Paulo W. Pires, BSc, MSc, PhD

Assistant Professor, Physiology

Assistant Professor, Surgery

Education:

Sao Paulo State University, BOTUCATU, SP, Brazil, 2004 (B.Sc., 1st class honors)
Campinas State University, CAMPINAS, SP, Brazil, 2007 (M.Sc. Cell and Structural Biology)
Michigan State University, 2013 (Ph.D. Pharmacology and Toxicology)
Michigan State University, 2014 ( Postdoctoral Fellow, Department of Pharmacology and Toxicology)
University of Nevada SOM, 2018 (Postdoctoral Fellow, Department of Pharmacology)

Honors and Awards:

Horacio Passos Diploma – Awarded to the student with the highest GPA in the 2004 class of the Bachelor’s in Biological Sciences – Sao Paulo State University, 2004
The Caroline tum Suden/Frances A. Hellebrant Professional Opportunity Award, 2010
Future Academic Scholars in Teaching (FAST) Fellowship, Michigan State University, 2011
APS Cardiovascular Section Young Investigator Research Recognition Award, 2012
ASPET Graduate Student Travel Award, 2012
ASPET Third Place in the Best Graduate Student Abstract Competition – Cardiovascular Pharmacology, 2013
APS Minority Travel Award, 2015
Travel Award for Junior Investigators – International Stroke Conference, 2016
Steven M. Horvath Professional Opportunity Award – Experimental Biology, 2016
Carl Storm Underrepresented Minority Fellowship – Gordon Research Conference on Calcium Signaling, 2017
APS Cardiovascular Section Second Place in the Young Investigator Award Competition – Experimental Biology, 2018

Major Areas of Research Interest:

Research in the Pires lab focuses on understanding the regulation of blood flow to the brain under normal and disease states. We are particularly interested in the communication between neurons, astrocytes (a type of glial cells) and endothelial cells that control blood flow to discrete regions of the cerebral cortex, a process called neurovascular coupling. Disease states, such as Alzheimer’s disease and hypertension, are known to alter neurovascular coupling in the brain, leading to improper blood flow delivery to neurons and, consequently, loss of brain cells and cognitive decline. Our lab studies particular receptors in endothelial cells that have their function diminished by Alzheimer’s disease and hypertension, and possible therapies that can improve their function.

Selected Publications:

Pires PW, Earley S. Neuroprotective effects of TRPA1 channels in the cerebral endothelium following ischemic stroke. Elife. Sep 21;7. pii: e35316, 2018. doi: 10.7554/eLife.35316. PMID: 30239332.

Pritchard HAT, Pires PW, Yamasaki E, Thakore P, Earley S. Nanoscale remodeling of ryanodine receptor cluster size underlies cerebral microvascular dysfunction in Duchenne muscular dystrophy. Proc Natl Acad Sci U S A. Sep 4. pii: 201804593, 2018. doi: 10.1073/pnas.1804593115. [Epub ahead of print]. PMID: 30181262.

Pires PW, McClain JL, Hayoz SF, Dorrance AM. Mineralocorticoid receptor antagonism prevents obesity-induced cerebral artery remodeling and reduces white matter injury in rats. Microcirculation, 25(5):e12460, 2018.

Pritchard HAT, Gonzales AL, Pires PW, Drumm BT, Ko EA, Sanders KM, Hennig GW, Earley S. Microtubule structures underlying the sarcoplasmic reticulum support peripheral coupling sites to regulate smooth muscle contractility. Science Signaling, 10(497). Pii eaan2694, 2017.

Pires PW*, Ko EA*, Pritchard HAT*, Rudokas M, Yamasaki E, Earley S. The angiotensin II receptor type 1b is the primary sensor of intraluminal pressure in cerebral artery smooth muscle cells. The Journal of Physiology, 595(14): 4735-4753, 2017.

Matin N*, Pires PW*, Garver H, Jackson WF, Dorrance AM. DOCA-Salt Hypertension Impairs Artery Function in Rat Middle Cerebral Artery and Parenchymal Arterioles. DOCA-salt hypertension impairs artery function in rat middle cerebral artery and parenchymal arterioles. Microcirculation, 23(7):571-579, 2016.

Pires PW, Dabertrand F, Earley S. Isolation and cannulation of mouse cerebral parenchymal arterioles. Journal of Visualized Experiments, 111, 2016.

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