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  • Ovid Technologies (Wolters Kluwer Health)  (62)
  • 1
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    Online Resource
    LARP7 Protects Against Heart Failure by Enhancing Mitochondrial Biogenesis
    Ovid Technologies (Wolters Kluwer Health) ; 2021
    In:  Circulation Vol. 143, No. 20 ( 2021-05-18), p. 2007-2022
    Details
    In: Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 143, No. 20 ( 2021-05-18), p. 2007-2022
    Abstract: Heart failure (HF) is among the leading causes of morbidity and mortality, and its prevalence continues to rise. LARP7 (La ribonucleoprotein domain family member 7) is a master regulator that governs the DNA damage response and RNAPII (RNA polymerase II) pausing pathway, but its role in HF pathogenesis is incompletely understood. Methods: We assessed LARP7 expression in human HF and in nonhuman primate and mouse HF models. To study the function of LARP7 in heart, we generated global and cardiac-specific LARP7 knockout mice. We acutely abolished LARP7 in mature cardiomyocytes by Cas9-mediated LARP7 somatic knockout. We overexpressed LARP7 in cardiomyocytes using adeno-associated virus serotype 9 and ATM (ataxia telangiectasia mutated protein) inhibitor. The therapeutic potential of LARP7-regulated pathways in HF was tested in a mouse myocardial infarction model. Results: LARP7 was profoundly downregulated in failing human hearts and in nonhuman primate and murine hearts after myocardial infarction. Low LARP7 levels in failing hearts were linked to elevated reactive oxygen species, which activated the ATM-mediated DNA damage response pathway and promoted LARP7 ubiquitination and degradation. Constitutive LARP7 knockout in mouse resulted in impaired mitochondrial biogenesis, myocardial hypoplasia, and midgestational lethality. Cardiac-specific inactivation resulted in defective mitochondrial biogenesis, impaired oxidative phosphorylation, elevated oxidative stress, and HF by 4 months of age. These abnormalities were accompanied by reduced SIRT1 (silent mating type information regulation 2 homolog 1) stability and deacetylase activity that impaired SIRT1-mediated transcription of genes for oxidative phosphorylation and energy metabolism and dampened cardiac function. Restoring LARP7 expression after myocardial infarction by either adeno-associated virus–mediated LARP7 expression or small molecule ATM inhibitor substantially improved the function of injured heart. Conclusions: LARP7 is essential for mitochondrial biogenesis, energy production, and cardiac function by modulating SIRT1 homeostasis and activity. Reduction of LARP7 in diseased hearts owing to activation of the ATM pathway contributes to HF pathogenesis and restoring LARP7 in the injured heart confers myocardial protection. These results identify the ATM-LARP7-SIRT1 pathway as a target for therapeutic intervention in HF.
    Type of Medium: Online Resource
    ISSN: 0009-7322 , 1524-4539
    URL: Article
    DOI: 10.1161/CIRCULATIONAHA.120.050812
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2021
    detail.hit.zdb_id: 1466401-X
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  • 2
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    Deacetylation of Septin4 by SIRT2 (Silent Mating Type Information Regulation 2 Homolog-2) Mitigates Damaging of Hypertensive Nephropathy
    Ovid Technologies (Wolters Kluwer Health) ; 2023
    In:  Circulation Research Vol. 132, No. 5 ( 2023-03-03), p. 601-624
    Details
    In: Circulation Research, Ovid Technologies (Wolters Kluwer Health), Vol. 132, No. 5 ( 2023-03-03), p. 601-624
    Abstract: Hypertension can lead to podocyte damage and subsequent apoptosis, eventually resulting in glomerulosclerosis. Although alleviating podocyte apoptosis has clinical significance for the treatment of hypertensive nephropathy, an effective therapeutic target has not yet been identified. The function of septin4, a proapoptotic protein and an important marker of organ damage, is regulated by post-translational modification. However, the exact role of septin4 in regulating podocyte apoptosis and its connection to hypertensive renal damage remains unclear. Methods: We investigated the function and mechanism of septin4 in hypertensive nephropathy to discover a theoretical basis for targeted treatment. Mouse models including Rosa 26 (Gt(ROSA)26Sor)- SIRT2 (silent mating type information regulation 2 homolog-2)-Flag-TG (transgenic) ( SIRT2 -TG) mice SIRT2 -knockout, and septin4 -K174Q mutant mice, combined with proteomic and acetyl proteomics analysis, followed by multiple molecular biological methodologies, were used to demonstrate mechanisms of SIRT2-mediated deacetylation of septin4-K174 in hypertensive nephropathy. Results: Using transgenic septin4 -K174Q mutant mice treated with the antioxidant Tempol, we found that hyperacetylation of the K174 site of septin4 exacerbates Ang II (angiotensin II)– induced hypertensive renal injury resulting from oxidative stress. Proteomics and Western blotting assays indicated that septin4-K174Q activates the cleaved-PARP1 (poly [ADP-ribose] polymerase family, member 1)-cleaved-caspase3 pathway. In septin4-knockdown human renal podocytes, septin4-K174R, which mimics deacetylation at K174, rescues podocyte apoptosis induced by Ang II. Immunoprecipitation and mass spectrometry analyses identified SIRT2 as a deacetylase that interacts with the septin4 GTPase domain and deacetylates septin4-K174. In Sirt2 -deficient mice and SIRT2-knockdown renal podocytes, septin4-K174 remains hyperacetylated and exacerbates hypertensive renal injury. By contrast, in Rosa26-Sirt2-Flag (SIRT2-TG) mice and SIRT2-knockdown renal podocytes reexpressing wild-type SIRT2, septin4-K174 is hypoacetylated and mitigates hypertensive renal injury. Conclusions: Septin4, when activated through acetylation of K174 (K174Q), promotes hypertensive renal injury. Septin4-K174R, which mimics deacetylation by SIRT2, inhibits the cleaved-PARP1-cleaved-caspase3 pathway. Septin4-K174R acts as a renal protective factor, mitigating Ang II–induced hypertensive renal injury. These findings indicate that septin4-K174 is a potential therapeutic target for the treatment of hypertensive renal injury.
    Type of Medium: Online Resource
    ISSN: 0009-7330 , 1524-4571
    URL: Article
    DOI: 10.1161/CIRCRESAHA.122.321591
    RVK:
    XA 10000
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2023
    detail.hit.zdb_id: 1467838-X
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  • 3
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    Cardiomyocyte PKA Ablation Enhances Basal Contractility While Eliminates Cardiac β-Adrenergic Response Without Adverse Effects on the Heart
    Ovid Technologies (Wolters Kluwer Health) ; 2019
    In:  Circulation Research Vol. 124, No. 12 ( 2019-06-07), p. 1760-1777
    Details
    In: Circulation Research, Ovid Technologies (Wolters Kluwer Health), Vol. 124, No. 12 ( 2019-06-07), p. 1760-1777
    Abstract: PKA (Protein Kinase A) is a major mediator of β-AR (β-adrenergic) regulation of cardiac function, but other mediators have also been suggested. Reduced PKA basal activity and activation are linked to cardiac diseases. However, how complete loss of PKA activity impacts on cardiac physiology and if it causes cardiac dysfunction have never been determined. Objectives: We set to determine how the heart adapts to the loss of cardiomyocyte PKA activity and if it elicits cardiac abnormalities. Methods and Results: (1) Cardiac PKA activity was almost completely inhibited by expressing a PKA inhibitor peptide in cardiomyocytes (cPKAi) in mice; (2) cPKAi reduced basal phosphorylation of 2 myofilament proteins (TnI [troponin I] and cardiac myosin binding protein C), and one longitudinal SR (sarcoplasmic reticulum) protein (PLB [phospholamban] ) but not of the sarcolemmal proteins (Cav1.2 α1c and PLM [phospholemman]), dyadic protein RyR2, and nuclear protein CREB (cAMP response element binding protein) at their PKA phosphorylation sites; (3) cPKAi increased the expression of CaMKII (Ca 2+ /calmodulin-dependent kinase II), the Cav1.2 β subunits and current, but decreased CaMKII phosphorylation and CaMKII-mediated phosphorylation of PLB and RyR2; (4) These changes resulted in significantly enhanced myofilament Ca 2+ sensitivity, prolonged contraction, slowed relaxation but increased myocyte Ca 2+ transient and contraction amplitudes; (5) Isoproterenol-induced PKA and CaMKII activation and their phosphorylation of proteins were prevented by cPKAi; (6) cPKAi abolished the increases of heart rate, and cardiac and myocyte contractility by a β-AR agonist (isoproterenol), showing an important role of PKA and a minimal role of PKA-independent β-AR signaling in acute cardiac regulation; (7) cPKAi mice have partial exercise capability probably by enhancing vascular constriction and ventricular filling during β-AR stimulation; and (8) cPKAi mice did not show any cardiac functional or structural abnormalities during the 1-year study period. Conclusions: PKA activity suppression induces a unique Ca 2+ handling phenotype, eliminates β-AR regulation of heart rates and cardiac contractility but does not cause cardiac abnormalities.
    Type of Medium: Online Resource
    ISSN: 0009-7330 , 1524-4571
    URL: Article
    DOI: 10.1161/CIRCRESAHA.118.313417
    RVK:
    XA 10000
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2019
    detail.hit.zdb_id: 1467838-X
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  • 4
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    Endothelial Intracellular ANG (Angiogenin) Protects Against Atherosclerosis by Decreasing Endoplasmic Reticulum Stress
    Ovid Technologies (Wolters Kluwer Health) ; 2022
    In:  Arteriosclerosis, Thrombosis, and Vascular Biology Vol. 42, No. 3 ( 2022-03), p. 305-325
    Details
    In: Arteriosclerosis, Thrombosis, and Vascular Biology, Ovid Technologies (Wolters Kluwer Health), Vol. 42, No. 3 ( 2022-03), p. 305-325
    Abstract: ANG (angiogenin) is essential for cellular adaptation to endoplasmic reticulum (ER) stress, a process closely associated with cardiovascular diseases, including atherosclerosis. We aimed to investigate the role of ANG in the progression of atherosclerosis and elucidate its underlying molecular mechanisms. Methods: We constructed adenoassociated virus 9 ANG overexpression vectors and endothelial ANG- and ApoE (apolipoprotein E)-deficient mice to determine the effects of ANG on ER stress and atherosclerotic lesions. RNA sequencing of endothelial ANG- and ApoE-deficient mice identified ANG-dependent downregulation of ST3GAL5 (ST3 beta-galactoside alpha-2,3-sialyltransferase 5) expression, and the direct regulation of ST3GAL5 by ANG was verified by chromatin immunoprecipitation sequencing and luciferase reporter assay results. Results: Reanalysis of expression profiling datasets indicated decreased ANG levels in patients’ atherosclerotic lesions, and these data were validated in aortas from ApoE −/− mice. ER stress marker and adhesion molecule levels, aortic root lesions and macrophage deposition were substantially reduced in ApoE −/− mice injected with an adenoassociated virus 9 ANG without signal peptide (ANG-ΔSP) overexpression vector compared with empty and full-length ANG overexpression vectors. Endothelial ANG deficiency significantly elevated ER stress and increased adhesion molecule expression, which aggravated atherosclerotic lesions and enhanced THP-1 monocyte adhesion to endothelial cells in vivo and in vitro, respectively. Furthermore, ANG-ΔSP overexpression significantly attenuated oxidized low-density lipoprotein-induced ER stress and THP-1 monocyte adhesion to endothelial cells, which were reversed by ST3GAL5 inhibition. Conclusions: These results suggest that endothelial intracellular ANG is a novel therapeutic against atherosclerosis and exerts atheroprotective effects via ST3GAL5-mediated ER stress suppression.
    Type of Medium: Online Resource
    ISSN: 1079-5642 , 1524-4636
    URL: Article
    DOI: 10.1161/ATVBAHA.121.317339
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2022
    detail.hit.zdb_id: 1494427-3
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  • 5
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    Assessment and management of radiation-induced trismus in patients with nasopharyngeal carcinoma: a best practice implementation project
    Ovid Technologies (Wolters Kluwer Health) ; 2022
    In:  JBI Evidence Implementation Vol. 21, No. 3 ( 2022-11-14), p. 208-217
    Details
    In: JBI Evidence Implementation, Ovid Technologies (Wolters Kluwer Health), Vol. 21, No. 3 ( 2022-11-14), p. 208-217
    Abstract: Intensity-modulated radiotherapy (IMRT) is the most commonly used radiotherapy technology in oncology, which enables precise conformation of the radiation dose to the target volume and reduces the risk of radiation damage to the adjacent normal structures. Nevertheless, it is still inevitable for IMRT of head and neck cancer to cause radiation-related toxic and side effects, such as dry mouth, mucositis, oral dysarthria, taste disorder, osteonecrosis, and trismus. Trismus is one of the most common late side effects caused by radiotherapy of nasopharyngeal carcinoma (NPC), which seriously affects the quality of life for patients with NPC. However, the current clinical assessment and management of trismus after radiotherapy for NPC are still imperfect. This best practice implementation project aimed to implement an evidence-based practice in assessing and managing trismus for NPC patients who underwent radiotherapy, thereby improving the compliance of clinical practice with the best evidence and the quality of life of patients with NPC. Methods: This evidence-based audit and feedback project was implemented using a three-phase approach at a third-class hospital in China, following JBI‘s Practical Application of Clinical Evidence System (PACES) and GRiP evidence application. The first phase included a baseline audit with six evidence-based audit criteria derived from the best available evidence. The second phase included analyzing the results of the baseline audit, identifying barriers to compliance with best practice principles, and developing and implementing strategies to address the barriers identified in the baseline audit. The third phase involved a follow-up audit to assess the results of the interventions implemented to improve practice. Results: After evidence application, the compliance rate for audit criterion 1 increased from 0% at baseline audit to 70% at follow-up audit. The compliance rate for audit criterion 2 increased from 0% to 100%. The compliance rate for audit criterion 3 increased from 22 to 62%. The compliance rate for audit criterion 4 increased from 88 to 100%. The compliance rate for audit criterion 5 was 100% at baseline audit and follow-up audit. The compliance rate for audit criterion 6 increased from 0 to 55%. Conclusion: Implementation of the best evidence for the assessment and management of trismus of patients with NPC after radiotherapy is conducive to improving the compliance of clinical practice with the best evidence, standardizing clinical nursing practice, improving the quality of clinical nursing, and better preventing severe trismus in patients with NPC after radiotherapy.
    Type of Medium: Online Resource
    ISSN: 2691-3321
    URL: Article
    DOI: 10.1097/XEB.0000000000000355
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2022
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  • 6
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    Genome-wide association study of personality traits in bipolar patients
    Ovid Technologies (Wolters Kluwer Health) ; 2011
    In:  Psychiatric Genetics Vol. 21, No. 4 ( 2011-08), p. 190-194
    Details
    In: Psychiatric Genetics, Ovid Technologies (Wolters Kluwer Health), Vol. 21, No. 4 ( 2011-08), p. 190-194
    Type of Medium: Online Resource
    ISSN: 0955-8829
    URL: Article
    DOI: 10.1097/YPG.0b013e3283457a31
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2011
    detail.hit.zdb_id: 2063156-X
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  • 7
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    Effectiveness of Apoptotic Factors Expressed on the Wounds of Patients With Stage III Pressure Ulcers
    Ovid Technologies (Wolters Kluwer Health) ; 2012
    In:  Journal of Wound, Ostomy & Continence Nursing Vol. 39, No. 4 ( 2012-07), p. 391-396
    Details
    In: Journal of Wound, Ostomy & Continence Nursing, Ovid Technologies (Wolters Kluwer Health), Vol. 39, No. 4 ( 2012-07), p. 391-396
    Type of Medium: Online Resource
    ISSN: 1071-5754
    URL: Article
    DOI: 10.1097/WON.0b013e318259c47e
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2012
    detail.hit.zdb_id: 2030787-1
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  • 8
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    Gastrin Protects Against Myocardial Ischemia/Reperfusion Injury via Activation of RISK (Reperfusion Injury Salvage Kinase) and SAFE (Survivor Activating Factor Enhancement) Pathways
    Ovid Technologies (Wolters Kluwer Health) ; 2018
    In:  Journal of the American Heart Association Vol. 7, No. 14 ( 2018-07-17)
    Details
    In: Journal of the American Heart Association, Ovid Technologies (Wolters Kluwer Health), Vol. 7, No. 14 ( 2018-07-17)
    Abstract: Ischemia/reperfusion injury (IRI) is one of the most predominant complications of ischemic heart disease. Gastrin has emerged as a regulator of cardiovascular function, playing a key protective role in hypoxia. Serum gastrin levels are increased in patients with myocardial infarction, but the pathophysiogical significance of this finding is unknown. The purpose of this study was to determine whether and how gastrin protects cardiac myocytes from IRI. Methods and Results Adult male Sprague‐Dawley rats were used in the experiments. The hearts in living rats or isolated Langendorff‐perfused rat hearts were subjected to ischemia followed by reperfusion to induce myocardial IRI. Gastrin, alone or with an antagonist, was administered before the induction of myocardial IRI. We found that gastrin improved myocardial function and reduced the expression of myocardial injury markers, infarct size, and cardiomyocyte apoptosis induced by IRI. Gastrin increased the phosphorylation levels of ERK 1/2 (extracellular signal‐regulated kinase 1/2), AKT (protein kinase B), and STAT 3 (signal transducer and activator of transcription 3), indicating its ability to activate the RISK (reperfusion injury salvage kinase) and SAFE (survivor activating factor enhancement) pathways. The presence of inhibitors of ERK 1/2, AKT , or STAT 3 abrogated the gastrin‐mediated protection. The protective effect of gastrin was via CCK2R (cholecystokinin 2 receptor) because the CCK 2R blocker CI 988 prevented the gastrin‐mediated protection of the heart with IRI. Moreover, we found a negative correlation between serum levels of cardiac troponin I and gastrin in patients with unstable angina pectoris undergoing percutaneous coronary intervention, suggesting a protective effect of gastrin in human cardiomyocytes. Conclusions These results indicate that gastrin can reduce myocardial IRI by activation of the RISK and SAFE pathways.
    Type of Medium: Online Resource
    ISSN: 2047-9980
    URL: Article
    DOI: 10.1161/JAHA.116.005171
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2018
    detail.hit.zdb_id: 2653953-6
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  • 9
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    Surgical Implications and Radiologic Classification for the Upward Bulging of the Planum Sphenoidale in Patients With Anterior Skull Base Meningiomas Involving the Tuberculum Sellae Area
    Ovid Technologies (Wolters Kluwer Health) ; 2023
    In:  Journal of Craniofacial Surgery Vol. 34, No. 2 ( 2023-03), p. 467-470
    Details
    In: Journal of Craniofacial Surgery, Ovid Technologies (Wolters Kluwer Health), Vol. 34, No. 2 ( 2023-03), p. 467-470
    Abstract: To investigate the surgical implications and morphologic type of upward bulging of the planum sphenoidale (PS) in anterior skull base meningiomas involving the tuberculum sellae area. Methods: Between January 2014 and June 2021, 96 patients with anterior skull base meningiomas underwent surgery at the Sanbo Brain Hospital of Capital Medical University. A total of 96 patients with nonintracranial space-occupying lesions were selected as the control group. The height of upward bulging of the PS was measured and classified. The authors performed univariate and multivariate analyses to evaluate the rate and effects of upward bulging of the PS. Results: The PS upward bulging rate was 23.00% versus 66.70% ( P 〈 0.001) between the control and meningioma groups. Multiple linear regression showed that it was correlated with the tumor midsagittal anteroposterior length ( P =0.025) and the midsagittal height diameter ( P =0.012). According to the height of PS upward bulging, it was divided into types 1, 2, and 3. The tumor gross-total resection rates were 96.9%, 92.3%, and 76.0%, respectively ( P =0.042). Conclusions: Anterior skull base meningiomas involving the tuberculum sellae area can cause PS upward bulging, which lowers the tumor resection rate and should be considered while determining the treatment approach.
    Type of Medium: Online Resource
    ISSN: 1049-2275
    URL: Article
    DOI: 10.1097/SCS.0000000000008851
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2023
    detail.hit.zdb_id: 2060546-8
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  • 10
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    Pineal region metastasis with intraventricular seeding : A case report and literature review
    Ovid Technologies (Wolters Kluwer Health) ; 2019
    In:  Medicine Vol. 98, No. 34 ( 2019-08), p. e16652-
    Details
    In: Medicine, Ovid Technologies (Wolters Kluwer Health), Vol. 98, No. 34 ( 2019-08), p. e16652-
    Abstract: Tumors of the pineal region are rare, and metastatic carcinoma occurring in the pineal region is extremely rare. No previous reports have described pineal region metastasis with intraventricular seeding. Patient concerns: We report a case of a 51-year-old woman presented with a 1-week history of severe headache, nausea, and vomiting. Imaging examination revealed 2 lesions in the pineal region and the right lateral ventricle. Diagnosis: Pinealocytoma or germinoma was considered as the preoperative diagnosis. The postoperative pathological diagnosis was small cell neuroendocrine carcinoma. After bronchoscopic biopsy, small cell lung cancer was confirmed. Interventions: A right frontal craniotomy and a translateral ventricle approach were performed to remove 2 lesions completely. And regular radiotherapy and chemotherapy were initiated after surgery. Outcomes: The patient was discharged from the hospital 2 weeks after operation and went to another cancer hospital for bronchoscopic biopsy, radiotherapy, and chemotherapy. Finally, the patient died 2 years after surgical treatment. Conclusion: Metastatic tumors of the pineal region are very rare. For patients with pineal lesions, a diagnosis of a metastatic tumor should be considered. Retrograde cerebrospinal fluid circulation might be the reason for a secondary metastasis.
    Type of Medium: Online Resource
    ISSN: 0025-7974 , 1536-5964
    URL: Article
    DOI: 10.1097/MD.0000000000016652
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2019
    detail.hit.zdb_id: 2049818-4
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