Hemochromatosis Drives Multi-Organ Failure in Response to Hyperyersiniabactin-Producing Yersinia Pseudotuberculosis

Abstract:

As a part of the PURPOSE program at the RCCB department of Albany Medical Center, I worked under Dr. Zhang’s Lab. Our lab focus is in kidney fibrosis, currently working on the LCN2-> HDAC2-> Et1-> Fibrosis pathway. We conducted experiments concerning hemochromatic mice infected with siderophillic bacteria. To determine fibrosis, we looked for the presence of fibrotic markers using these methods: Mason’s Trichome, Immuno-Fluorescence, RT-PCR, and Western Blot. Using the same methods, we looked for the presence of the pathway. Two conclusions can be made: First, hemochromatic mice infected with Yersinia pseudotuberculosis undergo multiorgan failure which can be observed through kidney and liver fibrosis and function reduction. Secondly, the LCN2->HDAC2->ET1 pathway is upregulated in hemochromatic and infected mice.

Title

Hemochromatosis Drives Multi-Organ Failure in Response to Hyperyersiniabactin-Producing Yersinia Pseudotuberculosis

Faculty Advisor

Dr. Wenzheng Zhang

Course

Summer Research

Presentation Type

Location

Table 12