Transcription Factor GATA-6 Recruits PPARα to Cooperatively Activate Glut4 Gene Expression

Yao, Chunxia; Xiong, Cheng-Juan; Wang, Weiping; Yang, Fen; Zhang, Shufeng; Wang, Tian-qi; Wang, Shuling; Yu, Huanling; Wei, Zhiru; Zang, Ming-Xi

doi:10.1016/j.jmb.2011.11.011

Cited by 17 publications

(22 citation statements)

References 54 publications

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“…Neonatal rat ventricular cardiomyocytes culture was performed as described previously 28 . Transfections were performed 24 h after plating cells using Lipofectamine 2000 reagent (Invitrogen) according to the manufacturer’s instructions.…”

Section: Methodsmentioning

confidence: 99%

“…RNA was extracted from C2C12, P19CL6 cells and neonatal rat ventricular cardiomyocytes using the TRIzol method (Invitrogen). First-strand cDNAs were synthesized and used as a template in subsequent real-time PCR reactions as described previously 28 . A comparative quantification method was used, and the levels of mRNA and miR-200b were normalized to those of the ribosomal protein S16 and U6, respectively.…”

Section: Methodsmentioning

confidence: 99%

“…Cell lysates were prepared from C2C12 cells stably expressing GATA-4, miR-200b or RNAi GATA-4, or from C2C12 cells transfected with miR-200b mimic, miR-200b inhibitor or control miRNAs as previously described 28 . Nuclear extracts were prepared from neonatal rat ventricular myocytes treated with 100 μM Phe and/or transfected with miR-200b mimic, miR-200b inhibitor or control miRNAs.…”

Section: Methodsmentioning

confidence: 99%

“…Nuclear extracts were prepared from neonatal rat ventricular myocytes treated with 100 μM Phe and/or transfected with miR-200b mimic, miR-200b inhibitor or control miRNAs. Western blotting was performed using cell lysates according to standard protocols as previously described 28 . Briefly, proteins were separated by SDS-PAGE, transferred to PVDF membranes and subjected to immunoblotting using antibodies specific for the sarcomeric MHC (MF-20, Developmental Studies Hybridoma Bank), GATA-4, cyclin D1, Histone H3, or tubulin and visualized using the standard ECL protocol (Pierce).…”

Section: Methodsmentioning

confidence: 99%

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miR-200b targets GATA-4 during cell growth and differentiation

et al. 2013

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GATA-4 is an important transcription factor involved in several developmental processes of the heart, such as cardiac myocyte proliferation, differentiation and survival. The precise mechanisms underlying the regulation of GATA-4 remain unclear, this is especially true for the mechanisms that mediate the post-transcriptional regulation of GATA-4. Here, we demonstrate that miR-200b, a member of the miR-200 family, is a critical regulator of GATA-4. Overexpression of miR-200b leads to the downregulation of GATA-4 mRNA and a decrease in GATA-4 protein levels. Moreover, miR-200b not only inhibits cell growth and differentiation but also reverses the growth response mediated by GATA-4, whereas depletion of miR-200b leads to a slight reversal of the anti-growth response achieved by knocking down endogenous GATA-4. More importantly, the cell cycle-associated gene cyclin D1, which is a downstream target of GATA-4, is also regulated by miR-200b. Thus, miR-200b targets GATA-4 to downregulate the expression of cyclin D1 and myosin heavy chain (MHC), thereby regulating cell growth and differentiation.

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Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

See 2 more Smart Citations

miR-200b targets GATA-4 during cell growth and differentiation

et al. 2013

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“…This promiscuity suggests that other factors may modulate the activity of favored complexes on transcriptional “hot spots”. Interactions with other transcription factors have been documented with HNF4α or GATA-6 in the control of Acot1 or Glut4 gene expression respectively [8], [9]. Occupancy of PPRE sites is also regulated during the fed/fasting cycle depending on the expression of the HNF4α target gene Hes6 which, through interaction with HNF4α co-represses PPARα target genes in fed states [10].…”

Section: Introductionmentioning

confidence: 99%

Sox17 Regulates Liver Lipid Metabolism and Adaptation to Fasting

et al. 2014

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Liver is a major regulator of lipid metabolism and adaptation to fasting, a process involving PPARalpha activation. We recently showed that the Vnn1 gene is a PPARalpha target gene in liver and that release of the Vanin-1 pantetheinase in serum is a biomarker of PPARalpha activation. Here we set up a screen to identify new regulators of adaptation to fasting using the serum Vanin-1 as a marker of PPARalpha activation. Mutagenized mice were screened for low serum Vanin-1 expression. Functional interactions with PPARalpha were investigated by combining transcriptomic, biochemical and metabolic approaches. We characterized a new mutant mouse in which hepatic and serum expression of Vanin-1 is depressed. This mouse carries a mutation in the HMG domain of the Sox17 transcription factor. Mutant mice display a metabolic phenotype featuring lipid abnormalities and inefficient adaptation to fasting. Upon fasting, a fraction of the PPARα-driven transcriptional program is no longer induced and associated with impaired fatty acid oxidation. The transcriptional phenotype is partially observed in heterozygous Sox17+/− mice. In mutant mice, the fasting phenotype but not all transcriptomic signature is rescued by the administration of the PPARalpha agonist fenofibrate. These results identify a novel role for Sox17 in adult liver as a modulator of the metabolic adaptation to fasting.

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Insulin induces C2C12 cell proliferation and apoptosis through regulation of cyclin D1 and BAD expression

Xiong

Ping-fa

Song

et al. 2013

J of Cellular Biochemistry

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Insulin is a secreted peptide hormone identified in human pancreas to promote glucose utilization. Insulin has been observed to induce cell proliferation and myogenesis in C2C12 cells. The precise mechanisms underlying the proliferation of C2C12 cells induced by insulin remain unclear. In this study, we observed for the first time that 10 nM insulin treatment promotes C2C12 cell proliferation. Additionally, 50 and 100 nM insulin treatment induces C2C12 cell apoptosis. By utilizing real-time PCR and Western blotting analysis, we found that the mRNA levels of cyclinD1 and BAD are induced upon 10 and 50 nM/100 nM insulin treatment, respectively. The similar results were observed in C2C12 cells expressing GATA-6 or PPARα. Our results identify for the first time the downstream targets of insulin, cyclin D1, and BAD, elucidate a new molecular mechanism of insulin in promoting cell proliferation and apoptosis.

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Transcription Factor GATA-6 Recruits PPARα to Cooperatively Activate Glut4 Gene Expression

Cited by 17 publications

References 54 publications

miR-200b targets GATA-4 during cell growth and differentiation

miR-200b targets GATA-4 during cell growth and differentiation

Sox17 Regulates Liver Lipid Metabolism and Adaptation to Fasting

Insulin induces C2C12 cell proliferation and apoptosis through regulation of cyclin D1 and BAD expression

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