Evon Wang
Program: Unspecified
Current advisor:
Undergraduate university: Tufts University
Research summary
The kidneys are responsible for maintaining the body’s homeostasis by controlling the ins and outs of fluids, electrolytes and metabolic waste. Acute kidney injury is characterized by a sudden loss of kidney function (AKI), where serum creatinine increases and urinary output decreases. The common causes of AKI are ischemia-reperfusion injury (IRI), sepsis and nephrotoxins. While clinical treatments can address the underlying cause and provide supportive care of hemodynamic function and fluid status, there is no definitive treatment for AKI to mitigate injury or accelerate recovery. Previous data in the Lenschow lab have shown that ISG15 acts as a negative regulator of necroptosis and mice lacking ISG15 exhibit increased susceptibility to AKI. Given the known crosstalk between programmed cell death pathways (PCD), loss of ISG15 might also activate apoptosis, pyroptosis or ferroptosis. My rotation project explored what forms of PCD are implicated using immunofluorescence staining on kidney tissue sections harvested from WT mice and ISG15-/- mice. In addition, I am interested in understanding which cell type(s) ISG15 is primarily involved in during AKI. By inducing IRI through hypoxia treatment of isolated mouse proximal tubule cells, the degree of apoptosis can help identify whether the proximal tubule cells are where ISG15 is primarily acting.
Graduate publications