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302 results on '"Luo, Xiang-Hang"'

11. Long noncoding RNA Bmncr regulates mesenchymal stem cell fate during skeletal aging

Author

Li, Chang-Jun, Xiao, Ye, Yang, Mi, Su, Tian, Sun, Xi, Guo, Qi, Huang, Yan, and Luo, Xiang-Hang

Subjects
Aging (Biology) -- Physiological aspects, Gene expression -- Research, Osteoporosis -- Causes of, Stem cells -- Research, Chromatin, Genetic engineering, Antisense RNA, Bone morphogenetic proteins, RNA, Bone density, Health care industry
Abstract

Bone marrow mesenchymal stem cells (BMSCs) exhibit an age-related lineage switch between osteogenic and adipogenic fates, which contributes to bone loss and adiposity. Here we identified a long noncoding RNA, Bmncr, which regulated the fate of BMSCs during aging. Mice depleted of Bmncr (Bmncr-KO) showed decreased bone mass and increased bone marrow adiposity, whereas transgenic overexpression of Bmncr (Bmncr-Tg) alleviated bone loss and bone marrow fat accumulation. Bmncr regulated the osteogenic niche of BMSCs by maintaining extracellular matrix protein fibromodulin (FMOD) and activation of the BMP2 pathway. Bmncr affected local 3D chromatin structure and transcription of Fmod. The absence of Fmod modified the bone phenotype of Bmncr-Tg mice. Further analysis revealed that Bmncr would serve as a scaffold to facilitate the interaction of TAZ and ABL, and thus facilitate the assembly of the TAZ and RUNX2/PPARG transcriptional complex, promoting osteogenesis and inhibiting adipogenesis. Adeno-associated viral-mediated overexpression of Taz in osteoprogenitors alleviated bone loss and marrow fat accumulation in Bmncr-KO mice. Furthermore, restoring BMNCR levels in human BMSCs reversed the age-related switch between osteoblast and adipocyte differentiation. Our findings indicate that Bmncr is a key regulator of the age-related osteogenic niche alteration and cell fate switch of BMSCs., IntroductionGuided by genetic and molecular mediators, as well as the local microenvironment, bone marrow mesenchymal stem cells (BMSCs) differentiate into various mature cell types, including adipocytes and osteoblasts (1-3). Age-related [...]

Published
2018
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18. MicroRNA-188 regulates age-related switch between osteoblast and adipocyte differentiation

Author

Li, Chang-Jun, Cheng, Peng, Liang, Meng-Ke, Chen, Yu-Si, Lu, Qiong, Wang, Jin-Yu, Xia, Zhu-Ying, Zhou, Hou-De, Cao, Xu, Xie, Hui, Liao, Er-Yuan, and Luo, Xiang-Hang

Subjects
Stem cells -- Genetic aspects, MicroRNA -- Properties, Cell differentiation -- Genetic aspects, Health care industry
Abstract

Bone marrow mesenchymal stem cells (BMSCs) exhibit an age-dependent reduction in osteogenesis that is accompanied by an increased propensity toward adipocyte differentiation. This switch increases adipocyte numbers and decreases the number of osteoblasts, contributing to age-related bone loss. Here, we found that the level of microRNA-188 (miR-188) is markedly higher in BMSCs from aged compared with young mice and humans. Compared with control mice, animals lacking miR-188 showed a substantial reduction of age-associated bone loss and fat accumulation in bone marrow. Conversely, mice with transgenic overexpression of miR-188 in [osterix.sup.+] osteoprogenitors had greater age-associated bone loss and fat accumulation in bone marrow relative to WT mice. Moreover, using an aptamer delivery system, we found that BMSC-specific overexpression of miR-188 in mice reduced bone formation and increased bone marrow fat accumulation. We identified histone deacetylase 9 (HDAC9) and RPTOR-independent companion of MTOR complex 2 (RICTOR) as the direct targets of miR-188. Notably, BMSC-specific inhibition of miR-188 by intra-bone marrow injection of aptamer-antagomiR-188 increased bone formation and decreased bone marrow fat accumulation in aged mice. Together, our results indicate that miR-188 is a key regulator of the age-related switch between osteogenesis and adipogenesis of BMSCs and may represent a potential therapeutic target for age-related bone loss., Introduction Bone marrow mesenchymal stem cells (BMSCs) have the potential to differentiate into various cell types, including adipocytes, chondrocytes, and osteoblasts (1, 2). Age-related osteoporosis is characterized by reduced bone [...]

Published
2015
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19. Senescent immune cells release grancalcin to promote skeletal aging

Author

Li, Chang-Jun, primary, Xiao, Ye, additional, Sun, Yu-Chen, additional, He, Wen-Zhen, additional, Liu, Ling, additional, Huang, Mei, additional, He, Chen, additional, Huang, Min, additional, Chen, Kai-Xuan, additional, Hou, Jing, additional, Feng, Xu, additional, Su, Tian, additional, Guo, Qi, additional, Huang, Yan, additional, Peng, Hui, additional, Yang, Mi, additional, Liu, Guang-Hui, additional, and Luo, Xiang-Hang, additional

Published
2022
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28. A novel microRNA targeting HDAC5 regulates osteoblast differentiation in mice and contributes to primary osteoporosis in humans

Author

Li, Hui, Xie, Hui, Liu, Wei, Hu, Rong, Huang, Bi, Tan, Yan-Fei, Liao, Er-Yuan, Xu, Kang, Sheng, Zhi-Feng, Zhou, Hou-De, Wu, Xian-Ping, and Luo, Xiang-Hang

Subjects
Messenger RNA -- Physiological aspects, Osteoporosis -- Physiological aspects, Bone morphogenetic proteins -- Physiological aspects, Targeting (Nuclear strategy) -- Physiological aspects
Abstract

MicroRNAs (miRNAs) interfere with translation of specific target mRNAs and are thought to thereby regulate many cellular processes. Recent studies have suggested that miRNAs might play a role in osteoblast differentiation and bone formation. Here, we identify a new miRNA (miR-2861) in primary mouse osteoblasts that promotes osteoblast differentiation by repressing histone deacetylase 5 (HDAC5) expression at the posttranscriptional level. miR-2861 was found to be transcribed in ST2 stromal cells during bone morphogenetic protein 2-induced (BMP2-induced) osteogenesis, and overexpression of miR-2861 enhanced BMP2-induced osteoblastogenesis, whereas inhibition of miR-2861 expression attenuated it. HDAC5, an enhancer of runtrelated transcription factor 2 (Runx2) degradation, was confirmed to be a target of miR-2861. In vivo silencing of miR-2861 in mice reduced Runx2 protein expression, inhibited bone formation, and decreased bone mass. Importantly, miR-2861 was found to be conserved in humans, and a homozygous mutation in pre-miR-2861 that blocked expression of miR-2861 was shown to cause primary osteoporosis in 2 related adolescents. Consistent with the mouse data, HDAC5 levels were increased and Runx2 levels decreased in bone samples from the 2 affected individuals. Thus, our studies show that miR-2861 plays an important physiological role in osteoblast differentiation and contributes to osteoporosis via its effect on osteoblasts., Introduction MicroRNAs (miRNAs) are a growing class of small (~22 nucleotides), single-stranded noncoding RNAs found in diverse organisms (1). They negatively regulate translation of specific mRNAs by base pairing with [...]

Published
2009
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30. The role of autophagy in bone homeostasis

Author

Guo, Yi‐Fan, primary, Su, Tian, additional, Yang, Mi, additional, Li, Chang‐jun, additional, Guo, Qi, additional, Xiao, Ye, additional, Huang, Yan, additional, Liu, Ya, additional, and Luo, Xiang‐Hang, additional

Published
2021
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