A5083383869- Cardiac Fibrosis and Remodeling
- Signaling Pathways in Disease
- Blood properties and coagulation
- Tissue Engineering and Regenerative Medicine
- Peptidase Inhibition and Analysis
- Electrospun Nanofibers in Biomedical Applications
- TGF-β signaling in diseases
- Cardiac Valve Diseases and Treatments
- Cardiovascular Function and Risk Factors
- Ion Channels and Receptors
- Cell Adhesion Molecules Research
- Cardiac Structural Anomalies and Repair
- Cellular Mechanics and Interactions
- GDF15 and Related Biomarkers
- Phytochemicals and Antioxidant Activities
- Galectins and Cancer Biology
- Congenital heart defects research
- Antimicrobial Resistance in Staphylococcus
- NF-κB Signaling Pathways
- Adipokines, Inflammation, and Metabolic Diseases
- Macrophage Migration Inhibitory Factor
- Protease and Inhibitor Mechanisms
- Streptococcal Infections and Treatments
- Monoclonal and Polyclonal Antibodies Research
- Neurobiology and Insect Physiology Research
Indiana University – Purdue University Indianapolis
2024
Indiana University School of Medicine
2024
Albert Einstein College of Medicine
2013-2022
Baylor College of Medicine
2013-2015
Duke University
2015
Albany Medical Center Hospital
2012-2014
University at Albany, State University of New York
2013
Johannes Kepler University of Linz
2013
Albany State University
2013
Eastern Virginia Medical School
2013
Transforming growth factor-βs regulate a wide range of cellular responses by activating Smad-dependent and Smad-independent cascades. In the infarcted heart, Smad3 signaling is activated in both cardiomyocytes interstitial cells. We hypothesized that cell-specific actions repair remodeling myocardium.To dissect myocardial infarction, we generated mice with loss fibroblasts or cardiomyocytes. Cardiac function was assessed after reperfused nonreperfused infarction using echocardiography. The...
Diabetes mellitus is associated with cardiac fibrosis. Matricellular proteins are induced in fibrotic conditions and modulate fibrogenic angiogenic responses by regulating growth factor signaling.Our aim was to test the hypothesis that prototypical matricellular protein thrombospondin (TSP)-1, a potent angiostatic molecule crucial activator of transforming factor-β, may play key role remodeling diabetic heart.Obese db/db mice exhibited marked myocardial TSP-1 upregulation interstitial...
The heart contains abundant interstitial and perivascular fibroblasts. Traditional views suggest that, under conditions of mechanical stress, cytokines, growth factors, neurohumoral mediators stimulate fibroblast activation, inducing ECM (extracellular matrix) protein synthesis promoting fibrosis diastolic dysfunction. Members the TGF (transforming factor)-β family are upregulated activated in remodeling myocardium modulate phenotype function all myocardial cell types through activation...
Through largely unknown mechanisms, Ca(2+) signaling plays important roles in vascular smooth muscle cell (VSMC) remodeling. Orai1-encoded store-operated entry has recently emerged as an player VSMC However, the role of exclusively mammalian Orai3 protein native pathways, its upregulation during remodeling, and contribution to neointima formation remain unknown.The goal this study was determine agonist-evoked pathway contributed by Orai3; potential after balloon injury rat carotid...
Background— Heart failure in diabetics is associated with cardiac hypertrophy, fibrosis and diastolic dysfunction. Activation of transforming growth factor-β/Smad3 signaling the diabetic myocardium may mediate heart failure, while preserving matrix homeostasis. We hypothesized that Smad3 play a key role pathogenesis cardiovascular remodeling diabetes mellitus obesity. Methods Results— generated leptin-resistant db/db null mice Smad3+/− animals. haploinsufficiency did not affect metabolic...
Repair of the infarcted heart requires TGF-β/Smad3 signaling in cardiac myofibroblasts. However, TGF-β–driven myofibroblast activation needs to be tightly regulated order prevent excessive fibrosis and adverse remodeling that may precipitate failure. We hypothesized induction inhibitory Smad, Smad7, restrain infarct activation, we examined molecular mechanisms Smad7 actions. In a mouse model nonreperfused infarction, Smad3 triggered synthesis α-SMA+ myofibroblasts, but not α-SMA–PDGFRα+...
The calcium sensor STIM1 disrupts the endothelial barrier by coupling thrombin receptor to actin cytoskeleton.
BACKGROUND: Cardiac fibroblast activation contributes to adverse remodeling, fibrosis, and dysfunction in the pressure-overloaded heart. Although early TGF-β (transforming growth factor-β)/Smad (small mother against decapentaplegic)-3 protects heart by preserving matrix, sustained is deleterious, accentuating fibrosis dysfunction. Thus, endogenous mechanisms that negatively regulate response fibroblasts may be required protect from progressive remodeling. We hypothesized Smad7, an inhibitory...
Tissue transglutaminase (tTG) is induced in injured and remodelling tissues, modulates cellular phenotype, while contributing to matrix cross-linking. Our study tested the hypothesis that tTG may be expressed pressure-overloaded myocardium, regulate cardiac function, myocardial fibrosis chamber remodelling.In order test hypothesis, wild-type null mice were subjected pressure overload through transverse aortic constriction. Moreover, we used isolated fibroblasts macrophages dissect mechanisms...
Wounds are known to serve as portals of entry for group A Streptococcus (GAS). Subsequent tissue colonization is mediated by interactions between GAS surface proteins and host extracellular matrix components. We recently reported that the streptococcal collagen-like protein-1, Scl1, selectively binds cellular form fibronectin (cFn) also contributes biofilm formation on abiotic surfaces. One structural feature cFn, which predominantly expressed in response injury, presence a spliced variant...
In patients with myocardial infarction (MI), cardiac rupture is an uncommon but catastrophic complication. the mouse model of nonreperfused MI, reported rates are highly variable and depend not only on genetic background sex animals also method used for documentation rupture. most studies, diagnosis based visual inspection during autopsy; however, criteria poorly defined. We performed systematic histopathological analysis whole hearts from C57BL/6J mice dying after MI evaluated reliability...
Transglutaminase 2 (TG2) expression is increased in infarcted and remodeling hearts modulates cellular responses through enzymatic effects non-enzymatic actions. In monocytic cells, TG2 predominantly expressed by M2 macrophages both mice humans. Although considered a preserved reliable marker of macrophages, its role regulation macrophage phenotype remains unknown. order to study the function homeostasis disease, we generated with myeloid cell-specific loss (MyTG2KO), examined their response...