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FAM172A在硬膜外纤维化过程中调控内质网应激引发的自噬。

FAM172A supervises ER (endoplasmic reticulum) stress-triggered autophagy in the epidural fibrosis process.

作者信息

Zheng Yufeng, Zhang Dianzhong, Su Le, Wen Yanhua, Wang Yucai

机构信息

Department of Orthopaedic Surgery, Tangdu Hospital Air Force Medical University Xi'an China.

Department of Orthopaedic Surgery The Fourth People's Hospital of Zibo Zibo China.

出版信息

JOR Spine. 2022 May 1;5(2):e1203. doi: 10.1002/jsp2.1203. eCollection 2022 Jun.

DOI:10.1002/jsp2.1203
PMID:35783909
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9238286/
Abstract

BACKGROUNDS

Lumbar laminectomy is usually utilized for lumbar disc herniation (LDH), but also causes epidural fibrosis (EF) process associated with abnormal proliferation of fibroblasts. FAM172A is associated with ER stress and cell proliferation, but its mechanism was unclear, especially in the process of EF.

METHODS

Therefore, the regulation of FAM172A on the calcium flux and autophagy in fibroblasts were investigated by inducing ER stress with tunicamycin and upexpression or downexpression of FAM172A. The calcium flux was determined using Fluo-3, and autophagy was examined with immunofluorescence or western blot for LC3, Beclin-1, ATG-5, and p62. Moreover, the apoptotic protein of Bax and Bcl-2 was detected, too. Furthermore, the laminectomy model was constructed and then dealt with overexpression of FAM172A.

RESULTS

Tunicamycin-induced endoplasmic reticulum (ER) stress and autophagy process in fibroblasts were associated with the calcium flux regulated by FAM172A, especially in EF cells. Besides, tunicamycin induced autophagy and suppressed cell apoptosis of fibroblasts. Furthermore, FAM72A repressed the proliferation of fibroblasts and the process of EF in the laminectomy model through the mediation of the autophagy process.

CONCLUSIONS

Tunicamycin-induced endoplasmic reticulum (ER) stress in fibroblasts was associated with calcium flux mediated by FAM172A. FAM72A participated in the autophagy regulation of fibroblasts and maybe the key interaction regulator of apoptosis and autophagy in fibroblasts, especially for epidural scar cells.

摘要

背景

腰椎椎板切除术通常用于治疗腰椎间盘突出症（LDH），但也会引发与成纤维细胞异常增殖相关的硬膜外纤维化（EF）过程。FAM172A与内质网应激和细胞增殖相关，但其机制尚不清楚，尤其是在EF过程中。

方法

因此，通过用衣霉素诱导内质网应激以及上调或下调FAM172A，研究FAM172A对成纤维细胞钙通量和自噬的调节作用。使用Fluo-3测定钙通量，并用免疫荧光或蛋白质印迹法检测LC3、Beclin-1、ATG-5和p62来检查自噬。此外，还检测了凋亡蛋白Bax和Bcl-2。此外，构建椎板切除术模型，然后进行FAM172A过表达处理。

结果

衣霉素诱导的成纤维细胞内质网（ER）应激和自噬过程与FAM172A调节的钙通量相关，尤其是在EF细胞中。此外，衣霉素诱导成纤维细胞自噬并抑制细胞凋亡。此外，FAM72A通过自噬过程的介导抑制成纤维细胞增殖和椎板切除术模型中的EF过程。

结论

衣霉素诱导的成纤维细胞内质网（ER）应激与FAM172A介导的钙通量相关。FAM72A参与成纤维细胞的自噬调节，可能是成纤维细胞，尤其是硬膜外瘢痕细胞中凋亡和自噬的关键相互作用调节因子。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c19f/9238286/53cd4923a7dd/JSP2-5-e1203-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c19f/9238286/2a21d0530555/JSP2-5-e1203-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c19f/9238286/ce28ddc7f926/JSP2-5-e1203-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c19f/9238286/1423a1b026b2/JSP2-5-e1203-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c19f/9238286/9eb6227ceedd/JSP2-5-e1203-g010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c19f/9238286/e289f3d41ff2/JSP2-5-e1203-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c19f/9238286/90fb2350bdad/JSP2-5-e1203-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c19f/9238286/faf7a5bb280e/JSP2-5-e1203-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c19f/9238286/1a7add8f8e11/JSP2-5-e1203-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c19f/9238286/53cd4923a7dd/JSP2-5-e1203-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c19f/9238286/2a21d0530555/JSP2-5-e1203-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c19f/9238286/ce28ddc7f926/JSP2-5-e1203-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c19f/9238286/1423a1b026b2/JSP2-5-e1203-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c19f/9238286/9eb6227ceedd/JSP2-5-e1203-g010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c19f/9238286/e289f3d41ff2/JSP2-5-e1203-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c19f/9238286/90fb2350bdad/JSP2-5-e1203-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c19f/9238286/faf7a5bb280e/JSP2-5-e1203-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c19f/9238286/1a7add8f8e11/JSP2-5-e1203-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c19f/9238286/53cd4923a7dd/JSP2-5-e1203-g001.jpg

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