Chondroitin sulfate-E mediates estrogen-induced osteoanabolism

Scientific Reports
Toshiyasu KoikeHiroshi Kitagawa

Abstract

Osteoporosis is an age-related disorder of bone remodeling in which bone resorption outstrips bone matrix deposition. Although anticatabolic agents are frequently used as first-line therapies for osteoporosis, alternative anabolic strategies that can enhance anabolic, osteogenic potential are actively sought. Sex steroid hormones, particularly estrogens, are bidirectional regulators for bone homeostasis; therefore, estrogen-mediated events are important potential targets for such anabolic therapies. Here, we show that estrogen-induced, osteoanabolic effects were mediated via enhanced production of chondroitin sulfate-E (CS-E), which could act as an osteogenic stimulant in our cell-based system. Conversely, estrogen deficiency caused reduced expression of CS-E-synthesizing enzymes, including GalNAc4S-6ST, and led to decreased CS-E production in cultures of bone marrow cells derived from ovariectomized mice. Moreover, Galnac4s6st-deficient mice had abnormally low bone mass that resulted from impaired osteoblast differentiation. These results indicated that strategies aimed at boosting CS-E biosynthesis are promising alternative therapies for osteoporosis.

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Citations

Oct 7, 2016·Glycoconjugate Journal·Tadahisa Mikami, Hiroshi Kitagawa
May 10, 2017·Molecules : a Journal of Synthetic Chemistry and Natural Product Chemistry·Marcelo LimaEdwin Yates
Jun 14, 2017·ACS Applied Materials & Interfaces·Hwan D KimNathaniel S Hwang
Apr 2, 2019·The FEBS Journal·Pinelopi KastanaEvangelia Papadimitriou
Nov 23, 2016·Journal of the American Society for Mass Spectrometry·Jonas NilssonGöran Larson
Dec 14, 2021·Frontiers in Cell and Developmental Biology·Shuji Mizumoto, Shuhei Yamada

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Methods Mentioned

BETA
gene-trap

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