Utilizing Experimental Mouse Model to Identify Effectors of Hepatocellular Carcinoma Induced by HBx Antigen

Yang, Ming Hui; Chen, Marcelo; Mo, Hsiao Hsuan; Tsai, Wan–Chi; Chang, Yu Chi; Chang, Chao‐Yuan; Chen, Ko Chin; Wu, Hsin‐Yi; Yuan, Cheng; Lee, Che Hsin; Chen, Yi Ming Arthur; Tyan, Yu‐Chang

doi:10.3390/cancers12020409

Cited by 14 publications

(11 citation statements)

References 63 publications

(65 reference statements)

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“…If there has a therapeutic strategy that can balance this pathological change? Previous studies have suggested that FSTL1 attenuated pathological injury of multiple organs by alleviating fibrosis, particularly in cardiac dysfunction ( Jiang et al, 2020 ; Hu et al, 2020 ; Li et al, 2021 ; Z.; Chen Z. et al, 2019 ; Yang et al, 2020 ). Our current findings are consistent with these aforementioned research findings that the upregulation of FSTL1 in DM compared with the control group, which was further increased in T2DM with MI.…”

Section: Discussionmentioning

confidence: 99%

FSTL1-USP10-Notch1 Signaling Axis Protects Against Cardiac Dysfunction Through Inhibition of Myocardial Fibrosis in Diabetic Mice

Yang

et al. 2021

Front. Cell Dev. Biol.

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The incidence of type 2 diabetes mellitus (T2DM) has been increasing globally, and T2DM patients are at an increased risk of major cardiac events such as myocardial infarction (MI). Nevertheless, the molecular mechanisms underlying MI injury in T2DM remain elusive. Ubiquitin-specific protease 10 (USP10) functions as a NICD1 (Notch1 receptor) deubiquitinase that fine-tunes the essential myocardial fibrosis regulator Notch signaling. Follistatin-like protein 1 (FSTL1) is a cardiokine with proven benefits in multiple pathological processes including cardiac fibrosis and insulin resistance. This study was designed to examine the roles of FSTL1/USP10/Notch1 signaling in MI-induced cardiac dysfunction in T2DM. High-fat-diet-treated, 8-week-old C57BL/6J mice and db/db T2DM mice were used. Intracardiac delivery of AAV9-FSTL1 was performed in T2DM mice following MI surgery with or without intraperitoneal injection of crenigacestat (LY3039478) and spautin-1. Our results demonstrated that FSTL1 improved cardiac function following MI under T2DM by reducing serum lactate dehydrogenase (LDH) and myocardial apoptosis as well as cardiac fibrosis. Further in vivo studies revealed that the protective role of FSTL1 against MI injury in T2DM was mediated by the activation of USP10/Notch1. FSTL1 protected cardiac fibroblasts (CFs) against DM-MI-induced cardiofibroblasts injury by suppressing the levels of fibrosis markers, and reducing LDH and MDA concentrations in a USP10/Notch1-dependent manner. In conclusion, FSTL1 treatment ameliorated cardiac dysfunction in MI with co-existent T2DM, possibly through inhibition of myocardial fibrosis and apoptosis by upregulating USP10/Notch1 signaling. This finding suggests the clinical relevance and therapeutic potential of FSTL1 in T2DM-associated MI and other cardiovascular diseases.

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Section: Discussionmentioning

confidence: 99%

FSTL1-USP10-Notch1 Signaling Axis Protects Against Cardiac Dysfunction Through Inhibition of Myocardial Fibrosis in Diabetic Mice

Yang

et al. 2021

Front. Cell Dev. Biol.

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“…BMP5 is widely expressed in many tissues, especially in the placenta, liver, and lung. [32][33][34] Immunofluorescent staining displayed that BMP5 was also abundantly present both in the epithelial and stromal cells of human and rat prostates. Similarly, BMP5 was strongly expressed in BPH-1 and WPMY-1 cells.…”

Section: Discussionmentioning

confidence: 99%

Upregulated bone morphogenetic protein 5 enhances proliferation and epithelial–mesenchymal transition process in benign prostatic hyperplasia via BMP/Smad signaling pathway

Liu

et al. 2021

The Prostate

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Background: Benign prostatic hyperplasia (BPH) is one of the most common illnesses in aging men. Recent studies found that bone morphogenetic protein 5 (BMP5) is upregulated in BPH tissues, however, the role of BMP5 in the development of BPH has not been examined. The current study aims to elucidate the potential roles of BMP5 and related signaling pathways in BPH.Methods: Human prostate cell lines (BPH-1, WPMY-1) and human/rat hyperplastic prostate tissues were utilized. Western blot, quantitative real-time polymerase chain reaction, immunofluorescent staining, and immunohistochemical staining were performed. BMP5-silenced and -overexpressed cell models were generated and then cell cycle progression, apoptosis, and proliferation were determined. The epithelial-mesenchymal transition (EMT) was also quantitated. And rescue experiments by BMP/Smad signaling pathway agonist or antagonist were accomplished.Moreover, BPH-related tissue microarray analysis was performed and associations between clinical parameters and expression of BMP5 were analyzed.Results: Our study demonstrated that BMP5 was upregulated in human and rat hyperplastic tissues and localized both in the epithelial and stromal compartments of the prostate tissues. E-cadherin was downregulated in hyperplastic tissues, while N-cadherin and vimentin were upregulated. Overexpression of BMP5 enhanced cell proliferation and the EMT process via phosphorylation of Smad1/5/8, while knockdown of BMP5 induced cell cycle arrest at G0/G1 phase and blocked the EMT process. Moreover, a BMP/Smad signaling pathway agonist and antagonist reversed the effects of BMP5 silencing and overexpression, respectively. In addition, BMP5

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“…The knockdown of circ_00004812 has been shown to lead to an increase in the mRNA and protein expression levels of IFN-α and IFN-β ( 37 ). FSTL1 and IFN-β have been reported to participate in the oncogenesis process induced by HBV infection ( 38 ). With regards to the association between HBV infection and liver fibrosis, hsa_circ_4099 enhances H 2 O 2 -mediated fibrosis, as well as exerts a sponge effect on miR-706 ( 39 ).…”

Section: Effect Of Circrnas On Viral Infectionsmentioning

confidence: 99%

Role of circRNAs in viral infection and their significance for diagnosis and treatment (Review)

Liu

et al. 2021

Int J Mol Med

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Circular RNAs (circRNAs) are a class of non-coding RNAs with a circular, covalent structure that lack both 5' ends and 3' poly(A) tails, which are stable and specific molecules that exist in eukaryotic cells and are highly conserved. The role of circRNAs in viral infections is being increasingly acknowledged, since circRNAs have been discovered to be involved in several viral infections (such as hepatitis B virus infection and human papilloma virus infection) through a range of circRNA/microRNA/mRNA regulatory axes. These findings have prompted investigations into the potential of circRNAs as targets for the diagnosis and treatment of viral infection-related diseases. The aim of the present review was to systematically examine and discuss the role of circRNAs in several common viral infections, as well as their potential as diagnostic markers and therapeutic targets.

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Utilizing Experimental Mouse Model to Identify Effectors of Hepatocellular Carcinoma Induced by HBx Antigen

Cited by 14 publications

References 63 publications

FSTL1-USP10-Notch1 Signaling Axis Protects Against Cardiac Dysfunction Through Inhibition of Myocardial Fibrosis in Diabetic Mice

FSTL1-USP10-Notch1 Signaling Axis Protects Against Cardiac Dysfunction Through Inhibition of Myocardial Fibrosis in Diabetic Mice

Upregulated bone morphogenetic protein 5 enhances proliferation and epithelial–mesenchymal transition process in benign prostatic hyperplasia via BMP/Smad signaling pathway

Role of circRNAs in viral infection and their significance for diagnosis and treatment (Review)

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