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  • 1
    Online Resource
    Online Resource
    Helix B Surface Peptide Protects against Acute Myocardial Ischemia-Reperfusion Injury via the RISK and SAFE Pathways in a Mouse Model
    S. Karger AG ; 2016
    In:  Cardiology Vol. 134, No. 2 ( 2016), p. 109-117
    Details
    In: Cardiology, S. Karger AG, Vol. 134, No. 2 ( 2016), p. 109-117
    Abstract: 〈 b 〉 〈 i 〉 Objective: 〈 /i 〉 〈 /b 〉 This study explores the effects of helix B surface peptide (HBSP) on myocardial infarct size (IS), cardiac function, cardiomyocyte apoptosis and oxidative stress damage in mouse hearts subjected to myocardial ischemia-reperfusion injury (MIRI) and also the mechanisms underlying the effects. 〈 b 〉 〈 i 〉 Method: 〈 /i 〉 〈 /b 〉 Male adult mice were subjected to 45 min of ischemia followed by 2 h of reperfusion; 5 min before the reperfusion, they were treated with HBSP or vehicle. MIRI-induced IS, cardiomyocyte apoptosis and cardiac functional impairment were determined and compared. Western blot analysis was then conducted to elucidate the mechanism of HBSP after treatment. 〈 b 〉 〈 i 〉 Results: 〈 /i 〉 〈 /b 〉 HBSP administration before reperfusion significantly reduced the myocardial IS, decreased cardiomyocyte apoptosis, reduced the activities of superoxide dismutase and malondialdehyde and partially preserved heart function. As demonstrated by the Western blot analysis, HBSP after treatment upregulated Akt/GSK-3β/ERK and STAT-3 phosphorylation; these inhibitors, in turn, weakened the beneficial effects of HBSP. 〈 b 〉 〈 i 〉 Conclusion: 〈 /i 〉 〈 /b 〉 HBSP plays a protective role in MIRI in mice by inhibiting cardiomyocyte apoptosis, reducing the MIRI-induced IS, oxidative stress and improving the heart function after MIRI. The mechanism underlying these effects of HBSP is related to the activation of the RISK (reperfusion injury salvage kinase, Akt/GSK-3β/ERK) and SAFE (STAT-3) pathways.
    Type of Medium: Online Resource
    ISSN: 0008-6312 , 1421-9751
    URL: Article
    DOI: 10.1159/000443680
    RVK:
    XA 36200
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2016
    detail.hit.zdb_id: 1482041-9
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  • 2
    Online Resource
    Online Resource
    The Common LncRNAs of Neuroinflammation-Related Diseases
    American Society for Pharmacology & Experimental Therapeutics (ASPET) ; 2023
    In:  Molecular Pharmacology Vol. 103, No. 3 ( 2023-03), p. 113-131
    Details
    In: Molecular Pharmacology, American Society for Pharmacology & Experimental Therapeutics (ASPET), Vol. 103, No. 3 ( 2023-03), p. 113-131
    Type of Medium: Online Resource
    ISSN: 0026-895X , 1521-0111
    URL: Article
    DOI: 10.1124/molpharm.122.000530
    Language: English
    Publisher: American Society for Pharmacology & Experimental Therapeutics (ASPET)
    Publication Date: 2023
    detail.hit.zdb_id: 1475030-2
    SSG: 15,3
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  • 3
    Online Resource
    Online Resource
    Helix B Surface Peptide Protects Cardiomyocytes From Hypoxia/Reoxygenation-induced Autophagy Through the PI3K/Akt Pathway
    Ovid Technologies (Wolters Kluwer Health) ; 2020
    In:  Journal of Cardiovascular Pharmacology Vol. 76, No. 2 ( 2020-08), p. 181-188
    Details
    In: Journal of Cardiovascular Pharmacology, Ovid Technologies (Wolters Kluwer Health), Vol. 76, No. 2 ( 2020-08), p. 181-188
    Abstract: Helix B surface peptide (HBSP) is a newly discovered tissue-protective erythropoietin derivative that provides benefits after myocardial ischemia/reperfusion. This study explores the cardioprotective effects of HBSP in myocardial cells in response to hypoxia/reoxygenation injury and its potential mechanism. Methods: In this study, rat ventricular (H9c2) cell cultures were established and pretreated with HBSP. H9c2 cardiomyocytes were randomly assigned to the control, H/R, H/R + LY294002 (a PI3K inhibitor), HBSP + H/R, and HBSP + H/R + LY294002 groups. The pretreated cardiomyocytes underwent H/R, and the cardiomyocytes were monitored for viability through a CCK-8 assay, whereas flow cytometry was used to test cell apoptosis. Orgotein Superoxide Dismutase (SOD) and lactate dehydrogenase (LDH) expression were monitored by SOD and LDH kits, respectively. The expression of LC3 autophagosomes was determined by immunocytochemistry. The expression of LC3II/LC3I, p-Mammalian Target of Rapamycin (mTOR) mTOR, mTOR, Beclin 1, p-PI3K, PI3K p-Akt, and Akt was determined by Western blotting. Results: HBSP increased cell viability and reduced SOD and LDH production, and it also reduced H/R-induced cell apoptosis. Moreover, the expression of the autophagy-related proteins (LC3II/LC3I) was inhibited by HBSP, whereas the expression of p-PI3K, p-Akt, and p-mTOR was enhanced. However, the PI3K inhibitor (LY294002) notably abolished these effects in H9c2 cells. Conclusions: HBSP inhibits excessive autophagy and apoptosis induced by H/R by activating the PI3K/Akt pathway. HBSP may potentially be a therapeutic intervention for myocardial ischemia/reperfusion injury.
    Type of Medium: Online Resource
    ISSN: 0160-2446
    URL: Article
    DOI: 10.1097/FJC.0000000000000849
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2020
    detail.hit.zdb_id: 2049700-3
    SSG: 15,3
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  • 4
    Online Resource
    Online Resource
    ROS Signaling-Mediated Novel Biological Targets: Brf1 and RNA Pol III Genes
    Hindawi Limited ; 2021
    In:  Oxidative Medicine and Cellular Longevity Vol. 2021 ( 2021-10-4), p. 1-9
    Details
    In: Oxidative Medicine and Cellular Longevity, Hindawi Limited, Vol. 2021 ( 2021-10-4), p. 1-9
    Abstract: Biomolecule metabolism produces ROS (reactive oxygen species) under physiological and pathophysiological conditions. Dietary factors (alcohol) and carcinogens (EGF, DEN, and MNNG) also induce the release of ROS. ROS often causes cell stress and tissue injury, eventually resulting in disorders or diseases of the body through different signaling pathways. Normal metabolism of protein is critically important to maintain cellular function and body health. Brf1 (transcript factor II B-related factor 1) and its target genes, RNA Pol III genes (RNA polymerase III-dependent genes), control the process of protein synthesis. Studies have demonstrated that the deregulation of Brf1 and its target genes is tightly linked to cell proliferation, cell transformation, tumor development, and human cancers, while alcohol, EGF, DEN, and MNNG are able to induce the deregulation of these genes through different signaling pathways. Therefore, it is very important to emphasize the roles of these signaling events mediating the processes of Brf1 and RNA Pol III gene transcription. In the present paper, we mainly summarize our studies on signaling events which mediate the deregulation of these genes in the past dozen years. These studies indicate that Brf1 and RNA Pol III genes are novel biological targets of ROS.
    Type of Medium: Online Resource
    ISSN: 1942-0994 , 1942-0900
    URL: Article
    DOI: 10.1155/2021/5888432
    Language: English
    Publisher: Hindawi Limited
    Publication Date: 2021
    detail.hit.zdb_id: 2455981-7
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  • 5
    Online Resource
    Online Resource
    Abstract P2020: A Novel Molecular Mechanism Of Cardiac Hypertrophy
    Ovid Technologies (Wolters Kluwer Health) ; 2022
    In:  Circulation Research Vol. 131, No. Suppl_1 ( 2022-08-05)
    Details
    In: Circulation Research, Ovid Technologies (Wolters Kluwer Health), Vol. 131, No. Suppl_1 ( 2022-08-05)
    Abstract: Proliferation of cardiac myocytes is accompanied by increases in cell mass to maintain myocyte size in fetal heart. In adult cardiac myocytes, cell growth becomes uncoupled from proliferation after growth stimuli, resulting in hypertrophic growth. Both proliferation and hypertrophy growth of cardiac myocytes require more protein synthesis. Brf1 (TF IIB-related factor 1) and Pol III genes (RNA Polymerase III-dependent genes) are the dominant factors of protein produce. Brf1 is a key regulator for Pol III genes. Cardiac hypertrophy is a critical risk factor for cardiovascular disease, including heart failure, arrhythmia, and sudden death. Cardiac hypertrophy involves both the processes of embryonic gene expression and transcriptional reprogramming. The processes are tightly modulated by different signal pathways and epigenetic regulation. Diabetic cardiomyopathy is associated with an increased risk for heart failure and death in patients with diabetes. To explore the molecular mechanism of cardiac hypertrophy, we investigate the alterations of Brf1 and Pol III gene transcription under glucose treatment by using cell culture model and animal model. We have found that glucose increases Brf1 expression and Pol III gene transcription. We identified that these genes are mediated by JNK1, MSK1, pAMPK and phosphorylated histone H3. inhibiting the pathways decrease Brf1 expression, reduce Pol III gene transcription, consequently repression of myocytes growth. It implies that developing an effective inhibitor to repress Brf1 expression may provide a potential approach for the therapy of cardiac hypertrophy. More studies on cardiac hypertrophy are going in our laboratory.
    Type of Medium: Online Resource
    ISSN: 0009-7330 , 1524-4571
    URL: Article
    DOI: 10.1161/res.131.suppl_1.P2020
    RVK:
    XA 10000
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2022
    detail.hit.zdb_id: 1467838-X
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  • 6
    Online Resource
    Online Resource
    Towards Low-Latency Batched Stream Processing by Pre-Scheduling
    Institute of Electrical and Electronics Engineers (IEEE) ; 2019
    In:  IEEE Transactions on Parallel and Distributed Systems Vol. 30, No. 3 ( 2019-3-1), p. 710-722
    Details
    In: IEEE Transactions on Parallel and Distributed Systems, Institute of Electrical and Electronics Engineers (IEEE), Vol. 30, No. 3 ( 2019-3-1), p. 710-722
    Type of Medium: Online Resource
    ISSN: 1045-9219 , 1558-2183 , 2161-9883
    URL: Article
    DOI: 10.1109/TPDS.2018.2866581
    RVK:
    SQ 1100
    RVK:
    SA 1000
    Language: Unknown
    Publisher: Institute of Electrical and Electronics Engineers (IEEE)
    Publication Date: 2019
    detail.hit.zdb_id: 2027774-X
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  • 7
    Online Resource
    Online Resource
    Helix B Surface Peptide Protects Cardiomyocytes Against Hypoxia/Reoxygenation-induced Apoptosis Through Mitochondrial Pathways
    Ovid Technologies (Wolters Kluwer Health) ; 2016
    In:  Journal of Cardiovascular Pharmacology Vol. 67, No. 5 ( 2016-05), p. 418-426
    Details
    In: Journal of Cardiovascular Pharmacology, Ovid Technologies (Wolters Kluwer Health), Vol. 67, No. 5 ( 2016-05), p. 418-426
    Type of Medium: Online Resource
    ISSN: 0160-2446
    URL: Article
    DOI: 10.1097/FJC.0000000000000367
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2016
    detail.hit.zdb_id: 2049700-3
    SSG: 15,3
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  • 8
    Online Resource
    Online Resource
    Significance and Prospect of Brf1 Overexpression
    Heighten Science Publications Corporation ; 2023
    In:  Archives of Pharmacy and Pharmaceutical Sciences Vol. 7, No. 1 ( 2023-08-22), p. 045-053
    Details
    In: Archives of Pharmacy and Pharmaceutical Sciences, Heighten Science Publications Corporation, Vol. 7, No. 1 ( 2023-08-22), p. 045-053
    Abstract: Brf1 (TFIIB-related factor 1) is a transcription factor, which specifically modulates the transcription of RNA polymerase III-dependent genes (RNA Pol III genes), such as tRNAs and 5S rRNA. The products of tRNAs and 5S rRNA transcription will be changed with the alteration of Brf1 expression. Whereas deregulation of Brf1 and RNA Pol III genes are tightly associated with cell proliferation and transformation, and tumorigenesis. In recent years, emerging studies indicate that Brf1 expression is increased in patients with cancers. In this review, we summarize the progress of the abnormal expression of Brf1 in different human cancers to explore an underlying mechanism and its clinical implication, as well as to prompt its application prospect. With the depth of the Brf1 study and the progress of biotechnology, the status of Brf1 expression may be used as a universal indicator of the early detection and prognosis observation of human cancers.
    Type of Medium: Online Resource
    ISSN: 2639-992X
    URL: Article
    DOI: 10.29328/journal.apps.1001043
    Language: Unknown
    Publisher: Heighten Science Publications Corporation
    Publication Date: 2023
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