KLF2 reduces dexamethasone-induced injury to growth plate chondrocytes by inhibiting the Runx2-mediated PI3K/AKT and ERK signalling pathways

Dexamethasone (Dex) is a type of glucocorticoid drug. Long term use can induce growth plate chondrocytes (GPCs) apoptosis, impair differentiation, and inhibit cell proliferation and bone growth. It has been reported that Krüppel-like factor 2 (KLF2) inhibits osteoblast damage induced by Dex, but the...

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Published in:Autoimmunity (Chur, Switzerland) Switzerland), 2023-01, Vol.56 (1), p.1-7
Main Authors: Ma, Yulong, Peng, Tao, Yao, Xudong, Sun, Chaonan, Wang, Xiaowei
Format: Article
Language:English
Subjects:
Animals
apoptosis
Chondrocytes - metabolism
Core Binding Factor Alpha 1 Subunit - genetics
Core Binding Factor Alpha 1 Subunit - metabolism
Dexamethasone - adverse effects
Growth Plate - metabolism
growth plate chondrocytes
KLF2
Kruppel-Like Transcription Factors - genetics
Kruppel-Like Transcription Factors - metabolism
Phosphatidylinositol 3-Kinases - metabolism
PI3K/AKT pathways
Proto-Oncogene Proteins c-akt
Rats
Runx2
Salter-Harris Fractures - metabolism
Transcription Factors - metabolism
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Summary:Dexamethasone (Dex) is a type of glucocorticoid drug. Long term use can induce growth plate chondrocytes (GPCs) apoptosis, impair differentiation, and inhibit cell proliferation and bone growth. It has been reported that Krüppel-like factor 2 (KLF2) inhibits osteoblast damage induced by Dex, but the role in Dex-induced GPCs remains unclear. Dex was used to construct a model of growth plate injury in vitro. CCK-8 and TUNEL kits were used to determine cell viability and apoptosis. A model of growth plate injury was established by intraperitoneal injection of Dex. Immunohistochemistry was used to investigate the expression of KLF2 in rats. The results showed that KLF2 expression of rat tibial GPCs was down-regulated after Dex stimulation. Overexpression of KLF2 promoted cell viability and cell cycle, while inhibited apoptosis of growth plate Dex-induced chondrocytes. Moreover, KLF2 inhibited Runx2-mediated PI3K/AKT and ERK signalling pathways. And PI3K/AKT and ERK signalling pathways, which were involved in the regulation of KLF2 on GPCs. Further studies showed that KLF2 alleviated growth plate injury in vivo. In conclusion, our study found that KLF2 promoted proliferation and inhibited apoptosis of Dex-induced GPCs by targeting the Runx2-mediated PI3K/AKT and ERK signalling pathways.
ISSN:0891-6934
1607-842X
DOI:10.1080/08916934.2022.2141233