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您的检索式：作者名="Jinlong Suo"
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| 1 | The RNA-binding protein Musashi2 governs osteoblast-adipocyte lineage commitment by suppressing PPARγsignaling显示文摘Osteoporosis caused by aging is characterized by reduced bone mass and accumulated adipocytes in the bone marrow cavity. How the balance between osteoblastogenesis and adipogenesis from bone marrow mesenchymal stem cells(BMSCs) is lost upon aging is still unclear. Here, we found that the RNA-binding protein Musashi2(Msi2) regulates BMSC lineage commitment. Msi2 is commonly enriched in stem cells and tumor cells. We found that its expression was downregulated during adipogenic differentiation and upregulated during osteogenic differentiation of BMSCs. Msi2 knockout mice exhibited decreased bone mass with substantial accumulation of marrow adipocytes, similar to aging-induced osteoporosis. Depletion of Msi2 in BMSCs led to increased adipocyte commitment. Transcriptional profiling analysis revealed that Msi2 deficiency led to increased PPARγ signaling.RNA-interacting protein immunoprecipitation assays demonstrated that Msi2 could inhibit the translation of the key adipogenic factor Cebpα, thereby inhibiting PPAR signaling. Furthermore, the expression of Msi2 decreased significantly during the aging process of mice, indicating that decreased Msi2 function during aging contributes to abnormal accumulation of adipocytes in bone marrow and osteoporosis. Thus, our results provide a putative biochemical mechanism for aging-related osteoporosis, suggesting that modulating Msi2 function may benefit the treatment of bone aging. | Jinlong Suo Sihai Zou Jinghui Wang Yujiao Han Lingli Zhang Chenchen Lv Bo Jiang Qian Ren Long Chen Lele Yang Ping Ji Xianyou Zheng Ping Hu Weiguo Zou | 2022 | Bone Research2022，10，3： | 5 |
| 2 | Premature aging of skeletal stem/progenitor cells rather than osteoblasts causes bone loss with decreased mechanosensation显示文摘A distinct population of skeletal stem/progenitor cells(SSPCs)has been identified that is indispensable for the maintenance and remodeling of the adult skeleton.However,the cell types that are responsible for age-related bone loss and the characteristic changes in these cells during aging remain to be determined.Here,we established models of premature aging by conditional depletion of Zmpste24(Z24)in mice and found that Prx1-dependent Z24 deletion,but not Osx-dependent Z24 deletion,caused significant bone loss.However,Acan-associated Z24 depletion caused only trabecular bone loss.Single-cell RNA sequencing(sc RNA-seq)revealed that two populations of SSPCs,one that differentiates into trabecular bone cells and another that differentiates into cortical bone cells,were significantly decreased in Prx1-Cre;Z24^(f/f)mice.Both premature SSPC populations exhibited apoptotic signaling pathway activation and decreased mechanosensation.Physical exercise reversed the effects of Z24depletion on cellular apoptosis,extracellular matrix expression and bone mass.This study identified two populations of SSPCs that are responsible for premature aging-related bone loss.The impairment of mechanosensation in Z24-deficient SSPCs provides new insight into how physical exercise can be used to prevent bone aging. | Ruici Yang Dandan Cao Jinlong Suo Lingli Zhang Chunyang Mo Miaomiao Wang Ningning Niu Rui Yue Weiguo Zou | 2023 | Bone Research2023，11，3： | 0 |
| 3 | A custom-designed panel sequencing study in 201 Chinese patients with craniosynostosis revealed novel variants and distinct mutation spectra显示文摘Craniosynostosis is a rare disease in which one or more of the cranial sutures in an infant skull prematurely fuses by turning into bone,with a prevalence of 1 in 2,000—2,500 individuals from reports in Western countries(Wilkie et al.,2017).It may restrict the growth of the brain,leading to some degree of morphological and functional abnormalities,and may affect the neurocognitive function of infants(Lattanzi et al.,2017).Genetic variants underlying craniosynostosis have been identified in cohort studies in Western populations. | Yingzhi Wu Meifang Peng Jieyi Chen Jinlong Suo Sihai Zou Yanqing Xu Andrew O.M.Wilkie Weiguo Zou Xiongzheng Mu Sijia Wang | 2021 | Journal of Genetics and Genomics2021，48，2： | 0 |
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