A5049967178- Cardiac Fibrosis and Remodeling
- Cardiac Ischemia and Reperfusion
- Tissue Engineering and Regenerative Medicine
- Mesenchymal stem cell research
- Receptor Mechanisms and Signaling
- Congenital heart defects research
- Heme Oxygenase-1 and Carbon Monoxide
- Signaling Pathways in Disease
- Cardiac Structural Anomalies and Repair
- Pharmacological Effects and Assays
- Nitric Oxide and Endothelin Effects
- Adipose Tissue and Metabolism
- Electrospun Nanofibers in Biomedical Applications
- Cardiac Arrest and Resuscitation
- Eicosanoids and Hypertension Pharmacology
- Chemokine receptors and signaling
- Viral Infections and Immunology Research
- Neuropeptides and Animal Physiology
- Neutrophil, Myeloperoxidase and Oxidative Mechanisms
- Cell Adhesion Molecules Research
- Mitochondrial Function and Pathology
- Cardiovascular Function and Risk Factors
- High Altitude and Hypoxia
- Cancer, Hypoxia, and Metabolism
- Anesthesia and Neurotoxicity Research
University of Missouri–St. Louis
2024
Washington University in St. Louis
2022-2024
University of Alabama at Birmingham
2015-2024
Oshkosh (United States)
2023
University of Louisville
2008-2019
Comprehensive Cardiovascular
2017-2019
Wenzhou Medical University
2017
Chengdu Medical College
2017
First Hospital of Jilin University
2017
Jilin University
2017
Administration of cardiac progenitor cells (CPCs) 4 hours after reperfusion ameliorates left ventricular function in rats with acute myocardial infarction (MI). Clinically, however, this approach is not feasible, because expansion autologous CPCs MI requires several weeks. Therefore, we sought to determine whether are beneficial the more clinically relevant setting an old (scar).One month coronary occlusion/reperfusion, received intracoronary infusion vehicle or enhanced green fluorescent...
Stromal cell-derived factor-1alpha (SDF-1alpha) binding to its cognate receptor, CXCR4, regulates a variety of cellular functions such as stem cell homing, trafficking, and differentiation. However, the role SDF-1alpha-CXCR4 axis in modulating myocardial ischemia/reperfusion injury is unknown.In mice subjected ischemic preconditioning, SDF-1alpha mRNA was found be increased 3 hours later (P<0.05). Myocardial CXCR4 protein were expressed both cardiac myocytes fibroblasts. production...
Inappropriately sustained inflammation is a hallmark of chronic ischemic heart failure (HF); however, the pathophysiological role T lymphocytes unclear.Permanent coronary ligation was performed in adult C57BL/6 mice. When compared with sham-operated mice, mice HF (8 weeks after ligation) exhibited following features: (1) significant (P<0.05) expansion circulating CD3+CD8+ cytotoxic and CD3+CD4+ helper (Th) lymphocytes, together increased Th1, Th2, Th17, regulatory T-cell (Treg) CD4+ subsets;...
Heart failure (HF) is a state of inappropriately sustained inflammation, suggesting the loss normal immunosuppressive mechanisms. Regulatory T-lymphocytes (Tregs) are considered key suppressors immune responses; however, their role in HF unknown. We hypothesized that Tregs dysfunctional ischemic cardiomyopathy and HF, they promote activation left ventricular (LV) remodeling.Adult male wild-type C57BL/6 mice, Foxp3-diphtheria toxin receptor transgenic tumor necrosis factor (TNF) α receptor-1...
Although chronic inflammation is a central feature of heart failure (HF), the immune cell profiles differ with different underlying causes. This suggests that for immunomodulatory therapy in HF to be successful, it needs tailored specific etiology. Here, authors demonstrate monocyte-derived C-C chemokine receptor 2 (CCR2)+ macrophages infiltrate early during pressure overload mice, and blocking this response either pharmacologically or antibody-mediated CCR2+ monocyte depletion alleviates...
Background— Heme oxygenase-1 (HO-1) is an inducible stress-response protein that imparts antioxidant and antiapoptotic effects. However, its pathophysiological role in cardiac remodeling chronic heart failure (HF) unknown. We hypothesized induction of HO-1 HF alleviates pathological remodeling. Methods Results— Adult male nontransgenic myocyte-restricted transgenic mice underwent either sham operation or coronary ligation to induce HF. Four weeks after ligation, exhibited postinfarction left...
α1-adrenergic receptors (ARs) play a major role in blood pressure regulation. The three α1-AR subtypes (A/C, B, and D) stimulate contraction of isolated arteries, but it is uncertain how different contribute to regulation the intact animal. We studied α1A/C subtype by using gene knockout. knockout (KO) mice were viable overtly normal. LacZ reporter replaced coding sequence KO, β-galactosidase staining was present resistance arteries arterioles, not thoracic aorta or its main branches. By...
Catecholamines and α1-adrenergic receptors (α1-ARs) cause cardiac hypertrophy in cultured myocytes transgenic mice, but heart size is normal single KOs of the main α1-AR subtypes, α1A/C α1B. Here we tested whether α1-ARs are required for developmental by generating α1B double KO (ABKO) which had no binding. In male ABKO growth after weaning was 40% less than WT, smaller due to myocytes. Body other organ weights were unchanged, indicating a specific effect on heart. Blood pressure mice same...
Cardiac progenitor cells (CPCs) improve left ventricular remodeling and function after acute or chronic myocardial infarction. However, the long-term (>5 weeks) effects, potential tumorigenicity, fate of transplanted CPCs are unknown.To assess outcome CPC therapy at 1 year.Female rats underwent a 90-minute coronary occlusion; 4 hours reperfusion, they received intracoronarily vehicle million male, syngeneic CPCs. One year later, CPC-treated exhibited smaller scars more viable myocardium in...
Rationale: Endothelial progenitor cells (EPCs) respond to stromal cell–derived factor 1 (SDF-1) through chemokine receptors CXCR7 and CXCR4. Whether SDF-1 involves in diabetes mellitus–induced EPCs dysfunction remains unknown. Objective: To determine the role of diabetic dysfunction. Methods Results: expression, but not CXCR4 was reduced from db/db mice, which coincided with impaired tube formation. Knockdown formation normal whereas upregulation rescued angiogenic function mice. In treated...
Persistent immune activation contributes significantly to left ventricular (LV) dysfunction and adverse remodeling in heart failure (HF). In contrast their well-known essential role acute myocardial infarction (MI) as first responders that clear dead cells facilitate subsequent reparative macrophage polarization, the of neutrophils pathobiology chronic ischemic HF is poorly defined. To determine importance progression cardiomyopathy, we measured production, levels, a mouse model 8 weeks...
The three cloned α1-adrenergic receptor (AR) subtypes, α1B, α1C, and α1D, can all couple to the same effector, phospholipase C, reason(s) for conservation of multiple subtypes remain uncertain. All α1-ARs are expressed natively in cultured neonatal rat cardiac myocytes, where chronic exposure agonist catecholamine norepinephrine (NE) induces hypertrophic growth gene transcription. We show here, using RNase protection, that α1-AR subtype mRNAs respond distinctly different ways during...
Catecholamines and α1-adrenergic receptors (α1-ARs) cause cardiac hypertrophy in cultured myocytes transgenic mice, but heart size is normal single KOs of the main α1-AR subtypes, α1A/C α1B. Here we tested whether α1-ARs are required for developmental by generating α1B double KO (ABKO) which had no binding. In male ABKO growth after weaning was 40% less than WT, smaller due to myocytes. Body other organ weights were unchanged, indicating a specific effect on heart. Blood pressure mice same...
Although Janus kinase (JAK)-mediated Tyr phosphorylation of signal transducers and activators transcription (STAT) 1 3 is essential for the upregulation cyclooxygenase-2 (COX-2) cardioprotection late preconditioning (PC), role Ser STAT1 STAT3 in PC upstream signaling mechanisms responsible mediating remain unknown.In mice preconditioned with six 4-minute coronary occlusion/4-minute reperfusion cycles, we found that (1) ischemic activates Raf1-mitogen-activated protein (MAPK)/extracellular...
Inducible nitric oxide synthase (iNOS) is an obligatory mediator of the late phase ischemic preconditioning, but mechanisms its cardioprotective actions are unknown. In addition, it remains unclear whether sustained elevation iNOS in myocytes provides chronic protection against ischemia/reperfusion injury.Constitutive overexpression transgenic mice (alpha-myosin heavy chain promoter) did not induce contractile dysfunction and affect mitochondrial respiration or biogenesis, profoundly...
Abstract —Cultured neonatal rat cardiac myocytes have been used extensively to study cellular and molecular mechanisms of hypertrophy. However, there are only a few studies in cultured mouse despite the increasing use genetically engineered models Therefore, we characterized hypertrophic responses low-density, serum-free cultures compared them with myocytes. In myocyte cultures, triiodothyronine (T3), norepinephrine (NE) through β-adrenergic receptor, leukemia inhibitory factor induced...
alpha 1-Adrenergic receptor (AR) activation in cardiac muscle has several different physiological effects that might be mediated through 1-AR subtypes. Two subtypes have been cloned from the rat, 1B and 1D; both are present adult rat heart. A third subtype, 1C, cow human, was reported to absent rat. However, we recently found 1C mRNA heart by using a partial cDNA. Thus, all three heart, but it is unknown whether each expressed myocytes or fibroblasts. In study, full-length 1C-AR cultured...
The role of endothelial nitric oxide synthase (eNOS) in ischemic preconditioning (PC) and cardioprotection is poorly understood. We addressed this issue using a genetic, rather than pharmacological, approach.In the nonpreconditioned state, eNOS-/- mice exhibited infarct sizes similar to those wild-type mice. A sequence six 4-minute coronary occlusion/4-minute reperfusion cycles (ischemic PC) induced late PC mice; genetic deletion eNOS abrogated by PC. In mice, membranous translocation...