Prolactin decreases expression of Runx2, osteoprotegerin, and RANKL in primary osteoblasts derived from tibiae of adult female rats

Canadian Journal of Physiology and Pharmacology - Tập 86 Số 5 - Trang 240-248 - 2008
Narattaphol Charoenphandhu1,2,3, Jarinthorn Teerapornpuntakit1,2,3, Mei Methawasin1,2,3, Kannikar Wongdee1,2,3, Kanogwun Thongchote1,2,3, Nateetip Krishnamra1,2,3
1Consortium for Calcium and Bone Research, Faculty of Science, Mahidol University, Bangkok, Thailand
2 Department of Pathobiology, Faculty of Science, Mahidol University, Bangkok, Thailand
3Department of Physiology, Faculty of Science, Mahidol University, Rama VI Road, Bangkok, 10400, Thailand

Tóm tắt

Hyperprolactinemia caused by physiological or pathological conditions, such as those occurring during lactation and prolactinoma, respectively, results in progressive osteopenia. The underlying mechanisms, however, are controversial. Prolactin (PRL) may directly attenuate the functions of osteoblasts, since these bone cells express PRL receptors. The present study therefore aimed to investigate the effects of PRL on the expression of genes related to the osteoblast functions by using quantitative real-time PCR technique. Herein, we used primary osteoblasts that were derived from the tibiae of adult rats and displayed characteristics of differentiated osteoblasts, including in vitro mineralization. Osteoblasts exposed for 48 h to 1000 ng/mL PRL, but not to 10 or 100 ng/mL PRL, showed decreases in the mRNA expression of Runx2, osteoprotegerin (OPG), and receptor activator of nuclear factor κB ligand (RANKL) by 60.49%, 72.74%, and 87.51%, respectively. Nevertheless, PRL did not change the RANKL/OPG ratio, since expression of OPG and RANKL were proportionally decreased. These concentrations of PRL had no effect on the mRNA expression of osteocalcin and osteopontin, nor on mineralization. High pathologic concentrations of PRL (1000 ng/mL) may downregulate expression of genes that are essential for osteoblast differentiation and functions. The present results explained the clinical findings of hyperprolactinemia-induced bone loss.

Từ khóa


Tài liệu tham khảo

10.1007/s00223-004-0074-4

10.1074/jbc.M701116200

10.1002/jcp.1041430203

Bakker, A., and Klein-Nulend, J. 2003. Osteoblast isolation from murine calvariae and long bones. In Methods in Molecular Medicine: Bone Research Protocols. Edited by M.H. Helfrich and S.H. Ralston. Humana Press, New Jersey. pp. 19–28.

10.1006/bbrc.1996.1800

10.1007/s00774-004-0549-4

Bezerra F.F., 2004, Am. J. Clin. Nutr., 80, 1322, 10.1093/ajcn/80.5.1322

10.1210/jc.75.3.692

10.1210/er.19.3.225

10.1139/Y07-041

10.1210/en.140.1.96

Coss D., 2000, Am. J. Physiol. Endocrinol. Metab., 279, E1216, 10.1152/ajpendo.2000.279.6.E1216

10.1359/jbmr.2001.16.6.1015

Grimaud E., 2003, Am. J. Pathol., 163, 2021, 10.1016/S0002-9440(10)63560-2

10.2165/00003495-200464200-00003

10.1111/j.1365-2141.2006.06218.x

10.1038/nature02079

10.1067/mob.2001.113910

Jung D.U., 2006, J. Clin. Psychiatry, 67, 1391, 10.4088/JCP.v67n0909

10.1038/nm1270

10.1016/S0092-8674(00)80258-5

10.1016/j.coph.2005.06.005

10.1139/cjpp-74-10-1157

10.1507/endocrj.44.257

10.1016/j.yexcr.2007.02.002

10.1196/annals.1314.044

10.1385/ENDO:20:1-2:163

10.1139/Y06-047

Ritchie L.D., 1998, Am. J. Clin. Nutr., 67, 693, 10.1093/ajcn/67.4.693

10.1016/j.jsbmb.2004.12.039

10.1023/B:HIJO.0000021151.31118.e3

10.1016/j.lfs.2006.11.037

10.1007/s00404-002-0410-8

Wang C., 1982, Endocrinology, 110, 1085, 10.1210/endo-110-4-1085

10.1016/0303-7207(80)90077-5

10.1074/jbc.M500750200

10.1002/jcb.20332

Thông tin
Thông tin xuất bản

Canadian Journal of Physiology and Pharmacology

Tập 86 Số 5

240-248

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