Phone: (706) 721-0698
Fax: (706) 721-7299
Email: wbollag@augusta.edu
Office: CA-1008
Lab: CA-1055
Learn more about Dr. Bollag's Research
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
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
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.
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.
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
Representative Publications
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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). |
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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). |
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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. |
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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 |
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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). |
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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) |
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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). |
| 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 |
Pictured left to right: Dr. Ismail Kaddour-Djebbar, Lawrence Olala, Dr. Wendy Bollag, Dr. Vivek Choudhary,
Dr. Sara Chen (2016)
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)
