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LRG-1 通过 RAB31 介导抑制缺氧诱导的细胞凋亡促进脂肪移植物存活。

LRG-1 promotes fat graft survival through the RAB31-mediated inhibition of hypoxia-induced apoptosis.

机构信息

Department of Plastic & Reconstructive Surgery, School of Medicine, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University, Shanghai, China.

出版信息

J Cell Mol Med. 2022 Jun;26(11):3153-3168. doi: 10.1111/jcmm.17280. Epub 2022 Mar 23.

DOI:10.1111/jcmm.17280
PMID:35322540
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9170820/
Abstract

Autologous adipose tissue is an ideal soft tissue filling material, and its biocompatibility is better than that of artificial tissue substitutes, foreign bodies and heterogeneous materials. Although autologous fat transplantation has many advantages, the low retention rate of adipose tissue limits its clinical application. Here, we identified a secretory glycoprotein, leucine-rich-alpha-2-glycoprotein 1 (LRG-1), that could promote fat graft survival through RAB31-mediated inhibition of hypoxia-induced apoptosis. We showed that LRG-1 injection significantly increased the maintenance of fat volume and weight compared with the control. In addition, higher fat integrity, more viable adipocytes and fewer apoptotic cells were observed in the LRG-1-treated groups. Furthermore, we discovered that LRG-1 could reduce the ADSC apoptosis induced by hypoxic conditions. The mechanism underlying the LRG-1-mediated suppression of the ADSC apoptosis induced by hypoxia was mediated by the upregulation of RAB31 expression. Using LRG-1 for fat grafts may prove to be clinically successful for increasing the retention rate of transplanted fat.

摘要

自体脂肪组织是一种理想的软组织填充材料,其生物相容性优于人工组织替代品、异物和异种材料。虽然自体脂肪移植有许多优点,但脂肪组织的低保留率限制了其临床应用。在这里,我们鉴定了一种分泌糖蛋白,富含亮氨酸的α-2-糖蛋白 1(LRG-1),它可以通过 RAB31 介导的抑制缺氧诱导的细胞凋亡来促进脂肪移植物的存活。我们发现,与对照组相比,LRG-1 注射显著增加了脂肪体积和重量的维持。此外,在 LRG-1 处理组中观察到更高的脂肪完整性、更多存活的脂肪细胞和更少的凋亡细胞。此外,我们发现 LRG-1 可以减少 ADSC 在缺氧条件下诱导的凋亡。LRG-1 介导的抑制缺氧诱导的 ADSC 凋亡的机制是通过上调 RAB31 表达来介导的。使用 LRG-1 进行脂肪移植可能被证明在临床上是成功的,可以提高移植脂肪的保留率。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0bfe/9170820/29314b4d877e/JCMM-26-3153-g007.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0bfe/9170820/65771605f397/JCMM-26-3153-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0bfe/9170820/07607dc21d25/JCMM-26-3153-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0bfe/9170820/29314b4d877e/JCMM-26-3153-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0bfe/9170820/37212aba13fe/JCMM-26-3153-g003.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0bfe/9170820/07fc31685bd7/JCMM-26-3153-g005.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0bfe/9170820/65771605f397/JCMM-26-3153-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0bfe/9170820/07607dc21d25/JCMM-26-3153-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0bfe/9170820/29314b4d877e/JCMM-26-3153-g007.jpg

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