Diane L. Rosin
Primary AppointmentAssistant Professor of Research, Pharmacology
- PhD, Virginia Commonwealth University
Central catecholamine dysfunction
I am interested in understanding immune mechanisms involved in acute and chronic kidney injury and the mechanisms that may underlie the progression of acute to chronic kidney disease. The availability of a large array of transgenic mice contributes important tools for teasing out these mechanisms. We use a variety of in vivo and in vitro models along with molecular, cell biological and immunological methods to study kidney injury and to guide development of novel pharmacological and cell based therapy approaches for modulating pathways that contribute to kidney injury. Some of our current work focuses on using ligands of adenosine 2A receptors and sphingosine 1 receptors to protect kidneys from insults that produce acute and chronic kidney injury. In addition we are exploring nanoparticle-mediated targeted delivery of drugs to kidney as a novel and possibly more selective treatment modality.
Some of the models that we use include:
1) Kidney ischemia-reperfusion injury as a model of acute kidney injury
2) Folic acid or aristolochic acid-induced kidney fibrosis. Interstitial fibrosis is one of the hallmarks of chronic kidney disease
3) Ischemia-reperfusion injury-induced fibrosis in mice maintained for longer time periods as a model of progression from acute to chronic kidney injury.
4) Hypoxia- or LPS-induced injury in cultured renal tubular epithelial cells, glomerular endothelial cells, and primary cultures of kidney fibroblasts.