A5065270119- Cardiac Fibrosis and Remodeling
- RNA Research and Splicing
- RNA and protein synthesis mechanisms
- Cardiovascular Effects of Exercise
- Pulmonary Hypertension Research and Treatments
- Cardiovascular Disease and Adiposity
- Signaling Pathways in Disease
- Tissue Engineering and Regenerative Medicine
- Peptidase Inhibition and Analysis
- RNA modifications and cancer
- Adipose Tissue and Metabolism
University of Cincinnati Medical Center
2022-2025
The Ohio State University Wexner Medical Center
2024-2025
Abstract The RNA‐binding protein human antigen R (HuR) has been shown to reduce cardiac remodeling following both myocardial infarction and pressure overload, but the full extent of HuR‐dependent mechanisms within cells myocardium yet be elucidated. Wild‐type mice were subjected 30 min ischemia (via LAD occlusion) treated with a novel small molecule inhibitor HuR at time reperfusion, followed by direct in vivo assessment structure function. Direct was done vitro using neonatal rat...
<b>Abstract ID 98908</b> <b>Poster Board 269</b> Our lab has previously published that Human antigen R (HuR) is necessary for myofibroblast (MF) activation of cultured primary cardiac fibroblasts (CFs) and identified <b>Wnt1-inducible signaling pathway protein-1</b> (WISP1; <i>Ccn4</i>) as a downstream HuR target gene. The objective this work was to identify the functional mechanistic role <b>WISP1</b> on initiation resolution MF activity. Wisp1 been shown be involved in several cellular...
<b>Abstract ID 25562</b> <b>Poster Board 305</b> We have previously shown that the RNA binding protein Human antigen R (HuR) directly mediates hypertrophic signaling in cardiac myocytes (CMs), and CM-specific genetic deletion or pharmacological inhibition of HuR reduces pathological remodeling preserves function following transverse aortic constriction (TAC)-induced pressure overload, part through a reduction pro-fibrotic gene expression. More recently, our lab demonstrated expression...
Obesity is a rapidly growing epidemic worldwide, especially in the United States, and associated with cardiovascular disease (CVD), diabetes, cancer, multitude of other comorbidities. Adipose tissue has been shown to act as an endocrine organ body mediate cardiac physiology. We have previously that deletion HuR specifically adipocytes (Adipo-HuR KO) induces fibrosis mice, independent traditional adipose/obesity co-morbidities (dyslipidemia, hypertension, diabetes). Deletion adipocyte...