L-Sox5 and Sox6 Proteins Enhance Chondrogenic miR-140 MicroRNA Expression by Strengthening Dimeric Sox9 Activity

Yamashita, Satoshi; Miyaki, Shigeru; Kato, Yoshio; Yokoyama, Shigetoshi; Sato, Tempei; Barrionuevo, Francisco; Akiyama, Haruhiko; Scherer, Gerd; Takada, Shuji; Asahara, Hiroshi

doi:10.1074/jbc.m112.343194

Cited by 86 publications

(62 citation statements)

References 40 publications

(56 reference statements)

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“…The mechanisms involved in miR-140-3p downregulation by TNF-␣ in HASM cells are yet to be determined. Recent studies in human chondrocytes showed that the proximal upstream region of pri-miR-140 has functional response elements for chondrogenic transcription factors Sox5/Sox6/ Sox9, indicating transcriptional regulation of miR-140-3p and miR-140-5p expressions (33). Different transcriptional regulators and epigenetic mechanisms such as DNA methylation may be involved in the altered miR-140-3p expression in AASM cells.…”

Section: Discussionmentioning

confidence: 99%

miR-140-3p regulation of TNF-α-induced CD38 expression in human airway smooth muscle cells

Jude

Dileepan

Subramanian

et al. 2012

American Journal of Physiology-Lung Cellular and Molecular Phys

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Section: Discussionmentioning

confidence: 99%

miR-140-3p regulation of TNF-α-induced CD38 expression in human airway smooth muscle cells

Jude

Dileepan

Subramanian

et al. 2012

American Journal of Physiology-Lung Cellular and Molecular Phys

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“…ChIP was performed as previously described 36,37) . In brief, cells were crosslinked with 1% formaldehyde for 10 min at room temperature before glycine was added to a final concentration of 0.125 M. Chromatin was sheared to 200 -1000 bp by sonication.…”

Section: Chromatin Immunoprecipitation (Chip) Assaymentioning

confidence: 99%

Crucial Role of the Aryl Hydrocarbon Receptor (AhR) in Indoxyl Sulfate-Induced Vascular Inflammation

Ito

Osaka

Edamatsu

et al. 2016

JAT

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Aim:The aryl hydrocarbon receptor (AhR), a ligand-inducible transcription factor mediating toxic effects of dioxins and uremic toxins, has recently emerged as a pathophysiological regulator of immune-inflammatory conditions. Indoxyl sulfate, a uremic toxin, is associated with cardiovascular disease in patients with chronic kidney disease and has been shown to be a ligand for AhR. The aim of this study was to investigate the potential role of AhR in indoxyl sulfate-induced leukocyte -endothelial interactions. Methods: Endothelial cell-specific AhR knockout (eAhR KO) mice were produced by crossing AhR floxed mice with Tie2 Cre mice. Indoxyl sulfate was administered for 2 weeks, followed by injection of TNF-. Leukocyte recruitment to the femoral artery was assessed by intravital microscopy. Vascular endothelial cells were transfected with siRNA specific to AhR (siAhR) and treated with indoxyl sulfate, followed by stimulation with TNF-. Results: Indoxyl sulfate dramatically enhanced TNF--induced leukocyte recruitment to the vascular wall in control animals but not in eAhR KO mice. In endothelial cells, siAhR significantly reduced indoxyl sulfate-enhanced leukocyte adhesion as well as E-selectin expression, whereas the activation of JNK and nuclear factor-B was not affected. A luciferase assay revealed that the region between 153 and 146 bps in the E-selectin promoter was responsible for indoxyl sulfate activity via AhR. Mutational analysis of this region revealed that activator protein-1 (AP-1) is responsible for indoxyl sulfate-triggered E-selectin expression via AhR. Conclusion: AhR mediates indoxyl sulfate-enhanced leukocyte -endothelial interactions through AP-1 transcriptional activity, which may constitute a new mechanism of vascular inflammation in patients with renal disease.

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“…Moreover, independent groups have developed miR-140-null mice, which displayed a concordant phenotype with major growth defects of endochondral bones (Miyaki et al 2010, Nakamura et al 2011, Papaioannou et al 2013. Interestingly, Sox9, L-Sox5, and Sox6 have been proved to cooperatively activate the miR-140 promoter in vivo and in vitro (Miyaki et al 2010, Yamashita et al 2012, as well as other chondrogenic differentiation-related miRNAs (Guerit et al 2013, Martinez-Sanchez & Murphy 2013. miR-181a is highly expressed in chondrocytes, and it has been suggested that it works as a negative feedback system to preserve the homeostasis of cartilage by targeting Ccn1 (Ccna2; which promotes chondrogenesis) and Acan (encoding the protein aggrecan, the major proteoglycan in the cartilage ECM) (Sumiyoshi et al 2013).…”

Section: Mirnas and Chondroblast Differentiationmentioning

confidence: 99%

MicroRNAs and post-transcriptional regulation of skeletal development

Gámez¹,

Rodríguez-Carballo²,

Ventura³

2014

Journal of Molecular Endocrinology

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MicroRNAs (miRNAs) have become integral nodes of post-transcriptional control of genes that confer cellular identity and regulate differentiation. Cell-specific signaling and transcriptional regulation in skeletal biology are extremely dynamic processes that are highly reliant on dose-dependent responses. As such, skeletal cell-determining genes are ideal targets for quantitative regulation by miRNAs. So far, large amounts of evidence have revealed a characteristic temporal miRNA signature in skeletal cell differentiation and confirmed the essential roles that numerous miRNAs play in bone development and homeostasis. In addition, microarray expression data have provided evidence for their role in several skeletal pathologies. Mouse models in which their expression is altered have provided evidence of causal links between miRNAs and bone abnormalities. Thus, a detailed understanding of the function of miRNAs and their tight relationship with bone diseases would constitute a powerful tool for early diagnosis and future therapeutic approaches.

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L-Sox5 and Sox6 Proteins Enhance Chondrogenic miR-140 MicroRNA Expression by Strengthening Dimeric Sox9 Activity

Cited by 86 publications

References 40 publications

miR-140-3p regulation of TNF-α-induced CD38 expression in human airway smooth muscle cells

miR-140-3p regulation of TNF-α-induced CD38 expression in human airway smooth muscle cells

Crucial Role of the Aryl Hydrocarbon Receptor (AhR) in Indoxyl Sulfate-Induced Vascular Inflammation

MicroRNAs and post-transcriptional regulation of skeletal development

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