Smad3 and Snail show circadian expression in human gingival fibroblasts, human mesenchymal stem cell, and in mouse liver

Sato, Fuyuki; Sato, Hiroyasu; Jin, Daiki; Bhawal, Ujjal K.; Wu, Yunyan; Noshiro, Mitsuhide; Kawamoto, Takeshi; Fujimoto, Katsumi; Seino, Hiroko; Morohashi, Satoko; Kato, Yukio; Kijima, Hiroshi

doi:10.1016/j.bbrc.2012.02.076

Cited by 32 publications

(35 citation statements)

References 30 publications

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“…In addition, we found that Bmal1 deficiency leads to significantly attenuated Smad3 activation and reporter activity, indicating that TGF-b signaling transduction could be subjected to temporal regulation as well. Indeed, circadian expression of Smad3 was detected in human gingival fibroblasts, mesenchymal stem cells and mouse liver (Sato et al, 2012). Furthermore, in epidermal stem cells (Janich et al, 2011;Karpowicz et al, 2013) and the central clock (the suprachiasmatic nuclei; Beynon et al, 2009), a circadian pattern of TGF-b signaling activity as indicated by Smad3 phosphorylation has been reported.…”

Section: Discussionmentioning

confidence: 97%

The adipocyte clock controls brown adipogenesis via TGF-β/BMP signaling pathway

Nam

Guo

Chatterjee

et al. 2015

Journal of Cell Science

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The molecular clock is intimately linked to metabolic regulation, and brown adipose tissue plays a key role in energy homeostasis. However, whether the cell-intrinsic clock machinery participates in brown adipocyte development is unknown. Here, we show that Bmal1 (also known as ARNTL), the essential clock transcription activator, inhibits brown adipogenesis to adversely affect brown fat formation and thermogenic capacity. Global ablation of Bmal1 in mice increases brown fat mass and cold tolerance, and adipocyteselective inactivation of Bmal1 recapitulates these effects and demonstrates its cell-autonomous role in brown adipocyte formation. Further loss-and gain-of-function studies in mesenchymal precursors and committed brown progenitors reveal that Bmal1 inhibits brown adipocyte lineage commitment and terminal differentiation. Mechanistically, Bmal1 inhibits brown adipogenesis through direct transcriptional control of key components of the TGF-b pathway together with reciprocally altered BMP signaling; activation of TGF-b or blockade of BMP pathways suppresses enhanced differentiation in Bmal1-deficient brown adipocytes. Collectively, our study demonstrates a novel temporal regulatory mechanism in finetuning brown adipocyte lineage progression to affect brown fat formation and thermogenic regulation, which could be targeted therapeutically to combat obesity.

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Section: Discussionmentioning

confidence: 97%

The adipocyte clock controls brown adipogenesis via TGF-β/BMP signaling pathway

Nam

Guo

Chatterjee

et al. 2015

Journal of Cell Science

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“…Six to 8-week-old male C57BL/6 mice were housed as previously described (26). The light in the mouse room was turned on at 7:00 a.m. (ZT 0 corresponds to 7:00 a.m., lights turned on) and turned off at 7:00 p.m. (ZT 12).…”

Section: Methodsmentioning

confidence: 99%

“…While DEC1 and DEC2 mRNA indicate a rhythmic expression in the suprachiasmatic nucleus (SCN), peripheral tissues, tumor cells and human mesenchymal stem cells (MSCs) (3,17,18,21,(25)(26)(27)(28)(29), whether DEC2 protein has rhythmic expression remains unclear. It seems likely that the rhythmic patterns of DEC1 and DEC2 are different in cell types (26), and what influences of DEC2 rhythmic expression under cell culture is poorly understood.…”

Section: Introductionmentioning

confidence: 99%

Rhythmic expression of DEC2 protein in vitro and in vivo

et al. 2016

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Basic helix-loop-helix (bHLH) transcription factor DEC2 (bHLHE41/Sharp1) is one of the clock genes that show a circadian rhythm in various tissues. DEC2 regulates differentiation, sleep length, tumor cell invasion and apoptosis. Although studies have been conducted on the rhythmic expression of DEC2 mRNA in various tissues, the precise molecular mechanism of DEC2 expression is poorly understood. In the present study, we examined whether DEC2 protein had a rhythmic expression. Western blot analysis for DEC2 protein revealed a rhythmic expression in mouse liver, lung and muscle and in MCF-7 and U2OS cells. In addition, AMP-activated protein kinase (AMPK) activity (phosphorylation of AMPK) in mouse embryonic fibroblasts (MEFs) exhibited a rhythmic expression under the condition of medium change or glucose-depleted medium. However, the rhythmic expression of DEC2 in MEF gradually decreased in time under these conditions. The medium change affected the levels of DEC2 protein and phosphorylation of AMPK. In addition, the levels of DEC2 protein showed a rhythmic expression and in MCF-7 and U2OS cells. The results showed that the phosphorylation of AMPK immunoreactivity was strongly detected in the liver and lung of knockout mice compared with that of wild-type mice. These results may provide new insights into rhythmic expression and the regulation between DEC2 protein and AMPK activity.

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“…The transcription factor DEC2 also plays an important role in the circadian rhythm (20). Previous studies showed a rhythmic expression of DEC1 and DEC2 mRNA in the suprachiasmatic nucleus, and peripheral tissues (21)(22)(23)(24)(25). DEC1 and were harvested and sub-cultured.…”

Section: Introductionmentioning

confidence: 99%

<b>Circadian Expression of Differentiated Embryonic Chondrocytes Expressed Genes 1 </b><b>and 2 in Human Oral Squamous Cell Carcinoma HSC-3 Cells </b>

et al. 2018

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Autonomous rhythmicity of clock genes controls the circadian rhythm and endogenous circadian rhythms regulates various biochemical, physiological, and biological processes, with a periodicity of about 24 h. Entrainment circadian clock of cells detects distinct patterns of circadian oscillation for clock genes. Although circadian disruptions have been implicated in cancer development, the altered circadian rhythm in human oral cancer remains largely unknown. Here we show that, upon entrainment by serum shock, cultured human oral epithelial cancer cell line, HSC-3, maintain an inner circadian oscillator, with key clock genes DEC1 and DEC2 oscillating in a circadian fashion. Serum-shocked HSC-3 cells exhibited an about 24 h oscillatory pattern of DEC1 and DEC2 protein and mRNA expression. Taken together, the results indicated that the transcription factors DEC1 and DEC2 modulate a rhythmic transcriptional regulation mechanism which can drive the expression of downstream genes involved in many cellular processes.

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Smad3 and Snail show circadian expression in human gingival fibroblasts, human mesenchymal stem cell, and in mouse liver

Cited by 32 publications

References 30 publications

The adipocyte clock controls brown adipogenesis via TGF-β/BMP signaling pathway

The adipocyte clock controls brown adipogenesis via TGF-β/BMP signaling pathway

Rhythmic expression of DEC2 protein in vitro and in vivo

<b>Circadian Expression of Differentiated Embryonic Chondrocytes Expressed Genes 1 </b><b>and 2 in Human Oral Squamous Cell Carcinoma HSC-3 Cells </b>

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