Chung Eunna, Sampson Alana Cherrell, Rylander Marissa Nichole
Virginia Tech-Wake Forest University School of Biomedical Engineering and Sciences, Virginia Tech, ICTAS Building, Stanger Street (MC 0298), Blacksburg, VA 24061, USA.
Virginia Tech-Wake Forest University School of Biomedical Engineering and Sciences, Virginia Tech, ICTAS Building, Stanger Street (MC 0298), Blacksburg, VA 24061, USA ; Department of Mechanical Engineering, Virginia Tech, ICTAS Building, Stanger Street (MC 0298), Blacksburg, VA 24061, USA.
Biomed Res Int. 2014;2014:354260. doi: 10.1155/2014/354260. Epub 2014 Jun 11.
Stress conditioning (e.g., thermal, shear, and tensile stress) of bone cells has been shown to enhance healing. However, prior studies have not investigated whether combined stress could synergistically promote bone regeneration. This study explored the impact of combined thermal and tensile stress on the induction of heat shock proteins (HSPs) and bone-related proteins by a murine preosteoblast cell line (MC3T3-E1). Cells were exposed to thermal stress using a water bath (44°C for 4 or 8 minutes) with postheating incubation (37°C for 4 hours) followed by exposure to cyclic strain (equibiaxial 3%, 0.2 Hz, cycle of 10-second tensile stress followed by 10-second rest). Combined thermal stress and tensile stress induced mRNA expression of HSP27 (1.41 relative fold induction (RFI) compared to sham-treated control), HSP70 (5.55 RFI), and osteopontin (1.44 RFI) but suppressed matrix metalloproteinase-9 (0.6 RFI) compared to the control. Combined thermal and tensile stress increased vascular endothelial growth factor (VEGF) secretion into the culture supernatant (1.54-fold increase compared to the control). Therefore, combined thermal and mechanical stress preconditioning can enhance HSP induction and influence protein expression important for bone tissue healing.
已证实对骨细胞进行应激预处理（如热应激、剪切应力和拉伸应力）可促进愈合。然而，此前的研究尚未探究联合应激是否能协同促进骨再生。本研究探讨了热应激与拉伸应力联合作用对小鼠前成骨细胞系（MC3T3-E1）诱导热休克蛋白（HSPs）和骨相关蛋白的影响。细胞先通过水浴（44°C，4或8分钟）进行热应激处理，加热后在37°C孵育4小时，随后施加循环应变（双轴3%，0.2 Hz，10秒拉伸应力后休息10秒的循环）。与对照组相比，热应激和拉伸应力联合作用诱导了HSP27（相对诱导倍数（RFI）为1.41，与假处理对照组相比）、HSP70（5.55 RFI）和骨桥蛋白（1.44 RFI）的mRNA表达，但抑制了基质金属蛋白酶-9（0.6 RFI）的表达。热应激和拉伸应力联合作用增加了培养上清液中血管内皮生长因子（VEGF）的分泌（与对照组相比增加了1.54倍）。因此，热应激与机械应力联合预处理可增强HSP的诱导，并影响对骨组织愈合重要的蛋白质表达。
