Dr. Abdulsalam Soofi

After moving to the US in 1997, I started my scientific research in aging and DNA repair at Wayne State University. Since 2000, my work at the University of Michigan has focused on the use and development of mouse models for renal disease, obesity, and cancer of the female reproductive tract. I have made significant contributions by generating several cell lines and mouse models to study and understand cell signaling and gene regulation in glomerular disease, fibrosis, and kidney development and diseases. Therapy for acute kidney injury (AKI) remains elusive, underlining the desperate need for the discovery of novel therapeutic approaches to prevent and treat kidney diseases. In this regard, I have previously demonstrated that overexpression of secreted protein KCP in the proximal tubular cells attenuates both acute and chronic renal injury by enhancing BMPs and suppressing TGBβ ligands’ interaction to their correspondent receptors, regulating the TGBβ/BMPs signaling axis. Also, evidence suggests that the process of AKI and subsequent tubular regeneration requires alterations or resetting of the epigenome in proximal tubule cells. To assess this requirement more directly, we utilized a conditional knockout (KO) of the Pax transactivation-domain interacting protein (PTIP) by deleting PTIP in the differentiated cells of proximal tubules. Our data demonstrated that PTIP and associated MLL3/4-mediated histone methylation is necessary for regenerating proximal tubules and maintaining or reestablishing the cellular epithelial phenotype. Also, it is well known that AKI causes upregulation of reactive oxygen species (ROS), thereby leading to the destabilization of heme-containing proteins and the release of toxic free heme, which causes oxidative stress, inflammation, and apoptosis. To better understand the participation of iron free (iron overload) in ROS and heme free groups’ influence on AKI and recovery, we have generated proximal tubular cell-specific ferroportin and hepcidin conditional KO to study their effects on injury-mediated responses and regeneration during AKI following folic acid intraperitoneal injection and renal ischemia reperfusion. 

In previous studies, we made significant breakthroughs in defining the mechanisms of Pax2 protein function in the urogenital system development and disease. In adult female mice both Pax2 and Pax8 genes are expressed in the oviduct and endometrium epithelial cells, but not in ovaries. Previously we generated conditional KO of Pax2 and Pax8 to study their specific deletion in epithelium secretory cells using the OVGP1-Cre tamoxifen inducible. This work holds promise as mouse oviduct secretory cells are the most frequently dividing cells of the oviductal epithelium. While the mechanisms underlying epithelial homoeostasis are still unknown, using a conditional KO mouse model of Pax2 and Pax8 will allow us to identify future therapeutic targets and progress towards the discovery of novel biomarkers for early detection, prevention, and treatments.

In addition to my research training and experience, I have acquired team leadership and administrative skills during 25 years of laboratory management. I am Fulbright US Scholar Award recipient (2021-2022): I developed a medical research project at the University of Sharjah (United Arab Emirates) as part of a project to study the role of disrupted iron metabolism in mouse models. I have supervised and trained nine graduate students and 20 undergraduate research students. I have a broad scientific background, with specific training and expertise in kidney disease research and the development of animal models