Trim47 is a critical regulator of cerebral ischemia-reperfusion injury through regulating apoptosis and inflammation

Hao, Miaoqing; Xie, Lanjun; Leng, Wei; Xue, Rui-Wen

doi:10.1016/j.bbrc.2019.05.065

Cited by 36 publications

(25 citation statements)

References 28 publications

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“…increasing evidence suggests that S100a8 can induce apoptosis in several cells of different origins such as skin and cancer cells (47)(48)(49). Consistent with previous findings (50,51), the results of the present study indicated markedly downregulated expression of the proapoptotic proteins, Bax and cleaved-caspase-3/pro-caspase-3, and upregulated expression of the antiapoptotic protein, Bcl-2, following S100a8 silencing and oGd/r exposure in BV2 cells, respectively. Taken together, these results suggest that S100a8 silencing suppresses the apoptosis of oGd/r-exposed BV2 cells.…”

Section: Discussionsupporting

confidence: 91%

S100a8 silencing attenuates inflammation, oxidative stress and apoptosis in BV2 cells induced by oxygen‑glucose deprivation and reoxygenation by upregulating GAB1 expression

Lin

2020

Mol Med Rep

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S100a8 serves an important role in cell differentiation and is abnormally expressed in common tumors, but there are few studies on the association between S100a8 and brain i/r injury. The present study aimed to investigate the role of S100a8 in oxygen-glucose deprivation and reoxygenation (oGd/r)-induced BV2 microglia cell injury, and to elucidate the potential underlying molecular mechanisms. BV2 cells were exposed to oGd/r to mimic ischemia/reperfusion (i/r) injury in vitro. S100a8 expression was detected via reverse transcription-quantitative Pcr and western blot analyses. Following transfection with short hairpin rnas targeting S100a8, the levels of inflammatory cytokines and oxidative stress-related factors were determined using commercial kits. Apoptosis was assessed using flow cytometric analysis and the expression levels of apoptosis-related proteins were determined using western blot analysis. Subsequently, the mrna and protein levels of Grb2-associated binder 1 (GaB1) were assessed following S100a8 silencing. immunoprecipitation (iP) was performed to verify the association between S100a8 and GAB1. The levels of inflammation, oxidative stress and apoptosis were assessed following GaB1 silencing, along with S100a8 silencing in BV2 cells subjected to oGd/r. The results indicated that exposure to oGd/R markedly upregulated S100a8 expression in BV2 cells. S100a8 silencing inhibited inflammation, oxidative stress and apoptosis, accompanied by changes in the expression of related proteins. The iP assay revealed a strong interaction between GaB1 and S100a8. in addition, GaB1 silencing reversed the inhibitory effects of S100a8 silencing on inflammation, oxidative stress and apoptosis in oGd/R-stimulated BV2 cells. Taken together, the results of the present study demonstrated that S100a8 silencing alleviated inflammation, oxidative stress and the apoptosis of BV2 cells induced by oGd/r, partly by upregulating the expression of GaB1. Thus, these findings may potentially provide a novel direction to develop therapeutic strategies for cerebral i/r injury.

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Section: Discussionsupporting

confidence: 91%

S100a8 silencing attenuates inflammation, oxidative stress and apoptosis in BV2 cells induced by oxygen‑glucose deprivation and reoxygenation by upregulating GAB1 expression

Lin

2020

Mol Med Rep

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“…Molecules with identical expression patterns usually Computational and Mathematical Methods in Medicine have a close association in function [20,22]. TRIM47 has been reported in multiple carcinomas, but its function is not clear [23]. We thus conducted related experiments to validate the mechanism and function.…”

Section: Discussionmentioning

confidence: 99%

Upregulated Tripartite Motif 47 Could Facilitate Glioma Cell Proliferation and Metastasis as a Tumorigenesis Promoter

Liu

Guo

Ming

et al. 2021

Computational and Mathematical Methods in Medicine

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Introduction. Tripartite motif 47 (TRIM47) belongs to a category of the TRIM family. It takes part in cancer tumorigenesis, thus demonstrating important functions across numerous carcinomas. Unfortunately, it is still elusive towards TRIM47 expression, characteristic, and biological function in brain gliomas. Methods. Public database analysis was applied to analyze TRIM47 expression, and quantitative real-time PCR (qRT-PCR) was applied to detect the expression of TRIM47 in 9 paired tissues of glioma. The Cancer Genome Atlas (TCGA) and the Chinese Glioma Genome Atlas (CGGA) databases were applied to evaluate the overall survival (OS). Gene Ontology (GO) term and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways were applied to analyze differentially expressed gene (DEG) functions. In vitro experiments were performed to validate TRIM47-mediated effects on glioma cell proliferation, migration, and invasion. Results. Compared to that in normal tissues, TRIM47 expression was greatly higher in glioma tissues, and its expression level was associated with different grades of glioma. Our data indicated that highly expressed TRIM47 displayed an association with the poor prognosis of glioma patients. Ablating TRIM47 obviously impeded glioma cell invasion and migration. Conclusion. TRIM47 could modulate glioma cell proliferation, invasion, and migration. Highly expressed TRIM47 exhibited a correlation with poor prognosis. All data imply that TRIM47 is a probable biomarker for glioma and has the potentiality to become a newly generated target for glioma treatment.

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“…( 6 ) Previous study reported that TRIM47 is a critical mediator of cerebral I/R injury through regulating inflammation. ( 7 ) Moreover, TRIM8 deficiency attenuated hepatic I/R injury by mediating inflammation responses and apoptosis. ( 8 ) As a member of the TRIM family, which contains similar domains of a RING (really interesting new gene) finger, B‐box zinc finger, and coiled‐coil domain, TRIM27 was first reported as a fusion protein of the RET proto‐oncogene in 1988.…”

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confidence: 99%

Tripartite Motif‐Containing 27 Attenuates Liver Ischemia/Reperfusion Injury by Suppressing Transforming Growth Factor β–Activated Kinase 1 (TAK1) by TAK1 Binding Protein 2/3 Degradation

Chen

Zhang

et al. 2021

Hepatology

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Background and Aims Hepatic ischemia‐reperfusion (I/R) injury, which mainly involves inflammatory responses and apoptosis, is a common cause of organ dysfunction in liver transplantation (LT). As a critical mediator of inflammation and apoptosis in various cell types, the role of tripartite motif‐containing (TRIM) 27 in hepatic I/R injury remains worthy of study. Approach and Results This study systemically evaluated the putative role of TRIM27/transforming growth factor β–activated kinase 1 (TAK1)/JNK (c‐Jun N‐terminal kinase)/p38 signaling in hepatic I/R injury. TRIM27 expression was significantly down‐regulated in liver tissue from LT patients, mice subjected to hepatic I/R surgery, and hepatocytes challenged by hypoxia/reoxygenation (H/R) treatment. Subsequently, using global Trim27 knockout mice (Trim27‐KO mice) and hepatocyte‐specific Trim27 transgenic mice (Trim27‐HTG mice), TRIM27 functions to ameliorate liver damage, reduce the inflammatory response, and prevent cell apoptosis. In parallel in vitro studies, activating TRIM27 also prevented H/R‐induced hepatocyte inflammation and apoptosis. Mechanistically, TRIM27 constitutively interacted with the critical components, TAK1 and TAK1 binding protein 2/3 (TAB2/3), and promoted the degradation of TAB2/3, leading to inactivation of TAK1 and the subsequent suppression of downstream JNK/p38 signaling. Conclusions TRIM27 is a key regulator of hepatic I/R injury by mediating the degradation of TAB2/3 and suppression of downstream TAK1‐JNK/p38 signaling. TRIM27 may be a promising approach to protect the liver against I/R‐mediated hepatocellular damage in transplant recipients.

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Trim47 is a critical regulator of cerebral ischemia-reperfusion injury through regulating apoptosis and inflammation

Cited by 36 publications

References 28 publications

S100a8 silencing attenuates inflammation, oxidative stress and apoptosis in BV2 cells induced by oxygen‑glucose deprivation and reoxygenation by upregulating GAB1 expression

S100a8 silencing attenuates inflammation, oxidative stress and apoptosis in BV2 cells induced by oxygen‑glucose deprivation and reoxygenation by upregulating GAB1 expression

Upregulated Tripartite Motif 47 Could Facilitate Glioma Cell Proliferation and Metastasis as a Tumorigenesis Promoter

Tripartite Motif‐Containing 27 Attenuates Liver Ischemia/Reperfusion Injury by Suppressing Transforming Growth Factor β–Activated Kinase 1 (TAK1) by TAK1 Binding Protein 2/3 Degradation

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Trim47 is a critical regulator of cerebral ischemia-reperfusion injury through regulating apoptosis and inflammation

Cited by 36 publications

References 28 publications

S100a8 silencing attenuates inflammation, oxidative stress and apoptosis in BV2&nbsp;cells induced by oxygen‑glucose deprivation and reoxygenation by upregulating GAB1 expression

S100a8 silencing attenuates inflammation, oxidative stress and apoptosis in BV2&nbsp;cells induced by oxygen‑glucose deprivation and reoxygenation by upregulating GAB1 expression

Upregulated Tripartite Motif 47 Could Facilitate Glioma Cell Proliferation and Metastasis as a Tumorigenesis Promoter

Tripartite Motif‐Containing 27 Attenuates Liver Ischemia/Reperfusion Injury by Suppressing Transforming Growth Factor β–Activated Kinase 1 (TAK1) by TAK1 Binding Protein 2/3 Degradation

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S100a8 silencing attenuates inflammation, oxidative stress and apoptosis in BV2 cells induced by oxygen‑glucose deprivation and reoxygenation by upregulating GAB1 expression

S100a8 silencing attenuates inflammation, oxidative stress and apoptosis in BV2 cells induced by oxygen‑glucose deprivation and reoxygenation by upregulating GAB1 expression