Nancy R. Webb, Ph.D. | Saha Cardiovascular Research Center

Nancy R. Webb, Ph.D.

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nrwebb1@uky.edu
(859) 218-1385
(859) 218-1386 (lab)
Inflammation and Lipo
535 C.T. Wethington Bldg, 900 S Limestone St, Lexington, KY 40536-0200
NRWebb CV January 2017.pdf
Imflammation and Lipoprotein Metabolism Research Group

Position(s):

Director for Nutritional Sciences Graduate Program

Professor

Graduate Faculty in Nutritional Sciences

Cardiovascular Research Center

Affiliation(s):

Pharmacology & Nutritional Sciences

Cardiovascular Research Center

Other Affiliation(s):

CVRC - Core Faculty

Inflammation and Lipoprotein Metabolism Research Group

Nutritional Sciences Graduate Faculty

Pharmacology and Nutritional Sciences Primary Faculty

Director for Nutritional Sciences Graduate Program

Interests / Specialties:

Cardiovascular

Obesity & Diabetes

Bio / Education:

University of Virginia, Charlottesville, VA	B.A.	1981	Biology
University of Kentucky, Lexington, KY	Ph.D.	1999	Molecular Biology

Research Description:

Research in the Webb laboratory focuses on mechanisms of cardiovascular disease, including atherosclerosis and abdominal aortic aneurysms. It has been recognized for decades that high levels of HDL in the blood reduce an individual's risk for heart attack and stroke, yet it is not well understood why HDL (the "good cholesterol") is cardioprotective. The Webb laboratory studies what regulates HDL levels in the blood, how HDL functions to reduce cardiovascular risk, and how inflammation, obesity, and diabetes alter the ability of HDL to function. Research projects integrate biochemical, cellular, and physiological analyses of HDLs obtained from transgenic mouse models as well as human subjects. Another area of research in the Webb laboratory focuses on a family of lipolytic enzymes, the secretory phospholipase A2’s (sPLA2), and their role in physiological and pathophysiological processes. The underlying hypothesis of the studies is that lipid products generated by sPLA2’s serve as bioactive mediators that have pleiotropic effects on fat, vascular, and immune cells.

Selected Publications:

1. Webb, N.R., Connell, P.M., Graf, G.A., Smart, E.J., de Williers, W.J.S., de Beer, F.C., and van der Westhuyzen, D.R. (1998) SR-BII, an isoform of the scavenger receptor BI containing an alternate cytoplasmic tail, mediates lipid transfer between high density lipoprotein and cells. J. Biol. Chem. 273:15241-15248.
2. Webb, N.R., Cai, L., Ziemba, K.S., Yu, J., Kindy, M.S., van der Westhuyzen, D.R., and de Beer, F.C. (2002) The fate of HDL particles in vivo after SR-BI mediated selective lipid uptake. J. Lipid Res. 43: 1890-1898.
3. Boyanovsky, B.B., van der Westhuyzen, D.R., Webb, N.R. (2005) Group V sPLA2-modified LDL promotes foam cell formation by a SR-A and CD36 independent process that involves cellular proteoglycans. J. Biol. Chem. 280:32746-52.
4. Bostrom, M.A., Boyanovsky, B.B., Jordan, C.T., Wadsworth, M.P., Taatjes, D.J., de Beer, F.C., and Webb, N.R. (2007) Group V secretory phospholipase A2 promotes atherosclerosis: Evidence from genetically altered mice. Arterioscler. Thromb. Vasc. Biol. 27:600-6.
5. Li, X., Shridas, P., Forrest, K., Baily, W., and Webb, N.R. (2010) Group X secretory phospholipase A2 negatively regulates adipogenesis in murine models. FASEB J. 24:4313-24. PMCID: PMC2974424
6. Boyanovsky, B. B., Bailey, W., Dixon, L., Shridas, P., and Webb, N.R. (2012) Group V secretory phospholipase A2 enhances the progression of angiotensin II-induced abdominal aortic aneurysms but confers protection against angiotensin II-induced cardiac fibrosis in apoE-deficient mice. Am. J. Pathol. 181:1088-98. PMCID: PMC3432434
7. De Beer, M.C., Wroblewski, J.M., Noffsinger, V.P., Rateri, D.L., Howatt, D.A., Balakrishnan, A., Ji, A., Shridas, P., Thompson, J., van der Westhuyzen, D.R., Tannock, L.R., Daugherty, A., Webb, N.R, de Beer F.C. (2014) Deficiency of endogenous acute phase serum amyloid A does not impact atherosclerotic lesions in apoE-/- mice. Arterioscler. Thromb. Vasc. Biol. 34: 255-261. PMCID: PMC3951741

PubMed Publications:

Thompson, J.C.;Wilson, P.G.;Shridas, P.;Ji, A.;Beer, M.;Beer, F.C.;Webb, N.R.;Tannock, L.R. "Serum amyloid A3 is pro-atherogenic." Atherosclerosis 268, (2018): 32-35. [PubMed Link] | [ Full text ]
Tannock, L.R.;De Beer, M.C.;Ji, A.;Shridas, P.;Noffsinger, V.P.;Hartigh, L.;Chait, A.;Beer, F.C.;Webb, N.R. "Serum amyloid A3 is a high density lipoprotein-associated acute-phase protein." Journal of lipid research 59, 2 (2018): 339-347. [PubMed Link] | [ Full text ]
Shridas, P.;Noffsinger, V.P.;Trumbauer, A.C.;Webb, N.R. "The dual role of group V secretory phospholipase A<sub>2</sub> in pancreatic β-cells." Endocrine 58, 1 (2017): 47-58. [PubMed Link] | [ Full text ]
Kim, M.H.;De Beer, M.C.;Wroblewski, J.M.;Charnigo, R.J.;Ji, A.;Webb, N.R.;Beer, F.C.;Westhuyzen, D.R. "Impact of individual acute phase serum amyloid A isoforms on HDL metabolism in mice." Journal of lipid research 57, 6 (2016): 969-79. [PubMed Link] | [ Full text ]
Rosenson, R.S.;Brewer HB, J.;Ansell, B.J.;Barter, P.;Chapman, M.J.;Heinecke, J.W.;Kontush, A.;Tall, A.R.;Webb, N.R. "Dysfunctional HDL and atherosclerotic cardiovascular disease." Nature reviews. Cardiology 13, 1 (2016): 48-60. [PubMed Link] | [ Full text ]