Long noncoding RNA TRG-AS1 protects against glucocorticoid-induced osteoporosis in a rat model by regulating miR-802-mediated CAB39/AMPK/SIRT-1/NF-κB axis

The long-term treatment of glucocorticoids is a common cause of osteoporosis (OP). This study concentrated on inquiring into the regulatory role and potential mechanisms of TRG-AS1 on dexamethasone (Dex)-induced OP in rats. We adopted Dex to treat rat osteoblasts and rats to simulate in-vitro and in...

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Published inHuman cell : official journal of Human Cell Research Society Vol. 35; no. 5; pp. 1424 - 1439
Main Authors Liu, Wen, Li, Guojuan, Li, Jing, Chen, Wei
Format Journal Article
LanguageEnglish
Published Singapore Springer Nature Singapore 01.09.2022
Springer Nature B.V
Subjects
Apoptosis
Biomedical and Life Sciences
Cell Biology
Dexamethasone
Glucocorticoids
Gynecology
Life Sciences
NF-κB protein
Oncology
Osteoblastogenesis
Osteoblasts
Osteoporosis
Reproductive Medicine
Research Article
Rodents
Stem Cells
Surgery
Osteoporosis
SIRT-1
NF-κB
CAB39
AMPK
TRG-AS1
Glucocorticoid
miR-802
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Summary:The long-term treatment of glucocorticoids is a common cause of osteoporosis (OP). This study concentrated on inquiring into the regulatory role and potential mechanisms of TRG-AS1 on dexamethasone (Dex)-induced OP in rats. We adopted Dex to treat rat osteoblasts and rats to simulate in-vitro and in-vivo OP models, respectively. Gain-of-function assays of TRG-AS1, miR-802 and CAB39 were constructed in rat osteoblasts to make certain the influence of TRG-AS1, miR-802 and CAB39 on differentiation, proliferation and apoptosis of rat osteoblasts. TRG-AS1 and CAB39 were down-regulated in the Dex-induced OP model in rats, in contrast to miR-802. Overexpression of TRG-AS1 restrained Dex-induced inhibition of osteogenic differentiation, promoted CAB39/AMPK/SIRT-1 and inhibited NF-κB, while overexpression of miR-802 bridled the inhibitory effect of TRG-AS1 on OP. miR-802 was targeted by TRG-AS1, and inhibited CAB39. Inhibition of either AMPK or SIRT-1 abated the osteogenic differentiation-promoting effect of CAB39. Animal experiments displayed that overexpressing TRG-AS1 alleviated Dex-induced OP in rats. In conclusion, up-regulation of TRG-AS1 protected against glucocorticoid-induced OP in rats by modulating the miR-802-mediated CAB39/AMPK/SIRT-1/NF-κB axis.
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ISSN:1749-0774
0914-7470
1749-0774
DOI:10.1007/s13577-022-00741-1