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

2009-present: Adjunct Professor, Departments of Cellular Biology and Anatomy,

                         Medicine (Dermatology) and Orthopaedic Surgery, Augusta University, Augusta, GA

2011-2016:  VA Research Career Scientist, Charlie Norwood VA Medical Center

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 particular PLD2, 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 skin diseases including non-melanoma skin cancers and psoriasis. One mechanism by which phosphatidylglycerol appears to function is through an ability to inhibit toll-like receptor activation by microbial products (pathogen-associated molecular patterns) and endogenous molecules such as anti-microbial peptides acting as danger- or damage-associated molecular patterns. These anti-microbial peptides are up-regulated in psoriasis, and we recently showed that phosphatidylglycerol can improve skin lesions in a mouse model of psoriasis. A similar aquaporin 3/PLD2/phosphatidylglycerol signaling pathway seems to play a role in corneal epithelial wound healing. 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

2019 Augusta University Research Institute Distinguished Researcher Award 

2018 Medical College of Georgia Exemplary Teaching Award

2018 Medical College of Georgia Institutional Service Award

2017 Medical College of Georgia Exemplary Teaching Award

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

(Go to Pub Med)

Choudhary V, S Griffith, X Chen & WB Bollag. Pathogen-associated molecular pattern-induced TLR2 and TLR4 activation increases keratinocyte production of inflammatory mediators and is inhibited by phosphatidylglycerol, Mol. Pharmacol., 97: 324-335, 2020 (e-published ahead of print March 15, 2020).

Yang R, S Chowdhury, V Choudhary, X Chen & WB Bollag. Aquaporin-3 expression induced by histone deacetylase inhibitors is mediated in part by peroxisome proliferator activated receptors (PPARs) in keratinocytes, Exp. Dermatol., 29: 380-386, 2020 (e-published ahead of print January 30, 2020).

Bollag WB, LO Olala, D Xie, X Lu, H Qin, V Choudhary, R Patel, D Bogorad, A Estes & MA Watsky. Dioleoylphosphatidylglycerol accelerates corneal epithelial wound healing. Invest. Ophthalmol. Vis. Sci., 61: 29, 2020.

Choudhary V*, R Uarantanawong*, R Patel, H Patel, W Bao, B Hartney, E Cohen, X Chen, Q Zhong, CM Isales & WB Bollag. Phosphatidylglycerol inhibits toll-like receptor-mediated inflammation by damage-associated molecular patterns. J. Invest. Dermatol., 139: 868-877, 2019 (e-published ahead of print October 31, 2018).

*contributed equally to this work

Tsai Y-Y, WE Rainey, MH Johnson & WB Bollag. VLDL-activated cell signaling pathways that stimulate adrenal cell aldosterone production, Mol. Cell. Endocrinol., 433: 138-146, 2016 (e-published ahead of print, May 21, 2016).

Bollag WB, L Aitkens, J White & KA Hyndman. Aquaporin-3 in the epidermis: More than skin deep. Am. J. Physiol. Cell Physiol., 318: C1144-c1153, 2020 (e-published ahead of print April 8, 2020). (Invited review)

Tsai Y-Y, WE Rainey & WB Bollag. Very low-density lipoprotein (VLDL)-induced signals mediating aldosterone production. J. Endocrinol. 232: R115-R129, 2017 (e-published ahead of print December 2, 2016).

 




Related Links

Dr. Bollag's Faculty Profile

Dr. Bollag on PubMed

LAB PERSONNEL

Sara Chen, MD
Research Manager
Vivek Choudhary, DVM, PhD
Assistant Research Scientist
Shinjini Spaulding
Graduate Student
Yonghong Luo
Graduate Student
Sam Melnyk
Graduate Student
Purnima Merai, MS
Part-time Research Assistant
Ismail Kaddour-Djebbar
Postdoctoral Fellow
 

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)