Current Research Projects

Single-cell RNA Sequencing of Latent Murine Cytomegalovirus Infected Lung and Kidney Transplants

• One of the major complications in transplantation is the reactivation and dissemination of cytomegalovirus (CMV). CMV is a ubiquitous beta-herpesvirus that establishes lifelong latency in the host in immunosufficient hosts but reactivates in immune-compromised patients, e.g. transplant recipients, causing significant morbidities and mortalities. There are a number of contributing factors that lead to CMV reactivation and disease in transplant patients, notably, seropositive donors and seronegative recipients, the type of organ transplanted, and immunosuppression (IS) of the recipient.
• We have previously shown that MCMV reactivation from transplant of a latently infected kidney (D+) into a naïve recipient (R-) is triggered by initial ischemia and reperfusion injury experienced during the transplant surgery and combined with IS facilitates dissemination to other organs. While these studies helped illuminate the conditional requirements for MCMV reactivation and dissemination, the specific cell types and pathways responsible remained elusive.
• Single-cell RNA sequencing has become a powerful tool for investigating the global gene regulation of thousands of individual cells from tissue. The purpose of this study is to analyze the transcriptomics of mouse lung and kidney cells with latent infection of cytomegalovirus (CMV) following transplantation and identify key cell types and molecular pathways responsible for CMV reactivation.

Targeting TGFb1 in UUO Model for Kidney Fibrosis

Transforming growth factor-β (TGF-β) is generally considered as a central mediator of fibrotic diseases, such as obstructive kidney diseases and acute kidney injury and chronic allograft rejection. TGF-β1 may be an ideal target for the treatment of kidney fibrotic diseases.  The mouse Unilateral Ureteral Obstruction (UUO) model is characterized by renal tubular dilation, interstitial expansion, loss of proximal tubular mass, hypertrophy, hydronephrosis, infiltration of leukocytes, tubular epithelial cell death and presence of fibroblasts, which altogether lead to progressive renal tubulointerstitial fibrosis associated with TGFb1.