Differentially expressed genes and signalling pathways are involved in mouse osteoblast-like MC3T3-E1 cells exposed to 17-β estradiol

Zhen-Zhen Shang , Xin Li , Hui-Qiang Sun , Guo-Ning Xiao , Cun-Wei Wang , Qi Gong

International Journal of Oral Science ›› 2014, Vol. 6 ›› Issue (3) : 142 -149.

PDF
International Journal of Oral Science ›› 2014, Vol. 6 ›› Issue (3) : 142 -149. DOI: 10.1038/ijos.2014.2
Article

Differentially expressed genes and signalling pathways are involved in mouse osteoblast-like MC3T3-E1 cells exposed to 17-β estradiol

Author information +
History +
PDF

Abstract

Bone-forming cells drastically alter their gene expression patterns in response to the hormone estrogen, according to researchers in China. A team led by Hui-Qiang Sun from Shandong University used microarray analyses to identify all the genes in a mouse bone-forming cell line (MC3T3-E1), where expression increased or decreased following treatment with a form of estrogen known as 17-β estradiol. Approximately 5 400 genes showed changed expression patterns. The researchers classified these genes into more than 1 500 different functional groups involved in approximately 50 different molecular pathways. In general, genes associated with cell proliferation and differentiation were switched on by estrogen, whereas genes involved in programmed cell death and bone resorption were switched off by the hormone treatment. The findings could guide therapies that aim to promote bone regeneration.

Keywords

17-β estradiol / MC3T3-E1 cell / microarray / signal transduction

Cite this article

Download citation ▾
Zhen-Zhen Shang, Xin Li, Hui-Qiang Sun, Guo-Ning Xiao, Cun-Wei Wang, Qi Gong. Differentially expressed genes and signalling pathways are involved in mouse osteoblast-like MC3T3-E1 cells exposed to 17-β estradiol. International Journal of Oral Science, 2014, 6(3): 142-149 DOI:10.1038/ijos.2014.2

登录浏览全文

4963

注册一个新账户 忘记密码

References

[1]

Syed F, Khosla S. Mechanism of sex steroid effects on bone. Biochem Biophys Res Commun, 2005, 328(3): 688-696.

[2]

Turner RT, Riggs BL, Spelsberg TC. Skeletal effects of estrogen. Endocr Rev, 1994, 15(3): 275-300.

[3]

Spelsberg TC, Subramaniam M, Riggs BL. The actions and interactions of sex steroids and growth factors/cytokines on the skeleton. Mol Endocrinol, 1999, 13(6): 819-828.

[4]

Richard DJ, Subramaniam M, Spelsberg TC. Molecular and cellular mechanisms of estrogen action on the skeleton. J Cell Biochem, 1999, 75(S32/S33): 123-132.

[5]

Kameda T, Mano H, Yuasa T. Estrogen inhibits bone resorption by directly inducing apoptosis of the bone-resorbing osteoclasts. J Exp Med, 1997, 186(4): 489-495.

[6]

Kassem M, Harris SA, Spelsberg TC. Estrogen inhibits interleukin-6 production and gene expression in a human osteoblastic cell line with high levels of estrogen receptors. J Bone Miner Res, 1996, 11(2): 193-199.

[7]

Oursler MJ, Cortese C, Keeting P. Modulation of transforming growth factor-β production in normal human osteoblast-like cells by 17β-estradiol and parathyroid hormone. Endocrinology, 1991, 129(6): 3313-3320.

[8]

Kousteni S, Chen JR, Bellido T. Reversal of bone loss in mice by nongenotropic signaling of sex steroids. Science, 2002, 298(5594): 843-846.

[9]

Boyce BF, Xing L. Functions of RANKL/RANK/OPG in bone modeling and remodeling. Arch Biochem Biophys, 2008, 473(2): 139-146.

[10]

Hofbauer LC, Khosla S, Dunstan CR. Estrogen stimulates gene expression and protein production of osteoprotegerin in human osteoblast cells. Endocrinology, 1999, 140(9): 4367-4370.

[11]

Krum SA, Miranda-Carboni GA, Hauschka PV. Estrogen protects bone by inducing Fas ligand in osteoblasts to regulate osteoclast survival. EMBO J, 2008, 27(3): 535-545.

[12]

Zhou S, Turgeman G, Harris SE. Estrogens activate bone morphogenetic protein-2 gene transcription in mouse mesenchymal stem cells. Mol Endocrinol, 2003, 17(1): 56-66.

[13]

Eriksen EF, Colvard DS, Berg NJ. Evidence of estrogen receptors in normal human osteoblast-like cells. Science, 1988, 241(4861): 84-86.

[14]

Komm BS, Terpening CM, Benz DJ. Estrogen binding, receptor mRNA, and biologic response in osteoblast-like osteosarcoma cells. Science, 1988, 241(4861): 81-84.

[15]

Qu Q, Perala-Heape M, Kapanen A. Estrogen enhances differentiation of osteoblasts in mouse bone marrow culture. Bone, 1998, 22(3): 201-209.

[16]

Tobias JH, Compston JE. Does estrogen stimulate osteoblast function in postmenopausal women?. Bone, 1999, 24(2): 121-124.

[17]

Bradford PG, Gerace KV, Roland RL. Estrogen regulation of apoptosis in osteoblasts. Physiol Behav, 2010, 99(2): 181-185.

[18]

Palmer RM, Loveridge N, Thomson BM. Effects of a polyclonal antiserum to rat growth hormone on circulating insulin-like growth factor (IGF)-I and IGF-binding protein concentrations and the growth of muscle and bone. J Endocrinol, 1994, 142: 85-91.

[19]

Pfaffl MW. A new mathematical model for relative quantification in real-time RT-PCR. Nucleic Acids Res, 2001, 29(9): e45.

[20]

Brazma A, Hingamp P, Quackenbush J. Minimum information about a microarray experiment (MIAME)-toward standards for microarray data. Nat Genet, 2001, 29(4): 365-371.

[21]

Ames MS, Hong S, Lee HR. Estrogen deficiency increases variability of tissue mineral density of alveolar bone surrounding teeth. Arch Oral Biol, 2010, 55(8): 599-605.

[22]

August M, Chung K, Chang Y. Influence of estrogen status on endosseous implant osseointegration. J Oral Maxillofac Surg, 2001, 59(11): 1285-1289.

[23]

Li YN, Wang D, Wang Z. The effect of 17β-estradiol on the osseointegration of dental implants in osteoporostic rats. Chin J Geriatr Dent, 2012, 10(3): 160-163.

[24]

Genetos DC, Geist DJ, Liu D. Fluid shear-induced ATP secretion mediates prostaglandin release in MC3T3-E1 osteoblast. J Bone Miner Res, 2005, 20(1): 41-49.

[25]

Park JB. Combination of simvastatin and bone morphogenetic protein-2 enhances the differentiation of osteoblasts by regulating the expressions of phospho-Smad1/5/8. Exp Ther Med, 2012, 4(2): 303-306.

[26]

Katsuyama H, Arii M, Tomita M. Association between estrogen receptor alpha polymorphisms and equol production, and its relation to bone mass. Int J Mol Med, 2009, 23(6): 793-798.

[27]

Deng Y, Chen X, Hu YF. Effects of estrogen versus letrozole on chicken embryo frontal bone osteoblast. J Clin Rehabil Tissue Eng Res, 2010, 14(7): 1157-1161.

[28]

Shen Q, Zhu S, Hu J. Recombinant human bone morphogenetic protein-4 (BMP-4)-stimulated cell differentiation and bone formation within the expanding calvarial suture in rats. J Craniofac Surg, 2009, 20(5): 1561-1565.

[29]

Valverde-Franco G, Liu H, Davidson D. Defective bone mineralization and osteopenia in young adult FGFR3−/− mice. Hum Mol Genet, 2004, 13(3): 271-284.

[30]

Bradford PG, Gerace KV, Roland RL. Estrogen regulation of apoptosis in osteoblasts. Physiol Behav, 2010, 99(2): 181-185.

[31]

Kim S, Koga T, Isobe M. Stat1 functions as a cytoplasmic attenuator of Runx2 in the transcriptional program of osteoblast differentiation. Genes Dev, 2003, 17(16): 1979-1991.

[32]

Tajima K, Takaishi H, Takito J. Inhibition of STAT1 accelerates bone fracture healing. J Orthop Res, 2010, 28(7): 937-941.

[33]

Woeckel VJ, Eijken M, van de Peppel J. IFNβ impairs extracellular matrix formation leading to inhibition of mineralization by effects in the early stage of human osteoblast differentiation. J Cell Physiol, 2012, 227(6): 2668-2676.

[34]

Yasuda H, Shima N, Nakagawa N. Osteoclast differentiation factor is a ligand for osteoprotegerin/osteoclastogenesis-inhibitory factor and is identical to TRANCE/RANKL. Proc Natl Acad Sci U S A, 1998, 95(7): 3597-3602.

[35]

Yasuda H, Shima N, Nakagawa N. Identity of osteoclastogenesis inhibitory factor(OCIF) and osteoprotegerin (OPG): a mechanism by which OPG/OCIF inhibits osteoclastogenesis in vitro. . Endocrinology, 1998, 139(3): 1329-1337.

[36]

Bucay N, Sarosi I, Dunstan CR. Osteoprotegerin-deficient mice develop early onset osteoporosis and arterial calcification. Genes Dev, 1998, 12(9): 1260-1268.

[37]

Bord S, Ireland DC, Beavan SR. The effects of estrogen on osteoprotegerin, RANKL, and estrogen receptor expression in human osteoblasts. Bone, 2003, 32(2): 136-141.

[38]

Babij P, Zhao W, Small C. High bone mass in mice expressing a mutant LRP5 gene. J Bone Miner Res, 2003, 18(6): 960-974.

[39]

Day TF, Guo X, Garrett-Beal L. Wnt/beta-catenin signaling in mesenchymal progenitors controls osteoblast and chondrocyte differentiation during vertebrate skeletogenesis. Dev Cell, 2005, 8(5): 739-750.

[40]

Hens JR, Wilson KM, Dann P. TOPGALl mice show that the canonical Wnt signaling pathway is active during bone development and growth and is activated by mechanical loading in vitro. . J Bone Miner Res, 2005, 20(7): 1103-1113.

[41]

Silkstone D, Hong H, Alman BA. Beta-catenin in the race to fracture repair: in it to Wnt. Nat Clin Pract Rheumatol, 2008, 4(8): 413-419.

[42]

Almeida M, Han L, Obrien CA. Classical genotropic versus kinase-initiated regulation of gene transcription by the estrogen receptor alpha. Endocrinology, 2006, 147(4): 1986-1996.

[43]

Kousteni S, Almeida M, Han L. Induction of osteoblast differentiation by selective activation of kinase-mediated actions of the estrogen receptor. Mol Cell Biol, 2007, 27(4): 1516-1530.

[44]

Holmen SL, Zylstra CR, Mukherjee A. Essential role of beta-catenin in postnatal bone acquisition. J Biol Chem, 2005, 280(22): 21162-21168.

[45]

Gaur T, Lengner CJ, Hovhannisyan H. Canonical WNT signaling promotes osteogenesis by directly stimulating Runx2 gene expression. J Biol Chem, 2005, 280(39): 33132-33140.

[46]

Vandenberg AL, Sassoon DA. Non-canonical Wnt signaling regulates cell polarity in female reproductive tract development via van Gogh-like 2. Development, 2009, 136(9): 1559-1570.

[47]

Hakeda Y, Yoshino T, Natakani Y. Prostaglandin E2 stimulates DNA synthesis by a cyclic AMP-independent pathway in osteoblastic clone MC3T3-E1 cells. J Cell Physiol, 1986, 128(2): 155-161.

[48]

Xiao G, Jiang D, Thomas P. MAPK pathways activate and phosphorylate the osteoblast-specific transcription factor, Cbfa1. J Biol Chem, 2000, 275(6): 4453-4459.

[49]

Wei P, Yuan GH, Yang MH. The Significance of the change of the gap junction protein connexin 43 expressed in osteoblasts and osteoclasts in ovaricetomized rats. J North Sichuan Med Coll, 2006, 21(4): 304-307.

[50]

Di WL, Lachelin GC, McGarrigle HH. Oestriol and oestradiol increase cell to cell communication and connexin43 protein expression in human myometrium. Mol Hum Reprod, 2001, 7(7): 671-679.

[51]

Chen CC, Lin CC, Lee TM. 17 Beta-estradiol decreases vulnerability to ventricular arrhythmias by preserving connexin43 protein in infracted rats. Eur J Pharmacol, 2010, 629(1/2/3): 73-81.

[52]

Ren J, Wang XH, Wang GC. 17β estradiol regulation of connexin 43-based gap junction and mechanosensitivity through classical estrogen receptor pathway in osteocyte-like MLO-Y4 cells. Bone, 2013, 53(2): 587-596.

[53]

Luo G, Hofmann C, Bronckers AL. BMP-7 is an inducer of nephrogenesis, and is also required for eye development and skeletal patterning. Genes Dev, 1995, 9(22): 2808-2820.

[54]

Ducy P, Zhang R, Geoffroy V. Osf2/Cbfa1: a transcriptional activator of osteoblast differentiation. Cell, 1997, 89(5): 747-754.

[55]

Takuwa Y, Ohse C, Wang EA. Bone morphogenetic protein-2 stimulates alkaline phosphatase activity and collagen synthesis in cultured osteoblastic cells, MC3T3-E1. Biochem Biophys Res Commun, 1991, 174(1): 96-101.

[56]

Maliakal JC, Asahina I, Hauschka PV. Osteogenic protein-1 (BMP-7) inhibits cell proliferation and stimulates the expression of markers characteristic of osteoblast phenotype in rat osteosarcoma (17/2.8) cells. Growth Factors, 1994, 11(3): 227-234.

[57]

Li IW, Cheifetz S, McCulloch CA. Effects of osteogenic protein-1 (OP-1, BMP-7) on bone matrix protein expression by fetal rat calvarial cells are differentiation stage specific. J Cell Physiol, 1996, 169(1): 115-125.

[58]

Yeh LC, Adamo ML, Olson MS. Osteogenic protein-1 and insulin-like growth factor I synergistically stimulate rat osteoblastic cell differentiation and proliferation. Endocrinology, 1997, 138(10): 4181-4190.

[59]

Bord S, Horner A, Hembry RM. Stromelysin-1 (MMP-3) and stromelysin-2 (MMP-10) expression in developing human bone: potential roles inskeletal development. Bone, 1998, 23(1): 7-12.

[60]

Breckon JJ, Papaioannou S, Kon LW. Stromelysin (MMP-3) synthesis is up-regulated in estrogen-deficient mouse osteoblasts in vivo and in vitro. . J Bone Miner Res, 1999, 14(11): 1880-1890.

[61]

Dew G, Murphy G, Stanton H. Localisation of matrix metalloproteinases and TIMP-2 in resorbing mouse bone. Cell Tissue Res, 2000, 299(3): 385-394.

[62]

Kusano K, Miyaura C, Inada M. Regulation of matrix metalloproteinases (MMP-2, -3, -9, and -13) by interleukin-1 and interleukin-6 in mousecalvaria: association of MMP induction with bone resorption. Endocrinology, 1998, 139(3): 1338-1345.

[63]

Inoue K, Mikuni-Takagaki Y, Oikawa K. A crucial role for matrix metalloproteinase 2 in osteocytic canalicular formation and bone metabolism. J Biol Chem, 2006, 281(44): 33814-33824.

[64]

Apte SS, Fukai N, Beier DR. The matrix metalloproteinase-14 (MMP-14) gene is structurally distinct from other MMP genes and is co-expressed with the TIMP-2 gene during mouse embryogenesis. J Biol Chem, 1997, 272(41): 25511-25517.

AI Summary AI Mindmap
PDF

141

Accesses

0

Citation

Detail

Sections
Recommended

AI思维导图

/