کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
3299315 | 1209926 | 2008 | 13 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Myosin Light Chain Kinase Is Central to Smooth Muscle Contraction and Required for Gastrointestinal Motility in Mice
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کلمات کلیدی
RLCROCK1MYPT1MLCKiAsCTRRT-PCRGFPBAC - LACACh - آهAcetylcholine - استیل کولینInternal anal sphincter - اسفنکتر مقعد داخلیsodium dodecyl sulfate–polyacrylamide gel electrophoresis - الکتروفورز ژل دوده سولفات سدیم پلی آکریل آمیدSDS-PAGE - الکتروفورز ژل پلی آکریل آمیدILK - اولregulatory light chain - زنجیره سبک قانونیmyosin light chain kinase - زنجیره کیناز سبک مایوسینembryonic stem - ساقه جنینknockout - ناکاوتreverse transcription–polymerase chain reaction - واکنش زنجیره ای رونویسی-پلیمراز معکوسgreen fluorescent protein - پروتئین فلورسنت سبزbacterial artificial chromosome - کروموزوم مصنوعی باکتریاییControl - کنترلintegrin-linked kinase - کیناز مرتبط با انتگرال
موضوعات مرتبط
علوم پزشکی و سلامت
پزشکی و دندانپزشکی
بیماریهای گوارشی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Background & Aims: Smooth muscle is essential for maintaining homeostasis for many body functions and provides adaptive responses to stresses imposed by pathologic disorders. Identified cell signaling networks have defined many potential mechanisms for initiating smooth muscle contraction with or without myosin regulatory light chain (RLC) phosphorylation by myosin light chain kinase (MLCK). We generated tamoxifen-inducible and smooth muscle-specific MLCK knockout (KO) mice and provide direct loss-of-function evidence that shows the primary importance of MLCK in phasic smooth muscle contractions. Methods: We used the Cre-loxP system to establish Mlck floxed mice in which exons 23, 24, and 25 were flanked by 2 loxP sites. Smooth muscle-specific MLCK KO mice were generated by crossing Mlck floxed mice with SM-CreERT2 (ki) mice followed by tamoxifen treatment. The phenotype was assessed by histologic, biochemical, molecular, cell biological, and physiologic analyses. Results: Targeted deletion of MLCK in adult mouse smooth muscle resulted in severe gut dysmotility characterized by weak peristalsis, dilation of the digestive tract, and reduction of feces excretion and food intake. There was also abnormal urinary bladder function and lower blood pressure. Isolated muscles showed a loss of RLC phosphorylation and force development induced by K+-depolarization. The kinase knockout also markedly reduced RLC phosphorylation and force development with acetylcholine which activates Ca2+-sensitizing signaling pathways. Conclusions: MLCK and its phosphorylation of RLC are required physiologically for smooth muscle contraction and are essential for normal gastrointestinal motility.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Gastroenterology - Volume 135, Issue 2, August 2008, Pages 610-620.e2
Journal: Gastroenterology - Volume 135, Issue 2, August 2008, Pages 610-620.e2
نویسندگان
Wei-Qi He, Ya-Jing Peng, Wen-Cheng Zhang, Ning Lv, Jing Tang, Chen Chen, Cheng-Hai Zhang, Song Gao, Hua-Qun Chen, Gang Zhi, Robert Feil, Kristine E. Kamm, James T. Stull, Xiang Gao, Min-Sheng Zhu,