Identification and characterization of the minimal promoter of &amp;lt;italic&amp;gt;Mipu1&amp;lt;/italic&amp;gt;: the role of GC boxes in the regulation of basal transcription

Lv, Ben; Tang, Yiting; Li, Xiayu; Wang, Guiliang; Yuan, Cheng; Liu, Ying; Jiang, Lei; Xiao, Xianzhong

doi:10.1093/abbs/gmp019

Cited by 4 publications

(6 citation statements)

References 17 publications

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“…We also searched transcription-factor-binding sites on the Mipu1 promoter using MatInspector and found some potential-binding sites of stress-response transcription factors, such as HIF alpha, HSF-1, Elk-1, Egr-1, and the GAGA-binding protein [34]. oxLDL can trigger HIF-1alpha accumulation [35] and induced of tissue factor gene expression mediated by both Egr-1 and Sp1 [36].…”

Section: Discussionmentioning

confidence: 99%

Mipu1 Inhibits Lipid Accumulation Through Down-Regulation of CD36 in RAW264.7 Cells

Fan

Zhang

et al. 2015

Cell Physiol Biochem

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Background/Aims: Our recent data indicated that Mipu1 overexpression reduces lipid intake and CD36 expression of macrophages in the presence of oxLDL. However, the mechanism of Mipu1 inhibiting lipid accumulation in macrophages is not elucidated. Methods: Real-time quantitative polymerase chain reaction (PCR) and western blot analysis were used to detect expression of Mipu1 and CD36. The promoter activity of CD36 was studied using luciferase assays. Chromatin immunoprecipitation (ChIP) was used to show the recruitment of Mipu1 onto the CD36 promoter. High-performance liquid chromatography and Dil-labeled lipoprotein were used to detect cholesterol accumulation. Results: Here, we show that CD36 overexpression rescues oxLDL-induced cholesterol accumulation in RAW264.7-Mipu1 cells. Analysis of the mouse CD36 promoter revealed two potential Mipu1-response elements (MRE), one of which (from -237bp to -244bp, ACTTAC) was shown, using mutagenesis and deletion analysis, to be functional. Mipu1 was demonstrated to bind to CD36 promoter, and oxLDL treatment resulted in increases in their interaction as assessed by ChIP. Conclusions: It was demonstrated that Mipu1 inhibited the lipid accumulation of macrophages and it down-regulated CD36 expression in the presence of oxLDL.

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Section: Discussionmentioning

confidence: 99%

Mipu1 Inhibits Lipid Accumulation Through Down-Regulation of CD36 in RAW264.7 Cells

Fan

Zhang

et al. 2015

Cell Physiol Biochem

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“…The assay was performed according to the instruction of Dual Luciferase Reporter System (Promega) and the methods described previously [ 16 - 18 ]. Mipu1 promoter (-1170/+233) was cloned into PGL3 reporter vector as described previously in our lab [ 16 ].…”

Section: Methodsmentioning

confidence: 99%

“…Recently, we evidenced that GC box is essential for regulating the constitutive expression of Mipu1 [ 18 ]. However, GC box is neither hypoxia-response nor stress-response elements, implying that other transcription factors binding sites within Mipu1 promoter region might be responsible for its up-regulation during pathological stress (ischemic or hypoxic stress).…”

Section: Introductionmentioning

confidence: 99%

Mipu1, a Novel Direct Target Gene, Is Involved in Hypoxia Inducible Factor 1-Mediated Cytoprotection

et al. 2013

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Mipu1 (myocardial ischemic preconditioning up-regulated protein 1), recently identified in our lab, is a novel zinc-finger transcription factor which is up-regulated during ischemic preconditioning. However, it is not clear what transcription factor contributes to its inducible expression. In the present study, we reported that HIF-1 regulates the inducible expression of Mipu1 which is involved in the cytoprotection of HIF-1α against oxidative stress by inhibiting Bax expression. Our results showed that the inducible expression of Mipu1 was associated with the expression and activation of transcription factor HIF-1 as indicated by cobalt chloride (CoCl2) treatment, HIF-1α overexpression and knockdown assays. EMSA and luciferase reporter gene assays showed that HIF-1α bound to the hypoxia response element (HRE) within Mipu1 promoter region and promoted its transcription. Moreover, our results revealed that Mipu1 inhibited the expression of Bax, an important pro-apoptosis protein associated with the intrinsic pathway of apoptosis, elevating the cytoprotection of HIF-1 against hydrogen peroxide (H2O2)-mediated injury in H9C2 cells. Our findings implied that Bax may be a potential target gene of transcription factor Mipu1, and provided a novel insight for understanding the cytoprotection of HIF-1 and new clues for further elucidating the mechanisms by which Mipu1 protects cell against pathological stress.

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“…Seven different deletion constructs were transiently transfected into an H9c2 cardiomyocyte cell line, and showed the luciferase activity of the seven constructs relative to the promoter-less construct. The results mapped the minimal promoter of Mipu1 to the region between -100 and +1 bp with respect to the transcription start site ( 30 ).…”

Section: Biological Characteristics Of Mipu1mentioning

confidence: 99%

“…Lv et al ( 30 ) showed that the GC box is essential for regulating the constitutive expression of Mipu1 . However, the GC box has neither hypoxia-response nor stress-response elements, implying that other transcription factor binding sites within the Mipu1 promoter region might be responsible for its upregulation during pathological stress (ischemic or hypoxic stress).…”

Section: Biological Characteristics Of Mipu1mentioning

confidence: 99%

Myocardial ischemic preconditioning upregulated protein 1(Mipu1):zinc finger protein 667 - a multifunctional KRAB/C2H2 zinc finger protein

Han

Zhang

Fan

et al. 2015

Braz J Med Biol Res

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Myocardial ischemic preconditioning upregulated protein 1 (Mipu1) is a newly discovered upregulated gene produced in rats during the myocardial ischemic preconditioning process. Mipu1 cDNA contains a 1824-base pair open reading frame and encodes a 608 amino acid protein with an N-terminal Krüppel-associated box (KRAB) domain and classical zinc finger C2H2 motifs in the C-terminus. Mipu1 protein is located in the cell nucleus. Recent studies found that Mipu1 has a protective effect on the ischemia-reperfusion injury of heart, brain, and other organs. As a nuclear factor, Mipu1 may perform its protective function through directly transcribing and repressing the expression of proapoptotic genes to repress cell apoptosis. In addition, Mipu1 also plays an important role in regulating the gene expression of downstream inflammatory mediators by inhibiting the activation of activator protein-1 and serum response element.

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Identification and characterization of the minimal promoter of <italic>Mipu1</italic>: the role of GC boxes in the regulation of basal transcription

Cited by 4 publications

References 17 publications

Mipu1 Inhibits Lipid Accumulation Through Down-Regulation of CD36 in RAW264.7 Cells

Mipu1 Inhibits Lipid Accumulation Through Down-Regulation of CD36 in RAW264.7 Cells

Mipu1, a Novel Direct Target Gene, Is Involved in Hypoxia Inducible Factor 1-Mediated Cytoprotection

Myocardial ischemic preconditioning upregulated protein 1(Mipu1):zinc finger protein 667 - a multifunctional KRAB/C2H2 zinc finger protein

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