Graduate Student - Ding Lab
B.A. in Biology and English Literature
I grew up in Olathe, Kansas and graduated from William Jewell College with a Bachelor of Arts in Biology and English Literature. After receiving my bachelor's degree, I worked at IBT Laboratories for five years where I developed immunology and allergy tests for study subjects enrolled in clinical trials for new drugs and vaccines. My work at IBT made me realize my passion for research and inspired me to pursue my graduate degree.
Under the guidance of my mentor Dr. Wen-Xing Ding, I am studying the role of Parkin-induced mitophagy in protection against liver injury using acetaminophen and ethanol mouse models. We found that autophagy is protective in acetaminophen-induced liver injury by removing damaged mitochondria. In addition, we found that autophagy is protective against alcohol-induced liver injury and steatosis by removing damaged mitochondria and lipid droplets. However, the mechanism for removal of these mitochondria and lipid droplets is unknown. Autophagy is an evolutionarily conserved process that results in degradation of cellular proteins and organelles due to a cell's "self-eating". Autophagy is a protective process that can be either selective or non-selective. Non-selective autophagy occurs during starvation to break down the cell's components in order to provide a source of energy and nutrients. Selective autophagy occurs in nutrient-rich or poor conditions as a protective mechanism by ridding the cell of protein aggregates and damaged organelles. Mitophagy is a selective form of autophagy specific for damaged mitochondria, and Parkin has been shown to be required for mitophagy induction in vitro. However, the role of Parkin for mitophagy induction in vivo in the liver is unknown. Parkin is an E3 ligase that is recruited to damaged mitochondria to initiate ubiquitination of mitochondrial outer membrane proteins and subsequent mitochondrial degradation by mitophagy. Parkin is mainly known for its protective role in the brain because loss of Parkin has been linked to autosomal recessive Parkinsonism. We recently found that Parkin is also expressed in liver. This led us to hypothesize that Parkin may protect against acetaminophen and ethanol-induced liver injury by removing damaged mitochondria.
1. Ni H., Williams JA., Jaeschke H., Ding WX.: Zonated Induction of Autophagy and Mitochondrial Spheroids to Limit Acetaminophen-induced Necrosis in the Liver. Redox Biology. In press.
2. Williams JA., Hou Y., Ni HM., Ding WX.: Role of Intracellular Calcium in Proteasome Inhibitor-induced Endoplasmic Reticulum Stress, Autophagy and Cell Death. Pharmaceutical Research. 30(9):2279-89, 2013.
3. Li G., Kong B., Zhu Y., Zhan L., Williams, JA., Tawfik O., Kassel KM., Luyendyk JP., Guo GL.: Small Heterodimer Partner Overexpression Partially Protects Against Liver Tumor Development in Farnesoid X Receptor knockout mice. Toxicol. Appl. Pharmacol. Epub June 26, 2013.
4. Manley S., Williams JA., Ding WX.: Role of p62/SQSTM1 in Liver Physiology and Pathogenesis. Experimental Biology and Medicine. 238(5):525-38, 2013.
5. Yang, H., Williams, J.A, Hou, Y., Xia, M., Shi, Y., Fan, .J. and Ding, W.X. Autophagy and Drug Discovery. 2013. Honggang Wang, Ed. Autophagy and Cancer (Springer Science).
6. Ni HM., Williams JA., Yang H., Shi YH., Fan J., Ding WX.: Targeting Autophagy for the Treatment of Liver Diseases. Pharmacological Research. 66 (6): 463-74, 2012.
7. Williams JA., Thomas AM., Li G., Kong B., Zhan L., Inaba Y., Xie W., Ding WX., Guo GL.: Tissue Specific Induction of p62/Sqstm1 by Farnesoid X Receptor. PLoS One. 7(8): e43961, 2012.
8. Li G., Thomas AM., Williams JA., Kong B., Liu J., Inaba Y., Xie W., Guo GL.: Farnesoid X Receptor Induces Murine Scavenger Receptor Class B Type 1 via Intron Binding. PLoS One. 7 (4):e35895, 2012.
Graduate Student - Ding Lab
4007 HLSIC; MS 1018
3901 Rainbow Blvd.
Kansas City, Kansas 66160
F: (913) 588-7501