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首页> 美国卫生研究院文献>Molecular Medicine Reports >Fluid shear stress induces osteoblast differentiation and arrests the cell cycle at the G0 phase via the ERK1/2 pathway
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Fluid shear stress induces osteoblast differentiation and arrests the cell cycle at the G0 phase via the ERK1/2 pathway

机译：流体剪切应力诱导成骨细胞分化并通过ERK1 / 2途径阻止G0期的细胞周期

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Numerous studies have demonstrated that fluid shear stress (FSS) may promote the proliferation and differentiation of osteoblast cells. However, proliferation and differentiation are mutually exclusive processes and are unlikely to be promoted by FSS simultaneously. Cell proliferation and differentiation induced by FSS has rarely been reported. In order to provide an insight into this process, the present study investigated the effects of FSS on osteoblast-like MC3T3 cells in the G0/G1 phase, the period during which the fate of a cell is determined. The results of the present study demonstrated that FSS promoted alkaline phosphatase (ALP) activity, and the mRNA expression and protein expression of osteocalcin, collagen type I and runt-related transcription factor 2 (Runx2), while inhibiting DNA synthesis and arresting the cell cycle at the G0/G1 phase. The increase in Runx2 and ALP activity was accompanied by the activation of calcium/calmodulin-dependent protein kinase type II (CaMK II) and extracellular signal-regulated kinases 1/2 (ERK1/2), which was completely abolished by treatment with KN93 and U0126, respectively. In addition, the inhibition of ERK1/2, although not CaMK II, decreased p21Cip/Kip activity, resulting in an increase in cell number and S phase re-entry. The results of the present study indicated that in the G0/G1 phase, FSS promoted osteoblast differentiation via the CaMK II and ERK1/2 signaling pathways, and blocked the cell cycle at the G0/G1 phase via the ERK1/2 pathway only. The present findings provided an increased understanding of osteoblastic mechanobiology.
机译：大量研究表明，流体剪切应力（FSS）可能促进成骨细胞的增殖和分化。但是，扩散和分化是相互排斥的过程，FSS不可能同时促进。由FSS诱导的细胞增殖和分化很少报道。为了提供对该过程的见解，本研究调查了FSS对G0 / G1期中成骨细胞样MC3T3细胞的影响，G0 / G1期是确定细胞命运的时期。本研究的结果表明，FSS可以促进碱性磷酸酶（ALP）的活性，并促进骨钙素，I型胶原和矮子相关转录因子2（Runx2）的mRNA表达和蛋白质表达，同时抑制DNA合成并阻止细胞周期在G0 / G1阶段。 Runx2和ALP活性的增加伴随着钙/钙调蛋白依赖性蛋白激酶II型（CaMK II）和细胞外信号调节激酶1/2（ERK1 / 2）的激活，而用KN93和U0126。此外，尽管不是CaMK II，但对ERK1 / 2的抑制作用会降低p21 Cip / Kip 活性，从而导致细胞数量增加和S期重入。本研究的结果表明，在G0 / G1期，FSS仅通过CaMK II和ERK1 / 2信号通路促进成骨细胞分化，而仅通过ERK1 / 2通路阻止G0 / G1期的细胞周期。目前的发现提供了对成骨细胞力学的进一步了解。

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