TY - JOUR AB - The ability of intermittent parathyroid hormone (1‑34) [PTH(1‑34)] treatment to enhance bone‑implant osseointegration was recently demonstrated in vivo. However, the mechanisms through which PTH (1‑34) regulates bone marrow‑derived stromal cells (BMSCs) remain unclear. The present study thus aimed to investigate the effects of PTH(1‑34) on the migration and adhesion of, and rictor/mammalian target of rapamycin complex 2 (mTORC2) signaling in BMSCs. In the present study, BMSCs were isolated from Sprague‑Dawley rats treated with various concentrations of PTH(1‑34) for different periods of time. PTH(1‑34) treatment was performed with or without an mTORC1 inhibitor (20 nM rapamycin) and mTORC1/2 inhibitor (10 µM PP242). Cell migration was assessed by Transwell cell migration assays and wound healing assays. Cell adhesion and related mRNA expression were investigated through adhesion assays and reverse transcription‑quantitative polymerase chain reaction (RT‑qPCR), respectively. The protein expression of chemokine receptors (CXCR4 and CCR2) and adhesion factors [intercellular adhesion molecule 1 (ICAM‑1), fibronectin and integrin β1] was examined by western blot analysis. The results revealed that various concentrations (1, 10, 20, 50 and 100 nM) of PTH(1‑34) significantly increased the migration and adhesion of BMSCs, as well as the expression of CXCR4, CCR2, ICAM‑1, fibronectin and integrin β1. In addition, the p‑Akt and p‑S6 levels were also upregulated by PTH(1‑34). BMSCs subjected to mTORC1/2 signaling pathway inhibition or rictor silencing exhibited a markedly reduced PTH‑induced migration and adhesion, while no such effect was observed for the BMSCs subjected to mTORC1 pathway inhibition or raptor silencing. These results indicate that PTH(1‑34) promotes BMSC migration and adhesion through rictor/mTORC2 signaling in vitro. Taken together, the results of the present study reveal an important mechanism for the therapeutic effects of PTH(1‑34) on bone‑implant osseointegration and suggest a potential treatment strategy based on the effect of PTH(1‑34) on BMSCs. AD - Department of Orthopedics, Guangzhou Panyu Central Hospital, Guangzhou, Guangdong 510080, P.R. China Department of Orthopedics, Peking University Third Hospital, Beijing 100191, P.R. China Guangdong Provincial Key Laboratory of Orthopedics and Traumatology, The First Affiliated Hospital of Sun Yat‑sen University, Guangzhou, Guangdong 510080, P.R. China Department of Orthopedics, Zhujiang Hospital of Southern Medical University, Guangzhou, Guangdong 510280, P.R. China AU - Lv,Zhong AU - Muheremu,Aikeremujiang AU - Bai,Xiaochun AU - Zou,Xuenong AU - Lin,Tao AU - Chen,Bailing DA - 2020/12/01 DO - 10.3892/ijmm.2020.4754 EP - 2101 IS - 6 JO - Int J Mol Med KW - PTH BMSCs rictor/mTORC2 pathway migration adhesion PY - 2020 SN - 1107-3756 1791-244X SP - 2089 ST - PTH(1‑34) activates the migration and adhesion of BMSCs through the rictor/mTORC2 pathway T2 - International Journal of Molecular Medicine TI - PTH(1‑34) activates the migration and adhesion of BMSCs through the rictor/mTORC2 pathway UR - https://doi.org/10.3892/ijmm.2020.4754 VL - 46 ER -