A5007128842- MicroRNA in disease regulation
- Cardiac Ischemia and Reperfusion
- Heat shock proteins research
- Ion channel regulation and function
- Extracellular vesicles in disease
- Cardiac electrophysiology and arrhythmias
- Cardiomyopathy and Myosin Studies
- Circular RNAs in diseases
- Calpain Protease Function and Regulation
- Cardiac Fibrosis and Remodeling
- Cardiovascular Effects of Exercise
- Endoplasmic Reticulum Stress and Disease
- Mitochondrial Function and Pathology
- Autophagy in Disease and Therapy
- Cell death mechanisms and regulation
- Signaling Pathways in Disease
- Immune cells in cancer
- Sepsis Diagnosis and Treatment
- Cardiovascular Disease and Adiposity
- Cancer-related Molecular Pathways
- Inflammasome and immune disorders
- Inflammation biomarkers and pathways
- Viral Infections and Immunology Research
- Chemotherapy-induced cardiotoxicity and mitigation
- Cardiovascular Function and Risk Factors
West China Hospital of Sichuan University
2025
Sichuan University
2025
University of Cincinnati Medical Center
2015-2024
Inner Mongolia Medical University
2024
University of Cincinnati
2010-2024
Beijing Institute of Technology
2024
Chinese Academy of Medical Sciences & Peking Union Medical College
2010-2024
Xian Yang Central Hospital
2024
Sabin Vaccine Institute
2004-2023
National Clinical Research
2023
The hydrophilic bile salt ursodeoxycholic acid (UDCA) protects against the membrane-damaging effects associated with hydrophobic acids. This study was undertaken to (a) determine if UDCA inhibits apoptosis from deoxycholic (DCA), as well ethanol, TGF-beta1, Fas ligand, and okadaic acid; (b) whether mitochondrial membrane perturbation is modulated by UDCA. DCA induced significant hepatocyte in vivo isolated hepatocytes determined terminal transferase-mediated dUTP-digoxigenin nick...
Background— Recent studies have identified critical roles for microRNAs (miRNAs) in a variety of cellular processes, including regulation cardiomyocyte death. However, the signature miRNA expression and possible ischemic heart been less well studied. Methods Results— We performed arrays to detect pattern miRNAs murine hearts subjected ischemia/reperfusion (I/R) vivo ex vivo. Surprisingly, we found that only miR-320 was significantly decreased on I/R This further confirmed by TaqMan real-time...
In human disease and experimental animal models, depressed Ca2+ handling in failing cardiomyocytes is widely attributed to impaired sarcoplasmic reticulum (SR) function. mice, disruption of the PLN gene encoding phospholamban (PLN) or expression dominant-negative mutants enhances SR cardiac function, but effects mutations humans are unknown. Here, a T116G point mutation, substituting termination codon for Leu-39 (L39stop), was identified two families with hereditary heart failure. The...
The sarcoplasmic reticulum Ca 2+ -cycling proteins are key regulators of cardiac contractility, and alterations in properties have been shown to be causal familial cardiomyopathies. Through genetic screening dilated cardiomyopathy patients, we identified a previously uncharacterized deletion arginine 14 (PLN-R14Del) the coding region phospholamban (PLN) gene large family with hereditary heart failure. No homozygous individuals were identified. By middle age, heterozygous developed left...
MicroRNAs (miRs) participate in many cardiac pathophysiological processes, including ischemia/reperfusion (I/R)-induced injury. Recently, we and others observed that miR-494 was downregulated murine I/R-injured human infarcted hearts. However, the functional consequence of response to I/R remains unknown.We generated a mouse model with cardiac-specific overexpression miR-494. Transgenic hearts wild-type from multiple lines were subjected global no-flow Langendorff system. exhibited improved...
Abstract Mesenchymal stem cells (MSCs) have been shown to elicit cardio-protective effects in sepsis. However, the underlying mechanism remains obscure. While recent studies indicated that miR-223 is highly enriched MSC-derived exosomes, whether exosomal contributes MSC-mediated cardio-protection sepsis unknown. In this study, loss-of-function approach was utilized and induced by cecal ligation puncture (CLP). We observed injection of miR-223-KO MSCs at 1 h post-CLP did not confer protection...
Decreased heat shock protein (Hsp) expression in type 1 and 2 diabetes has been implicated as a primary factor contributing to diabetes-induced organ damage. We recently showed that diabetic cardiomyocytes could release detrimental exosomes, which contain lower levels of Hsp20 than normal ones. To investigate whether such exosomes be modified by raising become protective, we used transgenic (TG) mouse model with cardiac-specific overexpression Hsp20. TG control wild-type (WT) mice were...
Heat-shock proteins (Hsps) have been shown to render cardioprotection from stress-induced injury; however, little is known about the role of another small heat-shock protein, Hsp20, which regulates activities vasodilation and platelet aggregation, in against ischemia injury. We recently reported that increased expression Hsp20 cardiomyocytes was associated with improved contraction protection beta-agonist-induced apoptosis.To investigate whether overexpression exerts protective effects both...
Abstract Although heat-shock preconditioning has been shown to promote cell survival under oxidative stress, the nature of response from different cells is variable and complex. Therefore, it remains unclear whether mesenchymal stem (MSCs) modified with a single protein (Hsp) gene are effective in repair damaged heart. In this study, we genetically engineered rat MSCs Hsp20 (Hsp20-MSCs) examined survival, revascularization, functional improvement left anterior descending ligation (LAD) model...
Doxorubicin (DOX) is a widely used antitumor drug, but its application limited because of cardiotoxic side effects. Heat shock protein (Hsp)20 has been recently shown to protect cardiomyocytes against apoptosis, induced by ischemia/reperfusion injury or prolonged β-agonist stimulation. However, it not clear whether Hsp20 would exert similar protective effects DOX-induced cardiac injury. Actually, DOX treatment was associated with downregulation in the heart. To elucidate role DOX-triggered...
Exosomes, a group of small vesicles (30-100 nm), originate when the inward budding endosomal membrane forms multivesicular bodies (MVBs). Exosomes are released into extracellular space MVBs fuse with plasma membrane. Numerous studies have indicated that exosomes play critical roles in mediating cell-to-cell communication. Also, believed to possess powerful capacity regulating cell survival/death, inflammation and tumor metastasis, depending on particular array molecules contained within...
Although remote ischemic stimuli have been shown to elicit cardioprotection against ischemia/reperfusion injury, there is little known about the effects of nonischemic stimuli. We previously described a cardioprotective effect surgical trauma (abdominal incision) called preconditioning (RPCT). In present study, we elucidate mechanisms underlying this phenomenon.We used murine model myocardial infarction evaluate and either abdominal incision, or application topical capsaicin,...
AimsWhile a wealth of data has uncovered distinct microRNA (miR) expression alterations in hypertrophic and ischaemic/reperfused (I/R) hearts, little is known about miR regulation response to ischaemic preconditioning (IPC).
Interferon regulatory factor 8 (IRF8) is known to affect the innate immune response, for example, by regulating differentiation and function of cells. However, whether IRF8 can influence cardiac hypertrophy unknown. Here we show that levels are decreased in human dilated/hypertrophic cardiomyopathic hearts murine hypertrophic hearts. Mice overexpressing Irf8 specifically heart resistant aortic banding (AB)-induced hypertrophy, whereas mice lacking either globally or cardiomyocytes develop an...
Calpain plays a critical role in cardiomyopathic changes type 1 diabetes (T1D). This study investigated how calpain regulates mitochondrial reactive oxygen species (ROS) generation the development of diabetic cardiomyopathy. T1D was induced transgenic mice overexpressing calpastatin, with cardiomyocyte-specific capn4 deletion, or their wild-type littermates by injection streptozotocin. Calpain-1 protein and activity mitochondria were elevated mouse hearts. The increased calpain-1 associated...