语
WOS记录号WOS:000266342500027
引用统计
被引频次:28[WOS]   [WOS记录]     [WOS相关记录]
文献类型期刊论文
条目标识符http://ir.bjmu.edu.cn/handle/400002259/65213
专题北京大学基础医学院_药理学系
北京大学基础医学院
作者单位1.Univ Pittsburgh, Sch Med & Vasc Surg Res, Dept Surg, Dept Vet Affairs Pittsburgh Healthcare Syst, Pittsburgh, PA 15240 USA
2.Peking Univ, Sch Basic Med Sci, Dept Pharmacol, Beijing 100871, Peoples R China
3.Peking Univ, Sch Basic Med Sci, Dept Physiol, Beijing 100871, Peoples R China
4.Univ Oxford, John Radcliffe Hosp, Dept Cardiovasc Med, Oxford OX3 9DU, England
推荐引用方式
GB/T 7714
Tie, Lu,Li, Xue-Jun,Wang, Xian,et al. Endothelium-specific GTP cyclohydrolase I overexpression accelerates refractory wound healing by suppressing oxidative stress in diabetes[J]. AMERICAN JOURNAL OF PHYSIOLOGY-ENDOCRINOLOGY AND METABOLISM,2009,296(6):E1423-E1429.
APA Tie, Lu,Li, Xue-Jun,Wang, Xian,Channon, Keith M.,&Chen, Alex F..(2009).Endothelium-specific GTP cyclohydrolase I overexpression accelerates refractory wound healing by suppressing oxidative stress in diabetes.AMERICAN JOURNAL OF PHYSIOLOGY-ENDOCRINOLOGY AND METABOLISM,296(6),E1423-E1429.
MLA Tie, Lu,et al."Endothelium-specific GTP cyclohydrolase I overexpression accelerates refractory wound healing by suppressing oxidative stress in diabetes".AMERICAN JOURNAL OF PHYSIOLOGY-ENDOCRINOLOGY AND METABOLISM 296.6(2009):E1423-E1429.
条目包含的文件
条目无相关文件。
个性服务
推荐该条目
保存到收藏夹
查看访问统计
导出为Endnote文件
谷歌学术
谷歌学术中相似的文章
[Tie, Lu]的文章
[Li, Xue-Jun]的文章
[Wang, Xian]的文章
百度学术
百度学术中相似的文章
[Tie, Lu]的文章
[Li, Xue-Jun]的文章
[Wang, Xian]的文章
必应学术
必应学术中相似的文章
[Tie, Lu]的文章
[Li, Xue-Jun]的文章
[Wang, Xian]的文章
相关权益政策
暂无数据
收藏/分享
所有评论 (0)
暂无评论
 

除非特别说明,本系统中所有内容都受版权保护,并保留所有权利。