Cyclic mechanical stretch regulates the AMPK/Egr1 pathway in tenocytes via Ca2+-mediated mechanosensing
Calcium in biology
Mechanotransduction
DOI:
10.1080/03008207.2022.2044321
Publication Date:
2022-03-01T10:33:25Z
AUTHORS (7)
ABSTRACT
Purpose Mechanical stimuli are essential for the maintenance of tendon tissue homeostasis. The study aims to elucidate mechanobiological mechanisms underlying tenocyte homeostasis by cyclic mechanical stretch under high-glucose (HG) condition.Materials and methods Primary tenocytes were isolated from rat Achilles 2D-cultured HG condition. in vitro effects a single bout, 2-h biaxial session (1 Hz, 8%) on primary explored through Flexcell system. Cell viability, tenogenic gene expression, intracellular calcium concentration, focal adhesion kinase (FAK) signaling pathway activation analyzed with or without stretch.Results increased proliferation upregulated early growth response protein 1 (Egr1) expression. An increase was observed after 30 min stretching. phosphorylated FAK, calmodulin-dependent 2 (CaMKK2), 5' adenosine monophosphate-activated (AMPK) time-dependent manner, these abrogated blocking calcium. Inhibition CaMKK2, AMPK downregulated expression Egr1. In addition, reinforced cytoskeletal organization via (Ca2+)/FAK signaling.Conclusions Our demonstrated that stretch-induced influx activated CaMKK2/AMPK FAK-cytoskeleton reorganization, thereby promoting Egr1, which may help maintain cell characteristics context diabetic tendinopathy.
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