کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8455430 | 1548022 | 2014 | 9 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Chronic alterations in growth hormone/insulin-like growth factor-I signaling lead to changes in mouse tendon structure
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کلمات کلیدی
ribosomal protein large P0TGF-βBGHCTRLGAPDHIGF-IRPLP0GHRIGF-IRAcromegaly - آکرومگالیTem - این استtransforming growth factor-beta - تبدیل فاکتور رشد بتاLaron syndrome - سندرم لارونInsulin-like growth factor-I - عامل رشد انسولین مانند ITransmission electron microscopy - میکروسکوپ الکترونی عبوریGrowth hormone - هورمون رشدbovine growth hormone - هورمون رشد گاوControl - کنترلCollagen turnover - گردش کلاژنglyceraldehyde 3-phosphate dehydrogenase - گلیسرولیدید 3-فسفات دهیدروژنازIGF-I receptor - گیرنده IGF-Iinsulin-like growth factor-I receptor - گیرنده فاکتور رشد مثل انسولینgrowth hormone receptor - گیرنده هورمون رشد
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
تحقیقات سرطان
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: Chronic alterations in growth hormone/insulin-like growth factor-I signaling lead to changes in mouse tendon structure Chronic alterations in growth hormone/insulin-like growth factor-I signaling lead to changes in mouse tendon structure](/preview/png/8455430.png)
چکیده انگلیسی
The growth hormone/insulin-like growth factor-I (GH/IGF-I) axis is an important stimulator of collagen synthesis in connective tissue, but the effect of chronically altered GH/IGF-I levels on connective tissue of the muscle-tendon unit is not known. We studied three groups of mice; 1) giant transgenic mice that expressed bovine GH (bGH) and had high circulating levels of GH and IGF-I, 2) dwarf mice with a disrupted GH receptor gene (GHR â/â) leading to GH resistance and low circulating IGF-I, and 3) a wild-type control group (CTRL). We measured the ultra-structure, collagen content and mRNA expression (targets: GAPDH, RPLP0, IGF-IEa, IGF-IR, COL1A1, COL3A1, TGF-β1, TGF-β2, TGF-β3, versican, scleraxis, tenascin C, fibronectin, fibromodulin, decorin) in the Achilles tendon, and the mRNA expression was also measured in calf muscle (same targets as tendon plus IGF-IEb, IGF-IEc). We found that GHR â/â mice had significantly lower collagen fibril volume fraction in Achilles tendon, as well as decreased mRNA expression of IGF-I isoforms and collagen types I and III in muscle compared to CTRL. In contrast, the mRNA expression of IGF-I isoforms and collagens in bGH mice was generally high in both tendon and muscle compared to CTRL. Mean collagen fibril diameter was significantly decreased with both high and low GH/IGF-I signaling, but the GHR â/â mouse tendons were most severely affected with a total loss of the normal bimodal diameter distribution. In conclusion, chronic manipulation of the GH/IGF-I axis influenced both morphology and mRNA levels of selected genes in the muscle-tendon unit of mice. Whereas only moderate structural changes were observed with up-regulation of GH/IGF-I axis, disruption of the GH receptor had pronounced effects upon tendon ultra-structure.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Matrix Biology - Volume 34, February 2014, Pages 96-104
Journal: Matrix Biology - Volume 34, February 2014, Pages 96-104
نویسندگان
R.H. Nielsen, N.M. Clausen, P. Schjerling, J.O. Larsen, T. Martinussen, E.O. List, J.J. Kopchick, M. Kjaer, K.M. Heinemeier,