Curculigoside Ameliorates Bone Loss by Influencing Mesenchymal Stem Cell Fate in Aging Mice

Senile osteoporosis is characterized by increased bone loss and fat accumulation in marrow. Curculigoside (CCG) is the major bioactive component of Curculigo orchioides, which has been used as anti-osteoporosis therapy for elder patients since antiquity. We aimed to investigate the underlying mechan...

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Published in:Frontiers in cell and developmental biology Vol. 9; p. 767006
Main Authors: Wang, Na, Li, Ziyi, Li, Shilun, Li, Yukun, Gao, Liu, Bao, Xiaoxue, Wang, Ke, Liu, Chang, Xue, Peng, Liu, Sijing
Format: Journal Article
Language:English
Published: Switzerland Frontiers Media S.A 03-12-2021
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Summary:Senile osteoporosis is characterized by increased bone loss and fat accumulation in marrow. Curculigoside (CCG) is the major bioactive component of Curculigo orchioides, which has been used as anti-osteoporosis therapy for elder patients since antiquity. We aimed to investigate the underlying mechanisms by which CCG regulated the bone-fat balance in marrow of aging mice. In our study, CCG treatment was identified to interfere with the stem cell lineage commitment both and . , CCG promoted the transcriptional co-activator with PDZ-binding motif (TAZ) expression to reverse age-related bone loss and marrow adiposity. , proper concentration of CCG upregulated TAZ expression to increase osteogenesis and decrease adipogenesis of bone marrow mesenchymal stem cells (BMSCs). This regulating effect was discounted by TAZ knockdown or the use of MEK-ERK pathway inhibitor, UO126. Above all, our study confirmed the rescuing effects of CCG on the differential shift from adipogenesis to osteogenesis of BMSCs in aging mice and provided a scientific basis for the clinical use of CCG in senile osteoporosis.
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Yinhe Wang, Nanjing University Medical School, China
Edited by: Ce Dou, Army Medical University, China
Reviewed by: Jiacan Su, Second Military Medical University, China
This article was submitted to Cellular Biochemistry, a section of the journal Frontiers in Cell and Developmental Biology
These authors have contributed equally to this work and share first authorship.
ISSN:2296-634X
2296-634X
DOI:10.3389/fcell.2021.767006