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MLT/MT1 信号对鹿茸间充质细胞生长的调控机制。

The Regulatory Mechanism of MLT/MT1 Signaling on the Growth of Antler Mesenchymal Cells.

机构信息

Key Lab of Agricultural Animal Genetics, Breeding and Reproduction of Ministry of Education, College of Animal Science and Technology, Huazhong Agricultural University, Wuhan 430070, China.

Department of Animal Husbandry and Veterinary, Wuhan Agricultural School, Wuhan 430043, China.

出版信息

Molecules. 2017 Oct 23;22(10):1793. doi: 10.3390/molecules22101793.

DOI:10.3390/molecules22101793
PMID:29065543
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6151843/
Abstract

Melatonin (MLT) plays an important role in regulating the physiological cycle of seasonal breeding animals. Melatonin receptor I (MT1) is effectively expressed in the cambium layer of deer antler. However, the function and metabolic mechanism of MLT/MT1 signaling in the mesenchymal cells of sika deer remain to be further elucidated. In this work, we detected the effects of MLT/MT1 signaling on mesenchymal cells proliferation and the interaction between MLT/MT1 and IGF1/IGF1-R signaling. The results show that (1) deer antler mesenchymal cells actually express MT1; (2) exogenous melatonin significantly promotes mesenchymal cells proliferation, while MT1 knock-down significantly impairs the positive effects of melatonin; and (3) melatonin significantly enhanced IGF1/IGF1-R signaling, as both the expression of IGF1 and IGF-1R increased, while MT1 knock-down significantly decreased IGF1-R expression and IGF1 synthesis. In summary, these data verified that MLT/MT1 signaling plays a crucial role in antler mesenchymal proliferation, which may be mediated by IGF1/IGF1-R.

摘要

褪黑素(MLT)在调节季节性繁殖动物的生理周期中起着重要作用。褪黑素受体 I(MT1)在鹿茸的形成层中有效表达。然而,MLT/MT1 信号在梅花鹿间充质细胞中的功能和代谢机制仍有待进一步阐明。在这项工作中,我们检测了 MLT/MT1 信号对间充质细胞增殖的影响以及 MLT/MT1 与 IGF1/IGF1-R 信号之间的相互作用。结果表明:(1)鹿茸间充质细胞实际上表达 MT1;(2)外源性褪黑素显著促进间充质细胞增殖,而 MT1 敲低则显著损害褪黑素的正向作用;(3)褪黑素显著增强 IGF1/IGF1-R 信号,因为 IGF1 和 IGF-1R 的表达均增加,而 MT1 敲低则显著降低 IGF1-R 表达和 IGF1 合成。总之,这些数据证实了 MLT/MT1 信号在鹿茸间充质增殖中起着至关重要的作用,其可能通过 IGF1/IGF1-R 介导。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6019/6151843/4f23022be8db/molecules-22-01793-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6019/6151843/41508fc843ea/molecules-22-01793-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6019/6151843/c8f883920924/molecules-22-01793-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6019/6151843/6c4c30406b3a/molecules-22-01793-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6019/6151843/045b8af40aa7/molecules-22-01793-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6019/6151843/025cee77836c/molecules-22-01793-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6019/6151843/4f23022be8db/molecules-22-01793-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6019/6151843/41508fc843ea/molecules-22-01793-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6019/6151843/c8f883920924/molecules-22-01793-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6019/6151843/6c4c30406b3a/molecules-22-01793-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6019/6151843/045b8af40aa7/molecules-22-01793-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6019/6151843/025cee77836c/molecules-22-01793-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6019/6151843/4f23022be8db/molecules-22-01793-g006.jpg

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