Dr. Stachelek is interested in the cellular and molecular mechanisms that control vasculature inflammation. Both acute and chronic inflammation contribute to a range of cardiovascular conditions such as atherosclerosis, ischemia-reperfusion injury, and in-stent restentosis, and addressing this represents an unmet need in medical research. At present, he is interested in the family of protein receptors that contain the Immunoreceptor Tyrosine-based Inhibitory Motif (ITIM) that function to limit or terminate an immune response.
Dr. Stachelek's current research on the topic focuses on the anti-inflammatory properties of the transmembrane protein CD47 and its ITIM expressing receptor Signal Regulatory Protein alpha (SIRPa). Dr. Stachelek's research program utilizes a variety of techniques and principles from bioengineering and cell/molecular biology to expand upon the body of knowledge related to SIRPa-CD47 signaling, with a particular focus on exploiting this immune inhibitory pathway to address the pathophysiology associated with cardiovascular devices. At present, his laboratory has received research funding from the National Institutes of Health to examine the anti-inflammatory properties of immobilized CD47 as a viable strategy to treat in-stent restenosis.
- The Stachelek Lab has shown that recombinant CD47, or its relevant peptide sequences, immobilized on a range of clinically relevant biomaterials significantly reduce monocyte activation and the release of pro-inflammatory cytokines.
- Working with an animal model, the lab demonstrated that CD47 immobilized on bare metal stents were able to resist thrombosis and restenotic related events up to four weeks.
- The lab demonstrated SIRPa expression in platelets and that platelet activation is also significantly reduced in blood exposed to CD47 modified surfaces.
- The lab demonstrated that CD47 plays a role in the attachment of endothelial precursor cells to cholesterol modified polymeric surfaces used for prosthetic heart valve leaflets.