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Metastasin S100A4 is a mediator of sex hormone-dependent formation of the cortical bone.

Journal article
Authors Malin Erlandsson
Li Bian
Ing-Marie Jonsson
Karin Andersson
Maria Bokarewa
Published in Molecular endocrinology (Baltimore, Md.)
Volume 27
Issue 8
Pages 1311-21
ISSN 1944-9917
Publication year 2013
Published at Institute of Medicine, Department of Rheumatology and Inflammation Research
Pages 1311-21
Language en
Links dx.doi.org/10.1210/me.2012-1398
Keywords Animals, Bone Density, Bone Resorption, genetics, Dehydroepiandrosterone, administration & dosage, metabolism, Estrogens, metabolism, Female, Femur, drug effects, metabolism, Mice, Mice, Knockout, Osteoblasts, metabolism, Osteocalcin, blood, Osteoclasts, metabolism, Osteogenesis, drug effects, physiology, Ovariectomy, RNA Interference, RNA, Small Interfering, S100 Proteins, genetics, metabolism
Subject categories Basic Medicine, Immunobiology

Abstract

S100A4 is a Ca-binding protein participating in regulation of cell growth, survival, and motility. Here we studied the role of S100A4 protein in sex hormone-regulated bone formation. Bone mineral density in the trabecular and cortical compartments was evaluated in female S100A4 knockout (KO), in matched wild-type (WT) counterparts, and in WT mice treated with lentiviral small hairpin RNA construct inhibiting the S100A4 gene transcription or with a nontargeting construct, by peripheral quantitative computed tomography. The effect of sex hormones on bone was measured 5 weeks after ovariectomy (OVX) and/or dehydroepiadrosterone treatment. S100A4KO had an excessive trabecular and cortical bone formation compared with the age- and sex-matched WT mice. S100A4KO had an increased periosteal circumference (P = .001), cortical thickness (P = .056), and cortical area (P = .003), which predicted 20% higher bone strength in S100A4KO (P = .013). WT mice treated with small hairpin RNA-S100A4 showed an increase of the cortical bone parameters in a fashion identical with S100A4KO mice, indicating the key role of S100A4 in the changed bone formation. S100A4KO mice had higher serum levels of osteocalcin and a higher number of osteocalcin-positive osteoblasts under the periosteum. OVX-S100A4 resulted in the loss of the cortical bone supported by high CTX-I levels, whereas no such changes were observed in OVX-WT mice. S100A4KO mice resisted the dehydroepiadrosterone -induced bone formation observed in the WT counterparts. Our study indicates that S100A4 is a regulator of bone formation, which inhibits bone excess in the estrogen-sufficient mice and prevents the cortical bone loss in the estrogen-deprived mice.

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