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Pharmacology and Toxicology Faculty

NAME: Stephanie W. Watts

Educational Background

1983-88 B.S., Advanced Chemistry, The University of Illinois

1988-92 Ph.D., Pharmacology & Toxicology, Indiana University

1992-95 Postdoctoral Fellow, Physiology, The University of Michigan

1995-00 Assistant Professor, Pharmacology & Toxicology, Michigan State

University

2000-05 Associate Professor, Pharmacology & Toxicology, Michigan State

University

2005-present Professor, Pharmacology & Toxicology, Michigan State University

2008-present Assistant Dean, The Graduate School, Michigan State University





CONTACT INFO Email: wattss@msu.edu Lab: B445 Life Sciences Ph: 517-353-3724 Fax: 517-353-8915



BIOGRAPHY AND CURRENT RESEARCH

Research Synopsis:



Click to enlarge lab

Welcome! Our laboratory focuses on vascular smooth muscle pharmacology, physiology and

function. Our reasons for focusing on the vasculature are many, but include the important fact that the

vasculature is involved in numerous cardiovascular diseases. For example, hypertension affects

approximately 20-30% of the world‟s population, and hypertension continues to be a killer because it

places individuals at a higher risk for heart disease, stroke and kidney failure. Our laboratory is dedicated towards

understanding the mechanisms by which the vasculature contributes to this and other diseases. We have a history of

investigating „non-classical‟ pathways or signal transduction mechanisms for smooth muscle contraction. For example, 5-

hydroxytryptamine or 5-HT has long been disputed as having the ability to alter blood vessel tone in vivo; we take the

stance that it can and does so in very different ways than classically envisioned. . At the present, our laboratory has two

on-going established scientific projects, and we have just initiated a third that spreads our wings as a group dedicated to

understanding smooth muscle function. A final fourth area investigates vascular mechanisms of the peptide hormone

endothelin (ET).



1) Role of 5-HT (serotonin, 5-hydroxytryptamine) and the 5-HT transporter in control of normal arterial tone and blood

pressure; upregulation and altered function of 5-HT receptors in hypertension; determination of whether a local 5-HT

generating system exists in peripheral smooth muscle.



2) Serotonylation/amidation of proteins to send a biological signal (e.g. internal functions of 5-HT and norepinephrine)



3) Pharmacology of uterine and cervical smooth muscle.



We use a multi-faceted technical and integrated approach towards studying these diseases so as to understand the

mechanism from a molecular to a whole animal level. My goal for a student is that they have, in their hands, a set of

integrative techniques when they leave the lab such that they can explore pharmacological studies in a thoughtful,

interrogative manner. Techniques in our lab include: isolated tissue bath system to measure smooth muscle contraction,

myograph to measure small artery contraction, Western analyses and protein work, real time RT-PCR, Super Arrays,

pathway mapping based on gene arrays, HPLC, immunohistochemistry, immunocytochemistry, cell culture, kinase

assays, animal surgery, blood pressure measurement and, of course, pharmacology!



We are fortunate that our laboratory works closely with a number of other laboratories in the department, and our students

benefit tremendously for the collegial and exciting exchanges and progress made by our laboratories, collectively.



Current Projects (and the questions we want to answer):



1. Function of intracellular 5-HT and primary amines (how does 5-HT modify proteins?)

2. Alteration of 5-HT receptor subtype(s) in high pressure (do different subtypes upregulate?)



3. Mechanism of blood pressure fall to 5-HT in chronic infusion (how does this occur?)



4. Endothelin (ET) signaling in arteries and veins: heterodimerization of ETA and ETB receptor (do these two

receptors „talk‟ to one another and how does this change their pharmacology?)



5. Role of calcium in ET-induced vasoconstriction (are different calcium sources used in an artery vs a vein?)



6. Pharmacology of isolated uterine and cervical smooth muscle (is the profile of relaxants/contractants similar?

Different? How do these tissues work together)



SELECTED AWARDS AND ACHIEVEMENTS

Selected Achievements:



Editorial Boards

 American Journal of Physiology: Heart, Lung and Circulatory

 American Journal of Physiology: Regulatory, Integrative and Comparative

 Clinical and Experimental Pharmacology and Physiology

 Clinical Science, Associate Editor

 Current Reviews of Hypertension

 Frontiers in Vascular Physiology, Associate Editor

 Hypertension

 Journal of Pharmacology and Experimental Therapeutics, Associate Editor (thru 2009)

 Molecular and Cellular Pharmacology (charter member, 2008)



Honors/Awards

 PhRMA Faculty Development Award, 1998-2000

 PhRMA Research Starter Award, 1998-2000

 Young Scholar Award, American Society of Hypertension, 2001

 Established Investigator of the American Heart Association, 2002

 Howard Hughes Medical Investigator Nominee, Michigan State University, 2004

 Bowditch Awardee of American Physiological Society, 2008 (Outstanding Research under age of 42)



COMMITTEES AND ACTIVITIES:

Committees/Service:

 Member, Pharmaceutical Research and Manufacturers Association Foundation (PhRMA) Basic Pharmacology

Research Advisory Board, 2001-present

 Pharmacology Study Section, NIH 2002-2004

 Charter Member of Hypertension and Microbiology Study Section, NIH, NHLBI October 2004, 2004-2008

 American Physiological Society, CV Section Nominating Committee, 2004-2007

 ASPET Centennial Celebration Planning Committee, 2004-2008

 Chair, ASPET Graduate Recruitment and Education Committee, 2005-2007

 Vice-Chair, Hypertension Summer School, Maritime Academy in Maine, 2005

 Chair, Hypertension 2007 Summer School (Ft. Collins, CO)

 Chair, Trainee Advocacy committee, CHBPR , 2005-2007

 Leadership of Council for High Blood Pressure research, 2005-2007, 2009.

• Chair of Keystone Conference “Dissecting the Vasculature”, held Feb 2009, Vancouver.

• Chair, NIH ZRG CVS-F (90S), AED.

• NIH RIBT Study Section (00201468), AHA SURF Peer Review Chair, NIH ZRG1 VH-D (58)R

Scientific review groups (2009); NIH RFA and F fellowship review committees (2010).

• AHA National Research Committee (2009)

• ASPET Cardiovascular Division Chair Elect (2011)



PUBLICATIONS AND ABSTRACTS (last 5 years)

•Thakali, K., Davenport, L., Fink, G. D. and Watts, S. W.: Pleiotropic effects of hydrogen peroxide in arteries and veins

from normotensive and deoxycorticosterone acetate-salt hypertensive rats, Hypertension, 47:482-487, 2006.



•Ni, W. and Watts, S. W.: 5-HT in the cardiovascular system: focus on the serotonin transporter (SERT), Clin. Exp.

Pharmacol. Physiol, 33:575-583, 2006.



•Thakali K. M., Lau, Y., Fink, G. D., Galligan, J. J., Chen, A. F. and Watts, S. W.: Mechanisms of hypertension

induced by nitric oxide (NO) deficiency: focus on venous function, J. Cardiovasc Pharmacol., 47:742-740, 2006.



•Ni, W., Lookingland, K. and Watts, S. W.: Arterial 5-HT transporter function is impaired in DOCA-salt hypertensive

but not spontaneously hypertensive rats, Hypertension, 48:134-140, 2006.



•Ogden, K., Thompson, J. M., Hickner, Z., Huang, T., Tang D. D. and Watts, S. W.: A new signaling paradigm for

serotonin: Use of Crk-Associated substrate in arterial contraction, Am. J. Physiology Heart Circ Phys, 291:H2857-

H2863, 2006.



•Ni, W.,Lookingland, L. and Watts, S. W.: Response to “Blood pressure in mutant rats lacking the 5-

hydroxytryptamine (5-HT) transporter, Hypertension, ePrint, Oct 2006.



•Szasz, T., Thakali, K., Fink, G. D. and Watts, S. W.: A comparison of arteries and veins in oxidative stress:

producers, destroyers, function and disease, Soc. Exp. Biol. Med, 232:27-37, 2007.



•Thakali, K., Davenport, L., Fink, G. D. and Watts, S. W.: Cyclooxygenase, p38 MAPK, Erk MAPK, Rho Kinase and

Src mediate hydrogen peroxide induced contraction of rat thoracic aorta and vena cava, J. Pharmacol. Exp. Ther.,

320:236-243, 2007.



•Rondelli, C. , Kayal, A., Szasz, T., Thakali, K., Watson, R. E., Rovner, A. S., Eddinger, T. J., Fink G. D. and Watts, S.

W. Preferential myosin heavy chain isoform B expression may contribute to the faster velocity of contraction in veins

vs arteries. J Vasc Res, 44:264-272, 2007.



• Watts, S. W., Rondelli, C., Thakali, K., Pervaiz, M., Watson, R. and Fink, G. D.: Morphologic and Biochemical

characterization of remodeling in aorta and vena cava of DOCA-salt hypertensive rats, Am. J. Physiology Heart Circ,

292:H2438-2448, 2007.



•Ni, W, Fink, G. D. and Watts, S. W.: The 5-HT2A receptor is involved in (+) norfenfluramine-induced arterial conraction

and blood pressure increase in DOCA-salt hypertension, J. Pharmacol. Exp. Ther. 321:485-491, 2007.



•Fink, G. D., Li, M., Lau, Y., Osborne, J. and Watts, S. W.: Chronic activation of endothelin ETB receptors: A new

model of experimental hypertension, Hypertension, 50:512-518, 2007.



•Linder, A. E., Ni, W., Diaz, J. L., Szasz, T., Burnett, R. and Watts, S. W.: 5-HT in veins: not all in vain, invited

Perspectives in Pharmacology J. Pharmacol. Exp. Ther., 323:415-421, 2007.



•Linder, A.E., Thakali, K., Thompson, J., Watts, S. W., Webb, R. C. and Leite, R.: Methyl-b-cyclodextrin prevents

angiotensin II-induced tachyphylactic contractile responses in rat aorta, J Pharmacol Exp Ther., 323:78-84, 2007.



•Ogden, K. K., Falck, J. R. and Watts, S. W.: The cytochrome P450 inhibitor ketoconazole potentiates 5-

hydroxytryptamine-induced contraction in rat aorta, J. Pharmacol. Exp. Ther., 323:606-613, 2007.



• Watts, S. W., Thakali, K., Rondelli, C and Fink, G. D.: Processing of big ET-1 into vasoactive peptides: comparison

of arteries and veins, Vascular Pharmacology, 47:302-312, 2007.



•Huang J, Lin SC, Nadershahi A, Watts SW, Sarkar R.Role of redox signaling and poly (adenosine

diphosphate-ribose) polymerase activation in vascular smooth muscle cell growth inhibition by nitric oxide and

peroxynitrite., J Vasc Surg. 47(3):599-607, 2008.

•Linder, A. E., Diaz, J., Ni, W., Szasz, T., Burnett, R. and Watts, S. W.: Vascular reactivity, 5-HT uptake and

blood pressure in the serotonin transporter knockout rat, Am J Physiol Heart Circ Physiol, 294:H1745-H1752,

2008.



•Thakali, K., Galligan, J. J., Fink, G. D., Gariepy, C. E. and Watts, S. W.: Pharmacological endothelin receptor

interaction occurs in veins but not arteries, Vascular Pharmacology, 49:6-13, 2008.



•Ni, W, Geddes, T. J., Priestly, J. R. C., Szasz, T., Kuhn, D. M. and Watts, S. W.: The existence of a local

serotonergic system in peripheral arteries, Br J Pharmacol, 154:663-674, 2008.



• Diaz, J., Ni, W., King, A., Fink, G. D. and Watts, S. W.: 5-hydroxytryptamine lowers blood pressure in

normotensive and hypertensive rats. J Pharmacol Exp Ther, 325:1031-1038, 2008.



•Linder, A. E., Ni, W., Szasz, T., Burnett, R., Diaz, J., Geddes, T. J., Kuhn, D. M. and Watts, S.W.: A

serotonergic system in veins: serotonin-transporter independent uptake, J. Pharmacol. Exp. Ther., 325:714-

722, 2008.



•Ni, W., Zhou, H., Diaz, J., Murphy, D. L., Haywood, J. R. and Watts, S. W.: Lack of the serotonin transporter does

not prevent mineralocorticoid hypertension in rat and mouse, Eur. J Pharmacol, 589:225-227, 2008.



•Szasz, T., Thompson, J. M. and Watts, S. W.: A comparison of reactive oxygen species metabolism in aorta

and vena cava of the normal rat: focus on xanthine oxidase, Am J Physiol Heart Circ Physiol 295:H1341-

H1350, 2008.



•Watts, S. W.: The beginning of a fantastic, unanswered question: is 5-HT involved in systemic hypertension,

Am J Physiol Heart Circ Physiology, 295:H915-H916, 2008.



•Li, M., Dai, X., Watts, S.W., Kreulen, D. and Fink, G. D.: Increased superoxide levels in ganglia and

sympathoexcitation are involved in S6c-induced hypertension. Am J Physiol Reg Integr Comp Physiol, 295:R1546-

R1554, 2008.



•Watts, S. W.: The love of a lifetime: 5-HT in the cardiovascular system, Am J Physiol Reg Integr Comp

Physiol, 296:R252-R256, 2009. PMID 18753260



•Szasz, T., Eddy, S., Paulauskis, J., Burnett, R., Ellekilde, M., Iovanna, J. L. and Watts, S. W.: Arterial vs venous

expression of genes: differences in inflammatory genes, J Vasc Res, 46:551-560, 2009.



•Linder, A. E., Beggs, K., Burnett, R. and Watts, S. W.: Body distribution of infused serotonin in rats, Clin.

Exp Pharmacol. Physiol, 36:599-601, 2009.



•Tykocki, N.R., Gariepy. C.E. and Watts, S. W.: ETB receptors in arteries and veins: multiple actions in veins, J.

Pharmacol. Exp. Ther., 329:875-881, 2009.



•Watts, S. W., Priestley J.R. C. and Thompson, J. M.: Serotonylation of vascular protein important to contraction,

PLoS One, May 25, e5682, 2009.



•Watts SW: Endothelin receptors: what do we know and what do we need to know? Am J Physiol Regul Integr Comp

Physiol, 298:R254-R260, 2010.



•Seymour E. M., Watts, S. W.: Whole grape intake impacts cardiac PPAR and NFkB activity, fibrosis and

cytokine expression in rats with diastolic heart failure, Hypertension, 55:1179-1185, 2010.



•Szasz, T. and Watts, S. W.: Uric acid does not impact endothelial function of aorta from normotensive and DOCA-sal

hypertensive rats, J. Pharmacol. Exp. Ther., 333: 758-763, 2010.

•Linder, A. E., Gaskell, G. L., Szasz, T., Thompson, J. M. and Watts, S. W.: Serotonin receptors in the rat jugular vein:

presence and involvement in contraction, J. Pharmacol. Exp. Ther., 334:116-123, 2010.



•Tykocki, N. and Watts, S. W.: Calcium and ET, Clin Sci, 119:361-372, 2010.



•Szasz, T, Linder AE, Davis RP, Burnett, R., Fink, G. D. and Watts, S. W.: Allopurinol does not decrease blood

pressure or prevent the development of hypertension in the DOCA-salt model, submitted, J Cardiovasc Pharmacol,

56:627-634, 2010.



•Johnson, K. B., Thompson, J. M., and Watts, S. W.: Modification of proteins by norepinephrine is important for

vascular contraction, Frontiers in Vascular Physiology, Front. Physio. 1:131. doi: 10.3389/fphys.2010.00131



•Northcott, C., Watts, S. W., Chen, Y., Morris, M., Chen, A. F., and Haywood, J. R.: Small hairpin RNA adenoviral

inhibition of AT1A receptors in the paraventricular nucleus inhibits acute increases in mean arterial blood pressure in

the rat. Am J Physiol Regul Integr Comp Physiol. Nov;299(5):R1202-1211, 2010.



•Invited Review: Watts SW and Davis P: 5-Hydroxtryptamine Receptors in Systemic Hypertension: an arterial focus,

Cardiovascular Therapeutics, 29:54-67, 2011.



•Ren W, Watts, S. W., Fanburg, B. L.: The serotonin transporter interacts with the PDGF (beta) receptor in PDGF-BB

induced signaling and mitogenesis in pulmonary artery smooth muscle cells. Am J Physiol. Lung Cell Mol Physiol,

300:L486-497, 2011.



•Davis, R., Linder A. E. and Watts, S W: Lack of the serotonin transporter (SERT) reduces the ability of 5-

hydroxytryptamine to lower blood pressure, Naunyn Schmied. Arch. Pharmacol, 383:543-546, 2011.



•Linder, A, Davis, R., Burnett, R. and Watts, S. W.: The serotonin transporter mediates vascular uptake of and

reactivity to serotonin in vessels from female rats, Clin. Exper. Pharmacol. Physiol., 38:314-322, 2011.



•Harrison, B., Watts, S.W. , Barrett, J. E., Coupet, J., Mazandarani, H., Nawoschik, S., Pangalos, M. N.,

Ramamoorthy, S., Schechter, L., Smith, D. L., Stack, G., Zhang, J., Zhange, G., Rosenzweig-Lipson, S. and Dunlop,

J.: Characterization of Vabicaserin (SCA-136), a functionally selective 5-HT2C receptor agonist, J. Pharmacol. Exp.

Ther., 337:673-680, 2011.



•Bush, C. J., Szasz, T., Johnson, K. B., Tykocki, N. R., Surewicz, W. K., Watson, R. E. and Watts, S. W.: Prior protein

is expressed in the vascular system, but recombinant human PrP does not protect vascular smooth muscle cells from

oxidative stress, accepted, Reinvention (Undergraduate Journal), 2011.



•Watts, S. W., Shaw, S., Burnett, R. and Dorrance, A. M.: Indoleamine 2,3-diooxygenase in perioaortic at:

mechanisms of inhibition of contraction, in press, Am. J. Physiol. Heart Circ. Physiol, 2011.



•Tan T, Watts, SW and Davis RP: Drug delivery: enabling technology for drug discovery and development.

IPRECIO micro infusion pump: programmable, refillable, and implantable. Front Pharmacol 2:44, Jul 29 2011.



•Davis RP, Pattison J, Thompson JM, Tiniakov R, Scrogin K





Updated 12/3/2011



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