A Core Omnigenic Non-coding Trait Governing Dex-Induced Osteoporotic Effects Identified Without DEXA

Iatrogenic glucocorticoid (GC)-induced osteoporosis (GIO) is an idiosyncratic form of secondary osteoporosis. Genetic predisposition among individuals may give rise to variant degree of phenotypic changes but there has yet been a documented unified pathway to explain the idiosyncrasy. In this study,...

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Autores principales:	Li Lu, Yanzhen Cai, Xiaoling Luo, Zhangting Wang, Sin Hang Fung, Huanhuan Jia, Chi Lam Yu, Wai Yee Chan, Kai Kei Miu, Wende Xiao
Formato:	article
Lenguaje:	EN
Publicado:	Frontiers Media S.A. 2021
Materias:	glucocorticoid glucocorticoid-induced osteoporosis bone loss bone morphogenetic protein signaling pathway osteoblasts differentiation cis-expression quantitative trait loci Therapeutics. Pharmacology RM1-950
Acceso en línea:	https://doaj.org/article/6d2c8ea5b86f45f8b7047596e82833d9
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spelling	oai:doaj.org-article:6d2c8ea5b86f45f8b7047596e82833d92021-11-30T16:27:05ZA Core Omnigenic Non-coding Trait Governing Dex-Induced Osteoporotic Effects Identified Without DEXA1663-981210.3389/fphar.2021.750959https://doaj.org/article/6d2c8ea5b86f45f8b7047596e82833d92021-11-01T00:00:00Zhttps://www.frontiersin.org/articles/10.3389/fphar.2021.750959/fullhttps://doaj.org/toc/1663-9812Iatrogenic glucocorticoid (GC)-induced osteoporosis (GIO) is an idiosyncratic form of secondary osteoporosis. Genetic predisposition among individuals may give rise to variant degree of phenotypic changes but there has yet been a documented unified pathway to explain the idiosyncrasy. In this study, we argue that the susceptibility to epigenetic changes governing molecular cross talks along the BMP and PI3K/Akt pathway may underline how genetic background dictate GC-induced bone loss. Concordantly, osteoblasts from BALB/c or C57BL/6 neonatal mice were treated with dexamethasone for transcriptome profiling. Furthermore, we also confirmed that GC-pre-conditioned mesenchymal stem cells (MSCs) would give rise to defective osteogenesis by instigating epigenetic changes which affected the accessibility of enhancer marks. In line with these epigenetic changes, we propose that GC modulates a key regulatory network involving the scavenger receptor Cd36 in osteoblasts pre-conditioning pharmacological idiosyncrasy in GIO.Li LuYanzhen CaiXiaoling LuoZhangting WangSin Hang FungHuanhuan JiaHuanhuan JiaChi Lam YuWai Yee ChanKai Kei MiuWende XiaoFrontiers Media S.A.articleglucocorticoidglucocorticoid-induced osteoporosisbone lossbone morphogenetic protein signaling pathwayosteoblasts differentiationcis-expression quantitative trait lociTherapeutics. PharmacologyRM1-950ENFrontiers in Pharmacology, Vol 12 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	glucocorticoid glucocorticoid-induced osteoporosis bone loss bone morphogenetic protein signaling pathway osteoblasts differentiation cis-expression quantitative trait loci Therapeutics. Pharmacology RM1-950
spellingShingle	glucocorticoid glucocorticoid-induced osteoporosis bone loss bone morphogenetic protein signaling pathway osteoblasts differentiation cis-expression quantitative trait loci Therapeutics. Pharmacology RM1-950 Li Lu Yanzhen Cai Xiaoling Luo Zhangting Wang Sin Hang Fung Huanhuan Jia Huanhuan Jia Chi Lam Yu Wai Yee Chan Kai Kei Miu Wende Xiao A Core Omnigenic Non-coding Trait Governing Dex-Induced Osteoporotic Effects Identified Without DEXA
description	Iatrogenic glucocorticoid (GC)-induced osteoporosis (GIO) is an idiosyncratic form of secondary osteoporosis. Genetic predisposition among individuals may give rise to variant degree of phenotypic changes but there has yet been a documented unified pathway to explain the idiosyncrasy. In this study, we argue that the susceptibility to epigenetic changes governing molecular cross talks along the BMP and PI3K/Akt pathway may underline how genetic background dictate GC-induced bone loss. Concordantly, osteoblasts from BALB/c or C57BL/6 neonatal mice were treated with dexamethasone for transcriptome profiling. Furthermore, we also confirmed that GC-pre-conditioned mesenchymal stem cells (MSCs) would give rise to defective osteogenesis by instigating epigenetic changes which affected the accessibility of enhancer marks. In line with these epigenetic changes, we propose that GC modulates a key regulatory network involving the scavenger receptor Cd36 in osteoblasts pre-conditioning pharmacological idiosyncrasy in GIO.
format	article
author	Li Lu Yanzhen Cai Xiaoling Luo Zhangting Wang Sin Hang Fung Huanhuan Jia Huanhuan Jia Chi Lam Yu Wai Yee Chan Kai Kei Miu Wende Xiao
author_facet	Li Lu Yanzhen Cai Xiaoling Luo Zhangting Wang Sin Hang Fung Huanhuan Jia Huanhuan Jia Chi Lam Yu Wai Yee Chan Kai Kei Miu Wende Xiao
author_sort	Li Lu
title	A Core Omnigenic Non-coding Trait Governing Dex-Induced Osteoporotic Effects Identified Without DEXA
title_short	A Core Omnigenic Non-coding Trait Governing Dex-Induced Osteoporotic Effects Identified Without DEXA
title_full	A Core Omnigenic Non-coding Trait Governing Dex-Induced Osteoporotic Effects Identified Without DEXA
title_fullStr	A Core Omnigenic Non-coding Trait Governing Dex-Induced Osteoporotic Effects Identified Without DEXA
title_full_unstemmed	A Core Omnigenic Non-coding Trait Governing Dex-Induced Osteoporotic Effects Identified Without DEXA
title_sort	core omnigenic non-coding trait governing dex-induced osteoporotic effects identified without dexa
publisher	Frontiers Media S.A.
publishDate	2021
url	https://doaj.org/article/6d2c8ea5b86f45f8b7047596e82833d9
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A Core Omnigenic Non-coding Trait Governing Dex-Induced Osteoporotic Effects Identified Without DEXA

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