Deficiency of the intermediate filament synemin reduces bone mass in vivo.

Autor:	Moorer MC; Department of Orthopaedics, University of Maryland School of Medicine, Baltimore, Maryland; and., Buo AM; Department of Orthopaedics, University of Maryland School of Medicine, Baltimore, Maryland; and., Garcia-Pelagio KP; Department of Physiology, University of Maryland School of Medicine, Baltimore, Maryland., Stains JP; Department of Orthopaedics, University of Maryland School of Medicine, Baltimore, Maryland; and jstains@som.umaryland.edu., Bloch RJ; Department of Physiology, University of Maryland School of Medicine, Baltimore, Maryland.
Jazyk:	angličtina
Zdroj:	American journal of physiology. Cell physiology [Am J Physiol Cell Physiol] 2016 Dec 01; Vol. 311 (6), pp. C839-C845. Date of Electronic Publication: 2016 Sep 07.
DOI:	10.1152/ajpcell.00218.2016
Abstrakt:	While the type IV intermediate filament protein, synemin, has been shown to play a role in striated muscle and neuronal tissue, its presence and function have not been described in skeletal tissue. Here, we report that genetic ablation of synemin in 14-wk-old male mice results in osteopenia that includes a more than 2-fold reduction in the trabecular bone fraction in the distal femur and a reduction in the cross-sectional area at the femoral middiaphysis due to an attendant reduction in both the periosteal and endosteal perimeter. Analysis of serum markers of bone formation and static histomorphometry revealed a statistically significant defect in osteoblast activity and osteoblast number in vivo. Interestingly, primary osteoblasts isolated from synemin-null mice demonstrate markedly enhanced osteogenic capacity with a concomitant reduction in cyclin D1 mRNA expression, which may explain the loss of osteoblast number observed in vivo. In total, these data suggest an important, previously unknown role for synemin in bone physiology. (Copyright © 2016 the American Physiological Society.)
Databáze:	MEDLINE
Externí odkaz:	Zobrazit plný text záznamu