Wendy Bollag, PhD, FAHA


Professor of PHYSIOLOGY, VA Research Career Scientist

Dr. Wendy Bollag

Phone: (706) 721-0698
Fax: (706) 721-7299
EmailWBOLLAG@augusta.edu
Office: CA-1008
Lab: CA-1055

 

 

 Learn more about Dr. Bollag's Research


Education and Training

Pennsylvania State University, University Park, PA, BS in Biochemistry, 1984

Yale University, New Haven, CT, MPhil (1987) and PhD in Cellular and Molecular Physiology, 1990  

Hoffmann-La Roche, Inc., Nutley, NJ, post-doctoral fellowship in Pre-Clinical Dermatologic Research, 1991


Academic Appointments

2009-present  Professor, Department of Physiology and College of Graduate Studies, Augusta University, Augusta, GA

2011-present  Adjunct Professor, Department of Oral Biology (Dental College of Georgia), Augusta University, Augusta, GA

2011-present  VA Research Career Scientist, Charlie Norwood VA Medical Center

2009-present  Adjunct Professor, Departments of Cellular Biology and Anatomy, Medicine (Dermatology) and Orthopaedic Surgery, Augusta University, Augusta, GA

2004-2009  Professor, Department of Medicine, Medical College of Georgia, Augusta, GA

1999-2004  Associate Professor, Department of Medicine, Medical College of Georgia, Augusta, GA

1993-1999  Assistant Professor, Department of Medicine, Medical College of Georgia, Augusta, GA

1992-1993  Assistant Professor, Department  of Biology, Seton Hall University, South Orange, NJ


Research Interests

My research interests lie in understanding the mechanisms by which hormones, growth factors, cytokines and other signaling molecules instruct cells to respond appropriately to perform their functions. My laboratory currently has one project investigating the regulation of keratinocyte growth and differentiation and a second defining the signaling mechanisms regulating aldosterone secretion from the adrenal gland. In the first project in skin, we are defining the role of the signaling enzymes phospholipase D (PLD) in promoting epidermal keratinocyte differentiation and protein kinase D (PKD) in supporting keratinocyte proliferation and survival. Our data suggest that PLD promotes keratinocyte differentiation and inhibits proliferation whereas PKD acts in an opposite fashion. By regulating these processes PLD and PKD may play a role in the development of skin diseases. Our second project investigates the mechanism by which very low-density lipoprotein (VLDL), the levels of which are elevated in obesity, stimulates the production of aldosterone. As a key hormone involved in sodium homeostasis, aldosterone is an important regulator of blood pressure, and abnormalities in its levels can contribute to various cardiovascular pathologies including hypertension. Since obesity is often associated with high blood pressure, our research may provide one mechanism by which excess weight contributes to hypertension.


Current Projects

In keratinocytes we have obtained data to suggest that PLD, in combination with the glycerol channel aquaporin-3, functions to produce the novel lipid signaling molecule, phosphatidylglycerol, which is involved in regulating early keratinocyte differentiation. By defining the function of this novel PLD-generated lipid signaling system in early keratinocyte differentiation, our research may identify new targets for therapeutic intervention in these skin diseases including non-melanoma skin cancers. In addition, our data indicate that PKD promotes proliferation and/or survival of epidermal keratinocytes. Furthermore, our studies suggest that PKD levels are increased in human basal cell carcinomas. The primary risk factor for the development of basal cell carcinoma is excessive exposure to the ultraviolet radiation of the sun, and we have recently demonstrated that ultraviolet light activates PKD. In addition, overexpression of PKD protects keratinocytes from ultraviolet exposure-induced apoptosis. Thus, we hypothesize that PKD plays a major role in epidermal tumorigenesis, with our results providing a link between PKD, sun exposure and tumorigenesis. Finally, we are also currently investigating the mechanism(s) by which VLDL increases aldosterone production, including possible roles of PLD and PKD, as well as its interaction with other aldosterone agonists such as angiotensin II. 


Awards and Accomplishments

2011-2016  VA Research Career Scientist Award

2014-2015  Completed the Augusta University Executive Leadership Excellence course

2008-2015  Outstanding Performance Award, Charlie Norwood VA Medical Center

2013            Distinguished Teaching Award, Augusta University, The Graduate School

2012            Distinguished Faculty Award, Basic Research, Augusta University, Medical College of Georgia

2012            Selected to attend the Association of American Medical Colleges Mid-Career Women Faculty, Professional Development Seminar in Austin, TX

2011            Nomination and selection as a Fellow of the American Heart Association

2010            Distinguished Research Award, Medical College of Georgia, College of Graduate Studies

2009            Distinguished Service Award, Medical College of Georgia, College of Graduate Studies

Representative Publications

(Go to Pub Med)

Bollag WB.  Role of phospholipases in adrenal steroidogenesis. J Endocrinol. 2016 Feb 15. pii: JOE-16-0007.

Bollag WB.  Lipid Signaling in Keratinocytes: Lipin-1 plays a PArt. J Lipid Res. 2016 Feb 6. pii: jlr.C067074.  

Arun SN, Xie D, Zhong Q, Howard AC, McNeil PL, Bollag WB. Phospholipase D activation by cell wounding and role in membrane repair. J. Lipid Res., 54: 581-591, 2013.

 Olala L, Seremwe M, Tsai Y-Y, Bollag WB. A role for phospholipase D in angiotensin II-induced protein kinase D activation in adrenal glomerulosa cells. Mol. Cell. Endocrinol., 66: 31-37, 2013.

Xing Y, Rainey WE, Apolzan JW, Francone OL, Harris RBS, Bollag WB. Adrenal cell aldosterone production is stimulated by very low density lipoprotein (VLDL). Endocrinology, 153: 721-731, 2012.

Voss K, Bollag RJ, Fussell N, By C, Sheehan DJ, Bollag WB. Abnormal aquaporin-3 protein expression in hyperproliferative skin disorders. Arch. Dermatol. Res., 303: 591-600, 2011.

Arun SN, Kaddour-Djebbar I, Shapiro BA, Bollag WB. UVB-induced activation of protein kinase D protects mouse keratinocytes from apoptosis. Oncogene, 30: 1586-1596, 2011.

 DR. BOLLAG'S FACULTY PROFILE

Dr. Bollag on PubMed

LAB PERSONNEL

Sara Chen, MD
Research Assistant and Laboratory Manager

Vivek Choudhary, DVM, PhD
Assistant Research Scientist

Purnima Merai, MS
Part-time Research Assistant

Rawipan "Amy" Uaratanawong, PhD
Visiting Faculty

Dr. Bollag Lab (2016)Pictured left to right: Dr. Ismail Kaddour-Djebbar,  Lawrence Olala, Dr. Wendy Bollag, Dr. Vivek Choudhary, Dr. Sara Chen (2016)

 

Dr. Bollag Lab (2013)

Pictured left to right: Back Row:  Dr. Ismail Kaddour-Djebbar, Dr. Vivek Choudhary, Inas Helwa, Lawrence Olala; Front Row:  Ying-Ying Tsai, Dr. Wendy Bollag, Purnima Merai, Dr. Sara Chen (2013)