Bcl-2 and Bax expression in cartilage and bone cells after high-dose corticosterone treatment in rats

Interactions between GH, IGF-I, Glucocorticoids, and Thyroid Hormones during Skeletal Growth

“…Furthermore, excess GC induce apoptosis of osteoblasts and osteocytes in rabbit trabecular bone (84), and in osteoblasts in rat long bones (85), resulting in an almost complete absence of new bone formation. In rats, GC excess also reduces growth plate width, possibly due to decreased numbers of proliferative chondrocytes and increased apoptosis in terminal hypertrophic chondrocytes (86). These results are also consistent with the dexamethasone-induced inhibition of chondrocyte proliferation and cartilage matrix production observed in 3-mo-old rats in vivo (87), suggesting that dexamethasone is a potent negative regulator of the progression of chondrogenesis.…”

Altered Chondrocyte Apoptosis Status in Developmental Hip Dysplasia in Rabbits

“…Next, we performed western blot analysis of several apoptosis related proteins. Previous studies have demonstrated that the expression of Bcl-2 plays an apoptosis-inhibiting role, whereas the expression of Bax plays a contrary role (19,20). survival of the cells.…”

Low-Intensity Ultrasound Inhibits Apoptosis and Enhances Viability of Human Mesenchymal Stem Cells in Three-Dimensional Alginate Culture During Chondrogenic Differentiation

“…34 Apoptosis is conserved in animal species and represents critical steps in the regulated development of multicellular organisms. [35][36][37][38][39] Apoptosis is a tightly regulated process mediated by a series of proteins involved in its execution and antiapoptotic events. 40 The p53 tumor suppressor is a key regulator of the apoptotic process, being activated by various stress signals at the protein level and transactivating a number of downstream genes including p21 WAF1/CIP1 , Gadd45 (growth arrest and DNA damage inducible gene 45), and Bax (Bcl-2 associated X protein).…”