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Welcome to the Dayal lab
The Dayal lab investigates mechanisms of thrombosis under a variety of pathological conditions using sophisticated animal models and clinically-relevant human samples. Specific research interests include thrombosis associated with aging, cardiovascular risk factors, and cancer.
Research
Thrombotic diseases such as myocardial infarction, stroke, deep vein thrombosis and pulmonary embolisms are the leading causes of morbidity and mortality worldwide. The primary focus of Dr. Dayal’s laboratory is to define the mechanisms of thrombosis using murine models and clinically-relevant human specimens. We are particularly interested in risk factors such as aging, hyperhomocysteinemia, and cancer. We have established methods for in vivo mouse models of experimental thrombosis (for arterial as well as venous systems). We have also developed assays to monitor ex vivo platelet activation, aggregation and thrombi formation in human samples. A new research direction is to study the involvement of NETs (neutrophil extracellular traps) and mitochondrial bioenergetics in thrombosis. A secondary interest is to investigate cognitive responses in aging and hyperhomocysteinemia. The Dayal laboratory is currently funded through a R01 from National Institute of Aging (NIA, NIH) as well as through internal and external collaborative research awards.
The Lab
Principal InvestigatorPostdoctoral Fellows |
Research Assistant/Lab ManagerUndergraduate Student |
Seminal Lab Publications
2017 |
*Dayal S, Baumbach GL, Arning E, Bottiglieri T, Faraci FM, Lentz SR. Deficiency of superoxide dismutase promotes cerebral vascular hypertrophy and vascular dysfunction in hyperhomocysteinemia. PLoS One. 2017 Apr 17;12(4):e0175732. doi: 10.1371/journal.pone.0175732. eCollection 2017. |
2015 |
*Dayal S, Gu SX, Hutchins RD, Wilson KM, Wang Y, Fu X, Lentz SR. Deficiency of Superoxide Dismutase Impairs Protein C Activation and Enhances Susceptibility to Experimental Thrombosis. Arterioscler Thromb Vasc Biol. 2015;35(8):1798-804. |
2013 |
*Dayal S, Wilson KM, Motto DG, Miller FJ, Chauhan A, Lentz SR. Hydrogen peroxide promotes aging-related platelet hyperactivation and thrombosis. Circulation, 2013, 127(12):1308-16. |
2012 |
*Dayal S, Chauhan AK, Jensen M, Leo L, Lynch CM, Faraci, FM, Kruger WD, Lentz SR. Paradoxical absence of a prothrombotic phenotype in a mouse model of severe hyperhomocysteinemia. Blood, 2012, 119(13):3176-83. |
2008 |
Chrissobolis S, Didion SP, Kinzenbaw D, Schrader LI, Dayal S, Lentz SR, Faraci FM. Glutathione peroxidase-1 plays a major role in protecting against angiotensin II-induced vascular dysfunction. Hypertension 2008;51:872-877. |
2007 |
Sontag E, Nunbhakdi-Craig V, Sontag JM, Diaz-Arrastia R, Ogris E, Dayal S, Lentz SR, Arning E, Bottiglieri T. Protein phosphatase 2A methyltransferase links homocysteine metabolism with tau and APP regulation. J. Neurosci. 2007:27:2751-2759 |
2006 |
Dayal S, Wilson KM, Leo L, Arning E, Bottiglieri T, Lentz SR. Enhanced susceptibility to arterial thrombosis in a murine model of hyperhomocysteinemia. Blood 2006;108:2237-43. |
2005 |
Dayal S, Devlin AM, McCaw RB, Liu M, Arning E, Bottiglieri T, Shane B, Faraci FM, Lentz SR. Cerebral vascular dysfunction in methionine synthase deficient mice. Circulation 2005;112:737-744 |
2004 |
Dayal S, Arning E, Bottiglieri T, Boger RH, Sigmund CT, Faraci FM, Lentz SR. Cerebral vascular dysfunction mediated by superoxide in hyperhomocysteinemia. Stroke 2004;35:1957-1962 |
2001 |
Dayal S, Bottiglieri T, Arning E, Maeda N, Malinow R, Sigmund CD, Heistad DD, Faraci FM, Lentz SR. Endothelial dysfunction and elevation of S-adenosylhomocysteine in cystathionine beta-synthase-deficient mice. Circ Res 2001;88:1203-1209 |
Contact Information
Medical Laboratories
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Locations:3160 ML (Laboratory) 25 S Grand Ave |
