GLORIA

GEOMAR Library Ocean Research Information Access

X

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
Filter
  • Ovid Technologies (Wolters Kluwer Health)  (3)
  • Li, Bin  (3)
  • Zhang, Ping  (3)
Material
Publisher
  • Ovid Technologies (Wolters Kluwer Health)  (3)
Person/Organisation
Language
Years
FID
  • 1
    Online Resource
    Online Resource
    Long Noncoding RNA Taurine-Upregulated Gene 1 Knockdown Protects Cardiomyocytes Against Hypoxia/Reoxygenation-induced Injury Through Regulating miR-532-5p/Sox8 Axis
    Ovid Technologies (Wolters Kluwer Health) ; 2020
    In:  Journal of Cardiovascular Pharmacology Vol. 76, No. 5 ( 2020-11), p. 556-563
    Details
    In: Journal of Cardiovascular Pharmacology, Ovid Technologies (Wolters Kluwer Health), Vol. 76, No. 5 ( 2020-11), p. 556-563
    Abstract: Long noncoding RNA taurine-upregulated gene 1 (TUG1) has been reported to involve in the processing of cardiac ischemia/reperfusion injury after myocardial infarction. Thus, this study further investigates the underlying mechanisms of TUG1 in hypoxia/reoxygenation (H/R)-induced cardiomyocyte injury in vitro. Methods: Cell viability, apoptosis, and migration and invasion were detected using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay, flow cytometry, and transwell assay, respectively. Western blot was used to examine the levels of matrix metallopeptidase 9, matrix metallopeptidase 2, and sex determining region Y-box transcription factor 8 (Sox8) protein. Levels of lactate dehydrogenase, malondialdehyde, superoxide dismutase, and glutathione peroxidase were detected using commercial kits. Levels of TUG1, microRNA-532-5p (miR-532-5p), and Sox8 were detected by quantitative real-time polymerase chain reaction. The interaction between miR-532-5p and Sox8 or TUG1 was confirmed by dual-luciferase reporter and RNA immunoprecipitation assay. Results: H/R induced rat cardiomyocyte H9c2 injury by inhibiting cell viability, migration and invasion, promoting cell apoptosis, and stimulating oxidative stress. H/R-induced H9c2 injury upregulated the level of TUG1, and TUG1 knockdown alleviated H/R-induced cardiomyocyte injury. TUG1 directly bound to miR-532-5p, and miR-532-5p inhibition reversed the action of TUG1 knockdown on H/R-induced cardiomyocyte injury. Sox8 was a target of miR-532-5p, and miR-532-5p blunted H/R-induced cardiomyocyte injury by targeting Sox8. In addition, TUG1 knockdown inhibited H/R-induced Sox8 elevation through miR-532-5p in H9c2 cells. Conclusion: TUG1 silence ameliorated H/R-induced cardiomyocytes injury through regulating miR-532-5p/Sox8 axis, suggesting a potential therapeutic target for preventing myocardial ischemia/reperfusion injury.
    Type of Medium: Online Resource
    ISSN: 0160-2446
    URL: Article
    DOI: 10.1097/FJC.0000000000000895
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2020
    detail.hit.zdb_id: 2049700-3
    SSG: 15,3
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 2
    Online Resource
    Online Resource
    Inhibition of miR-322-5p Protects Cardiac Myoblast Cells Against Hypoxia-Induced Apoptosis and Injury Through Regulating CIAPIN1
    Ovid Technologies (Wolters Kluwer Health) ; 2021
    In:  Journal of Cardiovascular Pharmacology Vol. 77, No. 2 ( 2021-02), p. 200-207
    Details
    In: Journal of Cardiovascular Pharmacology, Ovid Technologies (Wolters Kluwer Health), Vol. 77, No. 2 ( 2021-02), p. 200-207
    Abstract: Hypoxia leads to insufficient supply of blood and nutrients, which is major incentive for cardiomyocyte injury and apoptosis. Previous studies reported the regulation effects of microRNAs (miRNAs) in myocardial infarction, whereas function and molecular mechanisms of miR-322-5p were still unclear. Therefore, our study focused on the biological role of miR-322-5p in hypoxia-induced cardiac myoblast cells apoptosis and injury. The expression levels of miR-322-5p and cytokine-induced apoptosis inhibitor 1 (CIAPIN1) were measured by real-time quantitative polymerase chain reaction in cardiac myoblast cells. The 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-2H-tetrazol-3-ium bromide (MTT), lactic dehydrogenase, and flow cytometry assays were performed to examine proliferation, injury, and apoptosis of cardiac myoblast cells, respectively. The protein expression levels were evaluated with western blot assay. The relationship between miR-322-5p and CIAPIN1 was confirmed by dual-luciferase reporter analysis. We found that miR-322-5p level was increased in cardiac myoblast cells exposed to hypoxia. In addition, miR-322-5p silencing could weaken injury and apoptosis in cardiac myoblast cells induced by hypoxia; meanwhile, inhibition of miR-322-5p activation of phosphatidylinositol-3 kinases (PI3K)/protein kinase B (AKT) signal pathway. Besides, CIAPIN1 was a target mRNA of miR-322-5p based on bioinformatics prediction. CIAPIN1 knockdown reversed the effects of miR-322-5p silencing on hypoxic cardiac myoblast cells. Suppression of miR-322-5p protected cardiac myoblast cells against hypoxia-induced injury and apoptosis through regulation of CIAPIN1 expression and PI3K/AKT signal pathway.
    Type of Medium: Online Resource
    ISSN: 0160-2446
    URL: Article
    DOI: 10.1097/FJC.0000000000000949
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2021
    detail.hit.zdb_id: 2049700-3
    SSG: 15,3
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 3
    Online Resource
    Online Resource
    CircJARID2 Regulates Hypoxia-Induced Injury in H9c2 Cells by Affecting miR-9-5p–Mediated BNIP3
    Ovid Technologies (Wolters Kluwer Health) ; 2021
    In:  Journal of Cardiovascular Pharmacology Vol. 78, No. 1 ( 2021-07), p. e77-e85
    Details
    In: Journal of Cardiovascular Pharmacology, Ovid Technologies (Wolters Kluwer Health), Vol. 78, No. 1 ( 2021-07), p. e77-e85
    Abstract: Myocardial infarction (MI) is a common cardiovascular disease, and many circular RNAs (circRNAs) have been found to participate in the pathological process. This study was to research circRNA jumonji and AT-rich interaction domain containing 2 (circJARID2) in MI. MI cell model was established by hypoxia treatment in H9c2 cells. CircJARID2 and microRNA-9-5p (miR-9-5p) levels were examined using real-time polymerase chain reaction. Cell viability detection was performed by Cell Counting Kit-8 (CCK-8) and 5-ethynyl-2′-deoxyuridine (Edu) assays. Cell apoptosis was evaluated by flow cytometry and caspase-3 activity assay. Apoptotic markers and B-cell lymphoma-2 (Bcl-2) interacting protein 3 (BNIP3) were quantified by western blot. Inflammatory cytokines were determined via enzyme-linked immunosorbent assay. The genic interaction was analyzed through dual-luciferase reporter and RNA immunoprecipitation assays. Hypoxia induced the upregulation of circJARID2 expression in H9c2 cells. The hypoxia-induced cell viability inhibition, apoptosis promotion, and inflammatory response were all counterbalanced by knockdown of circJARID2. CircJARID2 interacted with miR-9-5p, and its function in regulating the hypoxia-induced cell injury was also dependent on targeting miR-9-5p. BNIP3 acted as a target gene of miR-9-5p, and circJARID2 had positive effect on BNIP3 expression by binding to miR-9-5p. MiR-9-5p played a protective role for H9c2 cells against the hypoxia-induced injury via targeting BNIP3. CircJARID2 overexpression contributed to the hypoxia-induced H9c2 cell injury by sponging miR-9-5p to upregulate BNIP3 expression, showing a novel molecular network of MI pathomechanism.
    Type of Medium: Online Resource
    ISSN: 0160-2446
    URL: Article
    DOI: 10.1097/FJC.0000000000001033
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2021
    detail.hit.zdb_id: 2049700-3
    SSG: 15,3
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...