Wong, Letitia - Date Last Updated: 09/21/2011

Letitia Wong - Email
PhD Candidate - Started Fall 2008
Hometown: Bartlett, IL
Wade Bushman, MD, PhD

Undergraduate Work
2008 - Bachelors in Pharmacology & Toxicology from UW-Madison

Interests
Cats

Why I Joined METC
Toxicology is a science of two sides: studying the adverse effect of the agents and then seeking for prevention and treatment through certain amount of effort. There are several reasons why I want to join the METC program. My PharmTox undergrad major has given me a strong interest in biological interaction of different chemicals and drugs. I spent most of my undergrad years in the pharmacology classes until taking toxicology courses in my senior year. The courses gave me a better understanding that science does not only focus on the favorable side but also concerns with the unfavorable aspect and thereby seeking for prevention. The concept I learned from the courses induces me striving for further knowledge in toxicology.

Funding/Awards

2011 AUA Foundation/NIDDK/SBUR Basic Science Symposium: “Stem Cells and Urologic Diseases” Young Investigator Travel Award
2011 AUA Foundation/SBUR Summer Research Conference “Aging and Urologic Diseases” Young Investigator Travel Award
09/2011 - 08/2012 - Herman Shapiro fellowship from the UW-Madison School of Medicine and Public Health
09/01/10 - 08/31/11 - National Institute of Environmental Health (NIEHS) Pre- and Post-Doctoral Training Grant

Research
Benign prostatic hyperplasia (BPH) is one of the leading health concerns among aging men in the United States. BPH is characterized by benign enlargement of the prostate gland from progressive hyperplasia of stromal and epithelial cells. Men diagnosed with BPH suffer from lower urinary tract symptoms that significantly reduce the quality of life. Because of its high prevalence in aging men, BPH has increasingly become a subject of interest for research scientists to study the mechanism of the pathogenesis of BPH.

Inflammation is a common feature in the aged adult prostate and is considered to be a major contributor to the development and progression of BPH. Previous studies have shown that the etiology of prostatic inflammation may be attributable to environmental factors such as infectious agents and dietary contaminants. A study of human BPH specimens obtained from 80 patients undergoing surgical treatment has found evidence of inflammation in all cases and 44% showed bacterial infection. In fact, transurethral instillation of uropathogenic E. coli results in prostatic inflammation in a mouse model. In addition, prostate tissues from animals that have ingested environmental contaminants such as heterocyclic amines and plasticizer phthalates displayed inflammation and reactive hyperplasia. These studies strongly demonstrate the relationship between environmental factors, prostatic inflammation and BPH; however, the mechanism of this disease is not well understood.

The presence of extracellular matrix within the stroma regulates normal prostate growth by providing structural support for the cells and regulating molecular signaling. Changes of extracellular matrix content can alter prostate function and predispose for prostate diseases. Previous studies have revealed that an increase in stromal connective tissues is one of the major changes in BPH. In fact, a retrospective study on connective tissues of prostate samples showed a significant increase in the number and thickness of collagen fibers within the stroma in BPH. In addition, the clinical lower urinary tract symptoms observed in BPH may in part be explained by the effect of increased collagen content in the prostate. Thus, these findings suggest that further investigation into the regulation of prostate collagen deposition is essential in understanding the development and progression of BPH.

Given the close association between inflammation and BPH, the molecular mechanism underpinning the changes in collagen in prostatic inflammation may correspond to that in BPH. In fact, collagen deposition and remodeling as a process of scar formation is a primary response of tissue repair to inflammation following injury. We have previously shown that interleukin-1 (IL-1) signaling is activated in the inflamed prostate and is required to induce reactive hyperplastic response to bacterial-induced inflammation in mouse prostate. Furthermore, IL-1 signaling has been demonstrated to induce collagen deposition in the skin, lung, and cartilagesom. Hence, this further leads us to speculate the role of IL-1 signaling in collagen deposition in prostatic inflammation. This study is considerably critical in understanding the mechanistic basis leading to BPH and providing insights into new therapeutic treatments for BPH patients.

Publications

Wong, L., Bushamn, W. Comment on basal epithelial stem cells as efficient targets for prostate cancer initiation. Stem Cell Res Ther. 2010 Jun 8;1(2):16

Zhu, L., Wong, L., Yu, L. Surface-Enhanced Crystallization of Amorphous Nifedipine. Molecular Pharmaceutics. 2008

Graduate Seminars Given

03/22/12
Effect of inflammation on collagen deposition in the Prostate

03/10 2011
Using Microfluidic Device to Study the
Role of Stromal Microenvironment in Prostate Progenitor Cell
Proliferation

03/18/10
The use of a simple microchannel device to study the role of stromal microenvironment, androgen and paracrine Hh signaling in prostatic epithelial progenitor cell proliferation

Date Last Updated: 09/21/2011 webteam@med.wisc.edu