Brian Su did a stem cell research internship this summer in the laboratory of Thomas Weimbs at University of California, Santa Barbara.
|Brian Su submitted this photo of his lab notebook to our #CIRMStemCellLab Instagram feed.|
I looked for up-regulation of dimeric IgA and pIgR in untreated cystic kidneys of mice and humans. Up-regulation of dimeric IgA and pIgR would suggest increased levels of transcytosis of IgA. My lab, the Weimbs lab at UCSB, had previously found pIgR to be up-regulated in mice. My research found IgA to be also up-regulated in mice. I confirmed this with beta-actin. I also ran western blots with ADPKD human cyst fluid. When probing for IgA, I found a band higher than dimeric IgA in mice, which was likely secretory IgA. When probing for pIgR, I saw the secretory component of pIgR from when pIgR cleaves at the apical surface. Secretory IgA is dimeric IgA with the secretory component of pIgR still bound to the J-chain. My data strongly suggests that the IgA-pIgR interaction exists in human cystic kidney epithelial cells. It also finds that IgA is up-regulated as well as pIgR in mouse cystic kidney epithelial cells.
My research furthered my lab’s goal of learning more about ADPKD in the search for a treatment or cure. It did this by showing the viability of using the IgA-pIgR interaction to distribute a cyst growth inhibiting drug throughout a renal cyst as a possible method of treatment. It also strongly suggested the existence and up-regulation of the IgA-pIgR interaction in cystic kidneys, which has been less studied than IgA-pIgR interactions in mucosal epithelial cells. While learning lab techniques and developing skills this summer, my research has taken steps to help the 12.5 million people world-wide that have the disease ADPKD.