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蝾螈来源的、经过人类优化的 nAG 蛋白可抑制原代人成纤维细胞的胶原蛋白合成并增加其降解。

Salamander-derived, human-optimized nAG protein suppresses collagen synthesis and increases collagen degradation in primary human fibroblasts.

机构信息

Department of Surgery, King Saud University, Riyadh, Saudi Arabia ; College of Medicine Research Center, King Saud University, Riyadh, Saudi Arabia.

出版信息

Biomed Res Int. 2013;2013:384091. doi: 10.1155/2013/384091. Epub 2013 Oct 31.

DOI:10.1155/2013/384091
PMID:24288677
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3833026/
Abstract

Unlike humans, salamanders regrow their amputated limbs. Regeneration depends on the presence of regenerating axons which upregulate the expression of newt anterior gradient (nAG) protein. We had the hypothesis that nAG might have an inhibitory effect on collagen production since excessive collagen production results in scarring, which is a major enemy to regeneration. nAG gene was designed, synthesized, and cloned. The cloned vector was then transfected into primary human fibroblasts. The results showed that the expression of nAG protein in primary human fibroblast cells suppresses the expression of collagen I and III, with or without TGF- β 1 stimulation. This suppression is due to a dual effect of nAG both by decreasing collagen synthesis and by increasing collagen degradation. Furthermore, nAG had an inhibitory effect on proliferation of transfected fibroblasts. It was concluded that nAG suppresses collagen through multiple effects.

摘要

与人类不同，蝾螈可以再生其截肢的肢体。再生取决于再生轴突的存在，再生轴突上调了蝾螈前部梯度（nAG）蛋白的表达。我们假设 nAG 可能对胶原蛋白的产生有抑制作用，因为过多的胶原蛋白产生会导致瘢痕形成，这是再生的主要敌人。设计、合成和克隆了 nAG 基因。然后将克隆载体转染到原代人成纤维细胞中。结果表明，nAG 蛋白在原代人成纤维细胞中的表达抑制了胶原 I 和 III 的表达，无论是否有 TGF-β1 刺激。这种抑制作用是由于 nAG 的双重作用，既通过减少胶原蛋白合成又通过增加胶原蛋白降解。此外，nAG 对转染成纤维细胞的增殖有抑制作用。结论是 nAG 通过多种作用抑制胶原蛋白。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/743f/3833026/2983cf90fb3e/BMRI2013-384091.007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/743f/3833026/3ce2d058afc8/BMRI2013-384091.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/743f/3833026/9ad153718cb1/BMRI2013-384091.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/743f/3833026/0f563bb9a911/BMRI2013-384091.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/743f/3833026/d37ef8e67570/BMRI2013-384091.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/743f/3833026/0f33b8138d83/BMRI2013-384091.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/743f/3833026/bc6e3859c438/BMRI2013-384091.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/743f/3833026/2983cf90fb3e/BMRI2013-384091.007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/743f/3833026/3ce2d058afc8/BMRI2013-384091.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/743f/3833026/9ad153718cb1/BMRI2013-384091.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/743f/3833026/0f563bb9a911/BMRI2013-384091.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/743f/3833026/d37ef8e67570/BMRI2013-384091.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/743f/3833026/0f33b8138d83/BMRI2013-384091.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/743f/3833026/bc6e3859c438/BMRI2013-384091.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/743f/3833026/2983cf90fb3e/BMRI2013-384091.007.jpg

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