2014  0,718
2013  0,739
2012  0,637
2011  0,658
2010  0,654
2009  0,570
2008  0,849
2007  0,805
2006  0,330
2005  0,435
2004  0,623
2003  0,567
2002  0,641
2001  0,490
2000  0,477
1999  0,762
1998  0,785
1997  0,507
1996  0,518
1995  0,502
Vol 51(2017) N 2 p. 300-312; DOI 10.1134/S0026893317020157 Full Text

J.Y. Li1, S.G. Liu3, G.N. Xiao4, M.Y. Mao1, X.W. Zhang1, H.Q. Sun1,2*

Fibroblast growth factor receptor 1 propagates estrogen and fluid shear stress driven proliferation and differentiation response in MC3T3-E1 cells

1Department of Prosthodontics, College of Stomatology, Shandong University, Jinan, Shandong Province, 250012 China
2Shandong Provincial Key Laboratory of Oral Biomedicine, Jinan, Shandong Province, 250012 China
3Guangdong Provincial Hospital of Stomatology, Guangzhou, Guangdong, 510280 China
4Dental ClinicTianjin Medical University General Hospital, Tianjin, 300052 China

Received - 2016-01-20; Accepted - 2016-03-03

Fluid shear stress (FSS) and estrogen exposure positively regulate bone metabolism. Fibroblast growth factor receptor 1 (FGFR1) plays a vital role in FSS-induced osteogenesis. An in vitro experiment with MC3T3-E1 cells combined with microarray analysis aided us in identification of the genes differentially expressed in response to FSS and highlighted the role of FGFR1 in this process. Both estrogen exposure and FSS increase methyl thiazol tetrazolium (MTT) values and alkaline phosphatase (ALP) activity, as well as the levels of Runt-related transcription factor 2 (Runx2) and osteocalcin (OCN). The effects of estrogen exposure and FSS were cumulative. Treatment with PD166866 inhibitor of the FGFR1 reduced the MTT values, increased ALP activity, and increased the levels of Runx2 and OCN. To investigate the regulation of FGFR1 signaling in stressed cells, a number of key components of the mitogen-activated protein kinase (MAPK) cascade were quantitatively examined. Neither estrogen nor FSS change the protein expression of extracellular signal-regulated kinase (ERK), Jun amino-terminal kinases (JNK) or p38, but positively influence their phosphorylation levels. Treatment with the FGFR1 inhibitor induced an increase in ERK phosphorylation levels only. In summary, estrogen exposure and FSS have a synergistic effect in osteogenesis. FGFR1 promotes osteoblast proliferation and inhibits the differentiation of osteoblasts. In MC3T3-E1 cells, FGFR1 signaling responds to independent and combined effects of estrogen and FSS. MAPK cascades participate in osteogenesis, but only the ERK signaling pathway responds to FGFR1.

MC3T3-E1 cells, estrogen, FSS, FGFR1, MAPK