Iron accumulation regulates osteoblast apoptosis through lncRNA XIST / miR ‐758‐3p/caspase 3 axis leading to osteoporosis

LncRNA XIST Relieves Hypoxia-Induced Damage in H9C2 Cells by Downregulating miR-429

Tobacco Regulatory Science ◽

10.18001/trs.7.5.41 ◽

2021 ◽

Vol 7 (5) ◽

pp. 1245-1253

Author(s):

Na Yu ◽

Xue Han ◽

Xueqin Wang ◽

Wanling Yu ◽

Liqiu Yan

Keyword(s):

Caspase 3 ◽

Luciferase Reporter ◽

Control Group ◽

H9c2 Cell ◽

H9c2 Cells ◽

Atp Content ◽

Xist Expression ◽

Gene Assay ◽

Lncrna Xist ◽

Group A

This paper aimed to investigate LncRNA XIST relieving hypoxia-induced damage in H9C2 cells by downregulating miR-429. Rat H9C2 cell lines were selected and divided into a normal control group, a hypoxia group, a XIST expression group, a XIST blank expression group, a miR-429 interference group and a blank interference group. qPCR was adopted for detecting LncRNA XIST and miR-429 expression. Western blot (WB) was adopted for detecting the expression of AMPK, PDH, FAT, MCPT-1, Caspase-3, Bax and Bcl-2, ATP content, and levels of SOD, MDA and LDH. Dual luciferase reporter gene assay (DLRGA) and RNA pull-down were adopted for verifying the correlation of LncRNA XIST with miR-429. Hypoxia-induced H9C2 cells had low LncRNA XIST expression and high miR-429 expression. LncRNA XIST upregulation or miR-429 downregulation could inhibit AMPK, PDH, Caspase-3 and Bax, upregulate FAT, MCPT-1 and Bcl-2, and increase ATP content and SOD activity, as well as reduce MDA content and LDH activity. miR-429 was the target gene of LncRNA XIST. LncRNA XIST can relieve hypoxia-induced damage in H9C2 cells via binding to and downregulating miR-429

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Compressive Force Induces Osteoblast Apoptosis via Caspase-8

Journal of Dental Research ◽

10.1177/154405910608500307 ◽

2006 ◽

Vol 85 (3) ◽

pp. 240-244 ◽

Cited By ~ 41

Author(s):

Y. Goga ◽

M. Chiba ◽

Y. Shimizu ◽

H. Mitani

Keyword(s):

Cell Death ◽

Caspase 3 ◽

Tooth Movement ◽

Orthodontic Tooth Movement ◽

Compressive Force ◽

Caspase 8 ◽

Dependent Manner ◽

Caspase 9 ◽

Osteoblast Apoptosis

Periodontal remodeling during orthodontic tooth movement is a result of mechanical stresses. The application of excessive orthodontic force induces cell death. However, the nature of compressive force-induced cell death is unclear. We examined whether the in vitro application of continuous compressive force would induce apoptosis in human osteoblast-like cells (MG-63 cells), and investigated the mechanism by which apoptosis was initiated. The cells became aligned irregularly, and cell viability decreased, indicating that the compressive force caused cell death. According to the TUNEL analysis, the number of apoptotic cells increased significantly in a time-and force-dependent manner. Caspase-3 activity increased with the magnitude of the compressive force, and this effect was reduced significantly by a caspase-8 inhibitor, whereas a caspase-9 inhibitor had no such effect. We conclude that the in vitro application of compressive force can induce apoptosis in MG-63 cells through the activation of caspase-3 via the caspase-8 signaling cascade.

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