Tissue expression and subcellular localization of Mipu1, a novel myocardial ischemia-related gene

Wang, Guanchao; Zuo, Xiao Xia; Jiang, Lei; Wang, K.; Wei, Xing; Zhang, B.; Xiao, Xianzhong

doi:10.1590/s0100-879x2009005000010

Cited by 7 publications

(11 citation statements)

References 12 publications

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“…Further important observations support a central role for ZNF667/Mipu1 in the survival of C2C12 myogenic cells, because ZNF667 overexpression could reduce the growth arrest induced by serum withdrawal [26] . It was also shown that ZNF667 protein was localized to the nucleus of H9c2 cardiomyocytes and was upregulated after the cells were treated with H 2 O 2 [2] - [5] . These observations indicated that ZNF667 might play a role in maintaining cell homeostasis and protecting the cells from being injured by oxidative stress.…”

Section: Discussionmentioning

confidence: 95%

“…The rat zinc finger protein 667, ZNF667, provisionally named m yocardial i schemic p reconditioning u pregulated protein 1 (Mipu1) in our lab due to its upregulation during myocardial ischemia/reperfusion, belongs to the KRAB/C 2 H 2 zinc finger proteins that contains a KRAB domain at its N-terminus and 14 zinc fingers at its C-terminus. Both the ZNF667 mRNA and protein are expressed abundantly and predominantly in the brain and heart [1] , [2] . It has also been shown that ZNF667 is a nuclear protein that is localized to the nucleus through its KRAB domain or the linker adjacent to its zinc finger region, unlike most of the KRAB/C 2 H 2 zinc finger proteins where their zinc finger motifs are required for nuclear targeting.…”

Section: Introductionmentioning

confidence: 99%

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ZNF667/Mipu1 Is a Novel Anti-Apoptotic Factor That Directly Regulates the Expression of the Rat Bax Gene in H9c2 Cells

et al. 2014

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ZNF667/Mipu1, a C2H2-type zinc finger transcription factor, was suggested to play an important role in oxidative stress. However, none of the target genes or potential roles of ZNF667 in cardiomyocytes have been elucidated. Here, we investigated the functional role of ZNF667 in H9c2 cell lines focusing on its molecular mechanism by which it protects the cells from apoptosis. We found that ZNF667 inhibited the expression and the promoter activity of the rat proapoptotic gene Bax gene, and at the same time prevented apoptosis of H9c2 cells, induced by H2O2 and Dox. Western immunoblotting analysis revealed that ZNF667 also inhibited Bax protein expression, accompanied by attenuation of the mitochondrial translocation of Bax protein, induced by H2O2. EMSA and target detection assay showed that the purified ZNF667 fusion proteins could interact with the Bax promoter sequence in vitro, and this interaction was dependent upon the ZNF667 DNA binding sequences or its core sequence in the promoter. Furthermore, ChIP assay demonstrated that a stimulus H2O2 could enhance the ability of ZNF667 protein binding to the promoter. Finally, a reporter gene assay showed that ZNF667 could repress the activity of the Bax gene promoter, and the repression was dependent upon its binding to the specific DNA sequence in the promoter. Our work demonstrates that ZNF667 that confers cytoprotection is a novel regulator of the rat Bax gene, mediating the inhibition of the Bax mRNA and protein expression in H9c2 cardiomyocytes in response to H2O2 treatment.

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Section: Discussionmentioning

confidence: 95%

Section: Introductionmentioning

confidence: 99%

ZNF667/Mipu1 Is a Novel Anti-Apoptotic Factor That Directly Regulates the Expression of the Rat Bax Gene in H9c2 Cells

et al. 2014

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“…Our experiments showed that KUS121, which has already been used in a clinical trial for ischemic retinal disease (UMIN000023979), upregulated gene expression and translation of Zfp667 in the retinal ganglion cells. Zfp667 has been reported to suppress apoptosis-related genes in ischemia-reperfusion injury 41,42 . KUS121 also upregulated the expression of a variety of genes such as Phkb, which is involved in glycogen metabolism 47 ; Ppargc1a, which is a strong activator of mitochondrial function and a regulator of energy metabolism [48][49][50] ; Ptcd2, which is involved in mitochondrial gene expression 51 ; Npm1, which promotes cell survival under stress 52 ; Dusp18, which may dephosphorylate and inactivate mitogen-activated protein kinase (MAPK) 47 ; Peg10, which is anti-apoptotic 53 .…”

Section: Discussionmentioning

confidence: 99%

“…Of the genes studied, we focused on Zfp667, which has been reported to suppress apoptosis-related genes and consequently prevent cell death in ischemia-reperfusion injury 41,42 . Western blot analysis of mouse retinal proteins showed that expression levels of Zfp667 was not significantly different between non-treated retinas and saline-treated NMDA-injected retinas (NMDA-saline as control) of wild-type mice (P = 0.61, Turkey HSD, Fig.…”

Section: Purification Of Retinal Ganglion Cells By Facsmentioning

confidence: 99%

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Effect of VCP modulators on gene expression profiles of retinal ganglion cells in an acute injury mouse model

Hasegawa

Ikeda

Gotoh

et al. 2020

Sci Rep

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In glaucoma, retinal ganglion cells are damaged, leading to the progressive constriction of the visual field. We have previously shown that the valosin-containing protein (VCP) modulators, Kyoto University Substance (KUS)121 and KUS187, prevent the death of retinal ganglion cells in animal models of glaucoma, including the one generated by N-methyl-D-aspartate (NMDA)-induced neurotoxicity. KUSs appeared to avert endoplasmic reticulum (ER) stress by maintaining ATP levels, resulting in the protection of ganglion cells from cell death. To further elucidate the protective mechanisms of KUSs, we examined gene expression profiles in affected ganglion cells. We first injected KUS-treated mice with NMDA and then isolated the affected retinal ganglion cells using fluorescence-activated cell sorting. Gene expression in the cells was quantified using a next-generation sequencer. Resultantly, we found that KUS121 upregulated several genes involved in energy metabolism. In addition, we observed the upregulation of Zfp667, which has been reported to suppress apoptosis-related genes and prevent cell death. These results further support the suitability of KUS121 as a therapeutic drug in protecting retinal ganglion cells in ophthalmic disorders, such as glaucoma.

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ZNF667 attenuates leukocyte‐endothelial adhesion via downregulation of P‐selectin in skin flap following remote limb ischemic preconditioning

Chen

Liu²,

et al. 2021

Cell Biology International

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We assessed the effects and potential mechanism of romote ischemic preconditioning (RIPC) on leukocytes‐endothelium cell adhesion in the flap microvessel after ischemia‐reperfusion (I/R) injury. Eight hours after reperfusion, edema and intravascular leukocyte aggregation were reduced and microvessels were more obvious in the group with superficial inferior epigastric artery (SIEA) perforator flap (SIEA‐flap) subjected to RIPC than in the I/R group. Zinc finger protein 667 (ZNF667) was significantly increased but P‐selectin was decreased in the flaps subjected to RIPC, compared to those in the I/R group. The low expression of P‐selectin was associated with ZNF667 expression and activation in human dermal microvascular endothelial cells in response to hypoxic preconditioning. ZNF667 bound to the P‐selectin promoter region, suppressing its transcription through a special core sequence. The ablation of P‐selectin by small interfering RNA effectively prevented the leukocytes‐endothelium cell adhesion effect of ZNF667‐knockdown. ZNF667 upregulation attenuates leukocyte‐endothelial cell adhesion by negatively regulating the expression of P‐selectin in SIEA‐flap subjected to RIPC.

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Tissue expression and subcellular localization of Mipu1, a novel myocardial ischemia-related gene

Cited by 7 publications

References 12 publications

ZNF667/Mipu1 Is a Novel Anti-Apoptotic Factor That Directly Regulates the Expression of the Rat Bax Gene in H9c2 Cells

ZNF667/Mipu1 Is a Novel Anti-Apoptotic Factor That Directly Regulates the Expression of the Rat Bax Gene in H9c2 Cells

Effect of VCP modulators on gene expression profiles of retinal ganglion cells in an acute injury mouse model

ZNF667 attenuates leukocyte‐endothelial adhesion via downregulation of P‐selectin in skin flap following remote limb ischemic preconditioning

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