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Estrogen receptor-α expression in neuronal cells affects bone mass.

Journal article
Authors Claes Ohlsson
Cecilia Engdahl
Anna E Börjesson
Sara H Windahl
Erik Studer
Lars Westberg
Elias Eriksson
Antti Koskela
Juha Tuukkanen
Andree Krust
Pierre Chambon
Hans Carlsten
Marie Lagerquist
Published in Proceedings of the National Academy of Sciences of the United States of America
Volume 109
Issue 3
Pages 983-988
ISSN 1091-6490
Publication year 2012
Published at Centre for Bone and Arthritis Research
Institute of Neuroscience and Physiology, Department of Pharmacology
Institute of Medicine, Department of Internal Medicine
Pages 983-988
Language en
Links dx.doi.org/10.1073/pnas.1111436109
Subject categories Endocrinology

Abstract

It has generally been assumed that bone mass is controlled by endocrine mechanisms and the local bone environment. Recent findings demonstrate that central pathways are involved in the regulation of bone mass. Estrogen is involved in the regulation of bone homeostasis and the CNS is also a target for estrogen actions. The aim of this study was to investigate in vivo the role of central estrogen receptor-α (ERα) expression for bone mass. Nestin-Cre mice were crossed with ERα(flox) mice to generate mice lacking ERα expression specifically in nervous tissue (nestin-ERα(-/-)). Bone mineral density was increased in both the trabecular and cortical bone compartments in nestin-ERα(-/-) mice compared with controls. Femoral bone strength was increased in nestin-ERα(-/-) mice, as demonstrated by increased stiffness and maximal load of failure. The high bone mass phenotype in nestin-ERα(-/-) mice was mainly caused by increased bone formation. Serum leptin levels were elevated as a result of increased leptin expression in white adipose tissue (WAT) and slightly increased amount of WAT in nestin-ERα(-/-) mice. Leptin receptor mRNA levels were reduced in the hypothalamus but not in bone. In conclusion, inactivation of central ERα signaling results in increased bone mass, demonstrating that the balance between peripheral stimulatory and central inhibitory ERα actions is important for the regulation of bone mass. We propose that the increased bone mass in nestin-ERα(-/-) mice is mediated via decreased central leptin sensitivity and thereby increased secretion of leptin from WAT, which, in turn, results in increased peripheral leptin-induced bone formation.

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