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Journal of Zhejiang University SCIENCE B 2005 Vol.6 No.7 P.699~704

http://doi.org/10.1631/jzus.2005.B0699


Effects of IGF-II on promoting proliferation and regulating nitric oxide synthase gene expression in mouse osteoblast-like cell


Author(s):  SUN Wei-lian, CHEN Li-li, YAN Jie, YU Zhong-sheng

Affiliation(s):  Department of Stomatology, Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou 310009, China; more

Corresponding email(s):   yanchen@mail.hz.zj.cn

Key Words:  Insulin-like growth factor II, Osteoblast, Proliferation, Nitric oxide synthase, Nitric oxide, Regulation


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SUN Wei-lian, CHEN Li-li, YAN Jie, YU Zhong-sheng. Effects of IGF-II on promoting proliferation and regulating nitric oxide synthase gene expression in mouse osteoblast-like cell[J]. Journal of Zhejiang University Science B, 2005, 6(7): 699~704.

@article{title="Effects of IGF-II on promoting proliferation and regulating nitric oxide synthase gene expression in mouse osteoblast-like cell",
author="SUN Wei-lian, CHEN Li-li, YAN Jie, YU Zhong-sheng",
journal="Journal of Zhejiang University Science B",
volume="6",
number="7",
pages="699~704",
year="2005",
publisher="Zhejiang University Press & Springer",
doi="10.1631/jzus.2005.B0699"
}

%0 Journal Article
%T Effects of IGF-II on promoting proliferation and regulating nitric oxide synthase gene expression in mouse osteoblast-like cell
%A SUN Wei-lian
%A CHEN Li-li
%A YAN Jie
%A YU Zhong-sheng
%J Journal of Zhejiang University SCIENCE B
%V 6
%N 7
%P 699~704
%@ 1673-1581
%D 2005
%I Zhejiang University Press & Springer
%DOI 10.1631/jzus.2005.B0699

TY - JOUR
T1 - Effects of IGF-II on promoting proliferation and regulating nitric oxide synthase gene expression in mouse osteoblast-like cell
A1 - SUN Wei-lian
A1 - CHEN Li-li
A1 - YAN Jie
A1 - YU Zhong-sheng
J0 - Journal of Zhejiang University Science B
VL - 6
IS - 7
SP - 699
EP - 704
%@ 1673-1581
Y1 - 2005
PB - Zhejiang University Press & Springer
ER -
DOI - 10.1631/jzus.2005.B0699


Abstract: 
Objective: To investigate the effects of insulin-like growth factor II (IGF-II) on promoting cell proliferation, regulating levels of cellular nitric oxide (NO) and mRNA transcriptions of inducible nitric oxide synthase%29&ck%5B%5D=abstract&ck%5B%5D=keyword'>nitric oxide synthase (iNOS) and endothelial NOS (eNOS) in mouse osteoblast-like cells. Methods: Mouse osteoblastic cell line MC3T3-E1 was selected as the effective cell of IGF-II. After the cells were treated with IGF-II at different concentrations for different time duration, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) colorimetric assay was used to examine cell proliferation, and nitrate reductase method was applied to detect NO concentrations in cell culture supernatants and quantitative reverse transcriptase-polymerase chain reaction (RT-PCR) was employed to determine transcription levels of cellular iNOS and eNOS mRNAs. Results: After the MC3T3-E1 cells were treated with IGF-II at concentration of 1 ng/ml for 72 h, 10 and 100 ng/ml for 24, 48 and 72 h respectively, all the MTT values increased (P<0.05 or P<0.01) with obvious dosage-time dependent pattern. NO levels of the MC3T3-E1 cells treated with 100 ng/ml IGF-II for 48 h, and with 1, 10 and 100 ng/ml IGF-II for 72 h were remarkably lower than that of the normal control, respectively (P<0.05 or P<0.01). After the cells were treated with 100 ng/ml IGF-II for 48 h cellular iNOS mRNA levels were significantly decreased (P<0.01). But the levels of eNOS mRNA in the cells treated with each of the used IGF-II dosages for different time duration did not show any differences compared with the normal control (P>0.05). Conclusion: IGF-II at different concentrations could promote proliferation of mouse MC3T3-E1 cell. This cell proliferation promotion was associated with the low NO levels maintained by IGF-II. Higher concentration of IGF-II could down-regulate iNOS gene expression at the level of transcription but not affect transcription of eNOS mRNA, which might be one of the mechanisms for IGF-II maintenance of the low NO levels in MC3T3-E1 cells.

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Reference

[1] Aguirre, J., Buttery, L., O’Shaughnessy, M., Afzal, F., Fernandez de Marticorena, I., Hukkanen, M., Huang, P., MacIntyre, I., Polak, J., 2001. Endothelial nitric oxide synthase gene-deficient mice demonstrate marked retardation in postnatal bone formation, reduced bone volume, and defects in osteoblast maturation and activity. Am J Pathol, 158:247-257.

[2] Armour, K.J., Armour, K.E., van’t Hof, R.J., Reid, D.M., Wei, X.Q., Liew, F.Y., Ralston, S.H., 2001a. Activation of the inducible nitric oxide synthase pathway contributes to inflammation-induced osteoporosis by suppressing bone formation and causing osteoblast apoptosis. Arthritis Rheum, 44:2790-2796.

[3] Armour, K.E., Armour, K.J., Gallagher, M.E., Godecke, A., Helfrich, M.H., Reid, D.M., Ralston, S.H., 2001b. Defective bone formation and anabolic response to exogenous estrogen in mice with targeted disruption of endothelial nitric oxide synthase. Endocrinology, 142:760-766.

[4] Batista, A.C., Silva, T.A., Chun, J.H., Lara, V.S., 2002. Nitric oxide synthesis and severity of human periodontal disease. Oral Dis, 8:254-260.

[5] Fournier, B., Ferralli, J.M., Price, P.A., Schlaeppi, J.M., 1993. Comparison of the effects of insulin-like growth factors-I and -II on the human osteosarcoma cell line OHS-4. J Endocrinol., 136:173-180.

[6] Gonzalez-Gay, M.A., Llorca, J., Sanchez, E., Lopez-Nevot, M.A., Amoli, M.M., Garcia-Porrua, C., Ollier, W.E., Martin, J., 2004. Inducible but not endothelial nitric oxide synthase polymorphism is associated with susceptibility to rheumatoid arthritis in northwest Spain. Rheumatology (Oxford), 43:1182-1185.

[7] Hill, D.J., Petrik, J., Arany, E., McDonald, T.J., Delovitch, T.L., 1999. Insulin-like growth factors prevent cytokine-mediated cell death in isolated islets of Langerhans from pre-diabetic non-obese diabetic mice. J Endocrinol, 161:153-165.

[8] Jessop, H.L., Rawlinson, S.C., Pitsillides, A.A., Lanyon, L.E., 2002. Mechanical strain and fluid movement both activate extracellular regulated kinase (ERK) in osteoblast-like cells but via different signaling pathways. Bone, 31:186-194.

[9] Kaliman, P., Canicio, J., Testar, X., Palacin, M., Zorzano, A., 1999. Insulin-like growth factor-II, phosphatidylinositol 3-kinase, nuclear factor-kappaB and inducible nitricoxide synthase define a common myogenic signaling pathway. J Biol Chem, 274:17437-17444.

[10] Kanamaru, Y., Takada, T., Saura, R., Mizuno, K., 2001. Effect of nitric oxide on mouse clonal osteogenic cell, MC3T3-E1, proliferation in vitro. Kobe J Med Sci, 47:1-11.

[11] Langdahl, B.L., Kassem, M., Moller, M.K., Eriksen, E.F., 1998. The effects of IGF-I and IGF-II on proliferation and differentiation of human osteoblasts and interactions with growth hormone. Eur J Clin Invest, 28:176-183.

[12] Laufs, U., Gertz, K., Huang, P., Nickenig, G., Bohm, M., Dirnagl, U., Endres, M., 2000. Atorvastatin upregulates type III nitric oxide synthase in thrombocytes, decreases platelet activation, and protects from cerebral ischemia in normocholesterolemic mice. Stroke, 31:2442-2449.

[13] Mancini, L., Moradi-Bidhendi, N., Becherini, L., Martineti, V., MacIntyre, I., 2000. The biphasic effects of nitric oxide in primary rat osteoblasts are cGMP dependent. Biochem Biophys Res Commun, 274:477-481.

[14] Otsuka, E., Hirano, K., Matsushita, S., Inoue, A., Hirose, S., Yamaguchi, A., Hagiwara, H., 1998. Effects of nitric oxide from exogenous nitric oxide donors on osteoblastic metabolism. Eur J Pharmacol, 349:345-350.

[15] Ralston, S.H., 1997. Nitric oxide and bone: What a gas! Br J Rheumatol, 36:831-838.

[16] Robinson, M.J., Cobb, M.H., 1997. Mitogen-activated protein kinase pathways. Curr Opin Cell Biol, 9:180-186.

[17] Schini, V.B., Catovsky, S., Schray-Utz, B., Busse, R., Vanhoutte, P.M., 1994. Insulin-like growth factor I inhibits induction of nitric oxide synthase in vascular smooth muscle cells. Circ Res, 74:24-32.

[18] Togari, A., Arai, M., Mogi, M., Kondo, A., Nagatsu, T., 1998. Coexpression of GTP cyclohydrolase I and inducible nitric oxide synthase mRNAs in mouse osteoblastic cells activated by proinflammatory cytokines. FEBS Lett., 428:212-216.

[19] van’t Hof, R.J., Ralston, S.H., 2001. Nitric oxide and bone. Immunology, 103:255-261.

[20] Vincent, A.M., Feldman, E.L., 2002. Control of cell survival by IGF signaling pathways. Growth Horm IGF Res, 12:193-197.

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