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脂多糖诱导的长链非编码RNA TMC3-AS1在骨质疏松症中高表达，并通过抑制成熟miR-708的形成促进成骨细胞凋亡。

Lipopolysaccharide-Induced lncRNA TMC3-AS1 is Highly Expressed in Osteoporosis and Promotes Osteoblast Apoptosis by Suppressing the Formation of Mature miR-708.

作者信息

Chen Sheng, Dai Min

机构信息

Orthopedics Department, the First Affiliated Hospital of Nanchang University, Nanchang City, Jiangxi Province, 330006, People's Republic of China.

出版信息

Int J Gen Med. 2022 Mar 25;15:3345-3352. doi: 10.2147/IJGM.S350081. eCollection 2022.

DOI:10.2147/IJGM.S350081
PMID:35368795
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8964444/
Abstract

BACKGROUND

LncRNA TMC3-AS1 expression is affected by lipopolysaccharide (LPS), a contributor to osteoporosis (OS). Therefore, we hypothesized that TMC3-AS1 could inhibit osteoblast apoptosis and interact with miR-708, a regulator of osteoblast apoptosis in OS.

METHODS

Differential expression of TMC3-AS1 and miR-708 (mature and premature) in OS patients and controls was analyzed using RT-qPCR. Subcellular location of TMC3-AS1 in osteoblasts was analyzed using subcellular fractionation assay. The direct interaction between TMC3-AS1 and premature miR-708 was analyzed using RNA pulldown assay. The role of TMC3-AS1 and miR-708 in the expression of each other was explored with overexpression assays. Cell apoptosis induced by LPS was analyzed using cell apoptosis assay.

RESULTS

TMC3-AS1 and premature miR-708 were highly expressed in OS and were upregulated by LPS in osteoblasts. In contrast, mature miR-708 was under-expressed in OS and downregulated by LPS. TMC3-AS1 directly interacted with premature miR-708 and was detected in both the nuclear and cytoplasm fractions. TMC3-AS1 decreased premature miR-708 level and increased mature miR-708 level. Moreover, TMC3-AS1 increased LPS-induced cell apoptosis and suppressed the role of miR-708 in cell apoptosis.

CONCLUSION

TMC3-AS1 is highly expressed in OS and promotes LPS-induced osteoblast apoptosis by reducing miR-708 maturation.

摘要

背景

长链非编码RNA TMC3-AS1的表达受脂多糖（LPS）影响，LPS是骨质疏松症（OS）的一个促成因素。因此，我们推测TMC3-AS1可能抑制成骨细胞凋亡，并与miR-708相互作用，miR-708是OS中成骨细胞凋亡的一个调节因子。

方法

采用逆转录定量聚合酶链反应（RT-qPCR）分析OS患者和对照组中TMC3-AS1和miR-708（成熟和前体）的差异表达。采用亚细胞分级分离试验分析TMC3-AS1在成骨细胞中的亚细胞定位。采用RNA下拉试验分析TMC3-AS1与前体miR-708之间的直接相互作用。通过过表达试验探讨TMC3-AS1和miR-708在彼此表达中的作用。采用细胞凋亡试验分析LPS诱导的细胞凋亡。

结果

TMC3-AS1和前体miR-708在OS中高表达，并在成骨细胞中被LPS上调。相反，成熟miR-708在OS中表达不足，并被LPS下调。TMC3-AS1与前体miR-708直接相互作用，在细胞核和细胞质组分中均有检测到。TMC3-AS1降低了前体miR-708水平，提高了成熟miR-708水平。此外，TMC3-AS1增加了LPS诱导的细胞凋亡，并抑制了miR-708在细胞凋亡中的作用。

结论

TMC3-AS1在OS中高表达，通过减少miR-708成熟促进LPS诱导的成骨细胞凋亡。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9aea/8964444/a46aa08f8ebc/IJGM-15-3345-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9aea/8964444/28019d1216aa/IJGM-15-3345-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9aea/8964444/a203033a18c7/IJGM-15-3345-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9aea/8964444/1ace889b756d/IJGM-15-3345-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9aea/8964444/f1c3c7efa54e/IJGM-15-3345-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9aea/8964444/a46aa08f8ebc/IJGM-15-3345-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9aea/8964444/28019d1216aa/IJGM-15-3345-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9aea/8964444/a203033a18c7/IJGM-15-3345-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9aea/8964444/1ace889b756d/IJGM-15-3345-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9aea/8964444/f1c3c7efa54e/IJGM-15-3345-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9aea/8964444/a46aa08f8ebc/IJGM-15-3345-g0005.jpg

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