Recruitment and subnuclear distribution of the regulatory machinery during 1α,25-dihydroxy vitamin D3-mediated transcriptional upregulation in osteoblasts

Arriagada, Gloria; Henríquez, Berta; Moena, Daniel; Merino, Paola; Ruiz-Tagle, Cinthya; Lian, Jane B.; Stein, Gary S.; Montecino, Martín

doi:10.1016/j.jsbmb.2010.02.013

Cited by 8 publications

(5 citation statements)

References 22 publications

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“…The first to hypothesize that osteoblasts coordinate osteoclast activity were Rodan and Martin [55], who elegantly depicted a model in which the osteoblasts responded to some osteoclast-seeking signals, first PTH and vitamin D3, stimulating bone resorption [56,57]. This theory has been fully confirmed by subsequent studies that discovered the many underlying pathways, including the RANKL/RANK axis and the various proosteoclastogenic and pro-inflammatory cytokines, such as IL-1, IL-6, IL-11, inhibin Aβ, and tumor necrosis factor-α, among others [28•].…”

Section: Bone-cell Cross-talkmentioning

confidence: 99%

Bone Development: Overview of Bone Cells and Signaling

Teti

2011

Curr Osteoporos Rep

110

115

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Vertebrates evolved elaborating a structure made up of more than 200 bones and cartilages articulated with one another to form the skeleton, through which locomotion, organ protection, lodging of hematopoiesis, and mineral homeostasis are allowed. Skeletogenesis starts at the fetal stage, along with marrow hematopoiesis, and evolves postnatally through modeling and remodeling processes that permit skeletal mass buildup. Preservation of skeletal mass is then implemented by balanced remodeling, which ensures continuous renovation of the tissue to allow its mechanical, structural, and metabolic properties to remain unaltered until ageing or diseases disrupt this equilibrium. Skeletal homeostasis is fulfilled by specialized bone cells in association with systemic and local regulators. Herein I review landmark discoveries that shed light on the intricate mesh connecting bone cells among themselves and with other systems, thus representing the cellular basis of normal and abnormal bone development and homeostasis.

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Section: Bone-cell Cross-talkmentioning

confidence: 99%

Bone Development: Overview of Bone Cells and Signaling

Teti

2011

Curr Osteoporos Rep

110

115

View full text Add to dashboard Cite

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“…Confirmation of the punctate intranuclear localization of the RUNX transcription factor by time-lapse fluorescence microscopy of cells with a fluorescent-tagged RUNX protein provides in situ validation of the punctate intranuclear organization [62]. Similar punctate intranuclear distribution has been confirmed for the vitamin D receptor (VDR) and co-regulatory molecules in bone-related cells [63, 64], indicating that transcriptional control of osteoblastic genes in response to vitamin D is also architecturally organized.…”

Section: Introductionmentioning

confidence: 81%

Multiple levels of epigenetic control for bone biology and pathology

Montecino

Stein

Zaidi

et al. 2015

Bone

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Multiple dimensions of epigenetic control contribute to regulation of gene expression that governs bone biology and pathology. Once confined to DNA methylation and a limited number of post-translational modifications of histone proteins, the definition of epigenetic mechanisms is expanding to include contributions of non-coding RNAs and mitotic bookmarking, a mechanism for retaining phenotype identity during cell proliferation. Together these different levels of epigenetic control of physiological processes and their perturbations that are associated with compromised gene expression during the onset and progression of disease, have contributed to an unprecedented understanding of the activities (operation) of the genomic landscape. Here, we address general concepts that explain the contribution of epigenetic control to the dynamic regulation of gene expression during eukaryotic transcription.

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“…This VDR/SRC‐1/p300 complex brings into place the intrinsic histone acetyl transferase activity of both SRC‐1 and p300 coactivators (Carvallo et al, 2007; Kim et al, 2005), which can then mediate the increased histone acetylation that has been shown as critical during 1,25(OH) 2 D 3 dependent CYP24A1 transcription activation (Moena et al, in press). Additionally, VDR‐containing complexes can activate transcription by directly interacting with the RNA polymerase II holoenzyme at target gene promoters (Arriagada et al, 2010; Chiba, Suldan, Freedman, & Parvin, 2000; Sutton & MacDonald, 2003), including CYP24A1 (Carvallo et al, 2008; Montecino et al, 2007).…”

Section: Discussionmentioning

confidence: 99%

Ezh2‐dependent H3K27me3 modification dynamically regulates vitamin D3‐dependent epigenetic control of CYP24A1 gene expression in osteoblastic cells

Moena

Nardocci

Acevedo

et al. 2020

Journal Cellular Physiology

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Epigenetic control is critical for the regulation of gene transcription in mammalian cells. Among the most important epigenetic mechanisms are those associated with posttranslational modifications of chromosomal histone proteins, which modulate chromatin structure and increased accessibility of promoter regulatory elements for competency to support transcription. A critical histone mark is trimethylation of histone H3 at lysine residue 27 (H3K27me3), which is mediated by Ezh2, the catalytic subunit of the polycomb group complex PRC2 to repress transcription. Treatment of cells with the active vitamin D metabolite 1,25(OH)2D3, results in transcriptional activation of the CYP24A1 gene, which encodes a 24‐hydroxylase enzyme, that is, essential for physiological control of vitamin D3 levels. We report that the Ezh2‐mediated deposition of H3K27me3 at the CYP24A1 gene promoter is a requisite regulatory component during transcriptional silencing of this gene in osteoblastic cells in the absence of 1,25(OH)2D3. 1,25(OH)2D3 dependent transcriptional activation of the CYP24A1 gene is accompanied by a rapid release of Ezh2 from the promoter, together with the binding of the H3K27me3‐specific demethylase Utx/Kdm6a and thereby subsequent erasing of the H3K27me3 mark. Importantly, we find that these changes in H3K27me3 enrichment at the CYP24A1 gene promoter are highly dynamic, as this modification is rapidly reacquired following the withdrawal of 1,25(OH)2D3.

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Recruitment and subnuclear distribution of the regulatory machinery during 1α,25-dihydroxy vitamin D3-mediated transcriptional upregulation in osteoblasts

Cited by 8 publications

References 22 publications

Bone Development: Overview of Bone Cells and Signaling

Bone Development: Overview of Bone Cells and Signaling

Multiple levels of epigenetic control for bone biology and pathology

Ezh2‐dependent H3K27me3 modification dynamically regulates vitamin D3‐dependent epigenetic control of CYP24A1 gene expression in osteoblastic cells

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