Karsten Peppel, PhD
Philadelphia, PA 19107
(215) 503-5731 fax
Ph.D. SUNY Albany, NY; Molecular Biology 1990
Associate Professor (2006)
Research & Clinical Interests
The current research in my lab seeks to further our understanding of the role of inflammation in vascular pathology. Specifically, we focus on:
The contributions of the two Tumor Necrosis Factor (TNF) receptors, TNFR1 and TNFR2, to vascular remodeling following injury.
The role of signal transduction cascades downstream of the TNF receptors that regulate growth, survival or apoptosis of cells that participate in the vascular repair response.
The potential efficacy of TNF-inhibitory molecules in attenuating pathophysiological vascular remodeling.
Cross-talk between cytokine and growth factor receptors.
My lab employs different in vivo models of vascular injury as well as in vitro culture of primary cells derived from mice with specific gene deletions to achieve these objectives.
In vivo we study the arterialization of murine inferior vena cava segments surgically grafted into the carotid circulation of recipient mice - a process that mimics venous remodeling following coronary artery bypass grafting in patients.
In vitro we focus on proliferation, migration and activation of regulatory factors and protein kinase cascades downstream of receptor activation.
Most Recent Peer-Reviewed Publications
- Tumor necrosis factor receptor-2 signaling attenuates vein graft neointima formation by promoting endothelial recovery
- Expression of tumor necrosis factor receptor-1 in arterial wall cells promotes atherosclerosis
- Activation of vascular smooth muscle cells by TNF and PDGF: Overlapping and complementary signal transduction mechanisms
- Vein graft neointimal hyperplasia is exacerbated by tumor necrosis factor receptor-1 signaling in graft-intrinsic cells
- Graft-Extrinsic Cells Predominate in Vein Graft Arterialization
- Phosphorylation of the platelet-derived growth factor receptor-β and epidermal growth factor receptor by G protein-coupled receptor kinase-2. Mechanisms for selectivity of desensitization
- Overexpression of G protein-coupled receptor kinase-2 in smooth muscle cells reduces neointimal hyperplasia
- Overexpression of G protein - Coupled receptor kinase-2 in smooth muscle cells attenuates mitogenic signaling via G protein - Coupled and platelet-derived growth factor receptors
- G protein-coupled receptor kinase 3 (GRK3) gene disruption leads to loss of odorant receptor desensitization
- A Tumor Necrosis Factor (TNF) receptor-IgG heavy chain chimeric protein as a bivalent antagonist of TNF activity