The Kevin Kim and Thomas Sisson labs (University of Michigan, Ann Arbor) are investigating the pathogenesis of pulmonary fibrosis which is a devastating disorder with limited medical therapy due to a poor understanding of the mechanisms of disease. We have funding and preliminary data to support studying a novel pathway in which alveolar epithelial cell (AEC2) injury/apoptosis results in a coordinated response in which the elaboration of CCL12 (the primary murine homolog of human CCL2) from injured AECs recruits monocyte-derived macrophages to the alveolar space where they engulf oxidized phospholipid-rich apoptotic AEC2s. In turn, the accumulation of oxidized phospholipid induces a phenotypic switch in the macrophage that is a critical driver of fibrosis. Our labs utilize a comprehensive array of experimental techniques including: 1)in vitro assays employing primary isolated murine cells and primary human cells from normal and diseased lung tissue for detailed biochemical and mechanistic analysis, 2) in vivo studies include several novel transgenic models including mice with AEC specific death (using AEC-promoter specific expression of diphtheria toxin receptor), floxed CCL12 mice enabling cell type-specific deletion, and mice deficient in LPLA2, the primary enzyme involved in degradation of surfactant phospholipid, and 3) in vivo studies with bone marrow chimeric mice, lineage tracing, and assays of fibrosis. This project has very high enthusiasm in the scientific community with a R01 proposal scoring at the 5th percentile in a recent NIH study section. In addition to co-mentorship by Dr. Kim and Dr. Sisson, post-doctoral personnel can expect to work in a highly collaborative environment with several prominent co-investigators. PhD or equivalent in biological sciences, chemistry, or related scientific field is required.
Experience handling mice desired but not required.
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