Osteoblast versus Adipocyte: Bone Marrow Microenvironment-Guided Epigenetic Control

Li, Jiao; Zuo, Bin; Zhang, Li; Dai, Liming; Xiao-ling, Zhang

doi:10.1159/000489053

Cited by 15 publications

(10 citation statements)

References 112 publications

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“…There is an inverse relationship between osteogenic and adipogenic differentiation. 27 This inverse relationship is indicated by the concurrent upregulation of RUNX-2 (a master regulator of osteogenesis) and downregulation of the adipogenic marker PPAR-γ (which induces cells to differentiate into adipocytes). [28][29][30] In addition, supplementation with a high (300 ng/mL) SeNP concentration results in excessive ROS generation with compromised antioxidant defense and decreased cell viability.…”

mentioning

confidence: 99%

Selenium Nanoparticles by Moderating Oxidative Stress Promote Differentiation of Mesenchymal Stem Cells to Osteoblasts

Fatima¹,

Alfrayh²,

Alrashed³

et al. 2021

IJN

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mentioning

confidence: 99%

Selenium Nanoparticles by Moderating Oxidative Stress Promote Differentiation of Mesenchymal Stem Cells to Osteoblasts

Fatima¹,

Alfrayh²,

Alrashed³

et al. 2021

IJN

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“…Recent studies have highlighted the importance of epigenetic changes in the lineage determination of adipogenesis and osteogenesis [ 35 , 36 ]. BMSC differentiation towards a lineage fate is associated with activation of lineage-specific gene expression and repression of other cell type-specific genes [ 37 ].…”

Section: Discussionmentioning

confidence: 99%

Adipocyte-induced transdifferentiation of osteoblasts and its potential role in age-related bone loss

et al. 2021

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Our preliminary findings have lead us to propose bone marrow adipocyte secretions as new contributors to bone loss. Indeed, using a coculture model based on human bone marrow stromal cells, we previously showed that soluble factors secreted by adipocytes induced the conversion of osteoblasts towards an adipocyte-like phenotype. In this study, microarray gene expression profiling showed profound transcriptomic changes in osteoblasts following coculture and confirmed the enrichment of the adipocyte gene signature. Double immunofluorescence microscopic analyses demonstrated the coexpression of adipogenic and osteoblastic specific markers in individual cells, providing evidence for a transdifferentiation event. At the molecular level, this conversion was associated with upregulated expression levels of reprogramming genes and a decrease in the DNA methylation level. In line with these in vitro results, preliminary immunohistochemical analysis of bone sections revealed adipogenic marker expression in osteoblasts from elderly subjects. Altogether, these data suggest that osteoblast transdifferentiation could contribute to decreased bone mass upon ageing.

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“…It has been suggested that the presence of ROS and pro-inflammatory cytokines provides a favorable environment for adipogenesis and fat accumulation, and impairs bone regeneration, thus leading to the development of osteoporosis. 51 …”

Section: Dna Damage Response In Osteogenesismentioning

confidence: 99%

DNA damage and repair in differentiation of stem cells and cells of connective cell lineages: A trigger or a complication?

Sjakste

Riekstiņa²

2021

Eur J Histochem

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The review summarizes literature data on the role of DNA breaks and DNA repair in differentiation of pluripotent stem cells (PSC) and connective cell lineages. PSC, including embryonic stem cells (ESC) and induced pluripotent stem cells (iPSC), are rapidly dividing cells with highly active DNA damage response (DDR) mechanisms to ensure the stability and integrity of the DNA. In PSCs, the most common DDR mechanism is error-free homologous recombination (HR) that is primarily active during S phase of the cell cycle, whereas in quiescent, slow-dividing or non-dividing tissue progenitors and terminally differentiated cells, error-prone non-homologous end joining (NHEJ) mechanism of the double-strand break (DSB) repair is dominating. Thus, it seems that reprogramming and differentiation induce DNA strand breaks in stem cells which itself may trigger the differentiation process. Somatic cell reprogramming to iPSCs is preceded by a transient increase of the DSBs induced presumably by the caspase-dependent DNase or reactive oxygen species (ROS). In general, pluripotent stem cells possess stronger DNA repair systems compared to the differentiated cells. Nonetheless, during a prolonged cell culture propagation, DNA breaks can accumulate due to the DNA polymerase stalling. Consequently, the DNA damage might trigger the differentiation of stem cells or a replicative senescence of somatic cells. Differentiation process per se is often accompanied by a decrease of the DNA repair capacity. Thus, the differentiation might be triggered by DNA breaks, alternatively the breaks can be a consequence of the decay in the DNA repair capacity of differentiated cells.

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Osteoblast versus Adipocyte: Bone Marrow Microenvironment-Guided Epigenetic Control

Cited by 15 publications

References 112 publications

Selenium Nanoparticles by Moderating Oxidative Stress Promote Differentiation of Mesenchymal Stem Cells to Osteoblasts

Selenium Nanoparticles by Moderating Oxidative Stress Promote Differentiation of Mesenchymal Stem Cells to Osteoblasts

Adipocyte-induced transdifferentiation of osteoblasts and its potential role in age-related bone loss

DNA damage and repair in differentiation of stem cells and cells of connective cell lineages: A trigger or a complication?

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