Victoria M. Bolotina, Ph.D.
B.Sc./Ph.D.: Moscow State University
Dr. Bolotina is a Professor of Medicine, Physiology and Biophysics, and a leading expert in calcium signaling and ion channels (with over 2000 citations of her work), who is well funded by NIH. The focus of her research is on the molecular mechanisms of calcium entry and its role in physiological and pathological function. Calcium signaling is an essential component of cell life and death, and is directly involved in virtually all cellular functions. Using an integrative multidisciplinary approach and multiple state-of-the-art techniques, investigators in Dr. Bolotina’s lab track each process from individual molecules and protein complexes, to Ca2+ signaling cascades within the cell and the function of the whole organs/systems, and translate it to the origins of different disease and potential cures. We combine molecular, biochemical and electrophysiological approaches with advanced imaging of live cells (confocal, FRET, TIRF, live imaging and other), and with studies of the main physiological functions of primary cells and cell lines (proliferation, migration, secretion, constriction and other). To study how targeted impairment of specific molecules translates into organ dysfunction and disease we develop and study new transgenic and KO mouse models.
Currently, there are several major projects underway in Dr. Bolotina’s lab:
- Molecular mechanism of the notorious store-operated Ca2+ entry pathway, and its role in health and disease
- New molecular determinants of cell migration, angiogenesis and wound healing
- New mechanism of Ca2+ oscillations and insulin secretion in beta cells, and new determinants of diabetes
- Identification of the mysterious calcium influx factor (CIF)
- Age-dependent progressive neurodegeneration (PD) in a new constitutive and inducible iPLA2β (park14)-deficient mouse models that have been developed in Dr. Bolotina’s lab.
Dr. Bolotina is also a Director of the Affinity Research Collaborative program (ARC) on Calcium Homeostasis in Health and Disease, which is supported by the Department of Medicine. This program promotes multidisciplinary research and collaboration of PI’s from different departments and scientific backgrounds, and opens new directions for integrative research.
Bolotina, V.M., Najibi, S., Palacino, J.J., Pagano, P.J., Cohen, R.A. Nitric oxide directly activates calcium- dependent potassium channels in vascular smooth muscle. Nature 368 :850-853, 1994.
Zakharov S.I., Mongayt D.A., Cohen R.A , Bolotina V.M. Monovalent cation and L-type Ca2+ channels participate in calcium paradox -like phenomenon in rabbit aortic smooth muscle cells. J Physiol 514(1):71-
81, 1999. link
Trepakova E.S., Cohen R.A., Bolotina V.M. Nitric oxide inhibits capacitative cation influx in human platelets by promoting SERCA-dependent refilling of Ca2+ stores. Circulation Research 84: 201-209, 1999. link
Cohen R.A., Weisbrod R.M., Gericke M., Yaghoubi M., Charlene Bierl, Bolotina V.M. Mechanism of nitric oxide-induced vasodilatation: refilling of intracellular stores by sarcoplasmic reticulum Ca2+ ATPase and inhibition of store-operated Ca2+ influx. Circulation Research 84: 210-219, 1999.
Hirakawa, Y., Gericke M., Cohen R.A., Bolotina V.M. Ca2+-dependent Cl- channels in smooth muscle cells from rabbit and mouse aorta: Regulation by intracellular Ca2+ and nitric oxide. Am.J.Physiol. 277: H1732-H1744 1999. link
Zakharov S.I., Cohen R.A., Bolotina V.M. The role of nonselective cation conductance in regulation of membrane potential in vascular smooth muscle cells. In: Endothelium-derived hyperpolarizing factor. (Eds: P.M. Vanhoutte, Harwood Academic Publishers): 243-252, 1999.
Trepakova E.S., Csutora P., Gericke M., Hunton D.L., Marchase R.B., Cohen R.A., Bolotina V.M. Calcium Influx factor (CIF) directly activates store-operated cation channels in vascular smooth muscle. J.Biol.Chem. 275 :26158-26163, 2000. link
Trepakova E.S., Gericke M., Hirakawa Y., Weisbrod R.M., Cohen R.A., Bolotina V.M. Properties of a native cation channel activated by Ca2+ store depletion in vascular smooth muscle cells. J.Biol.Chem.276 : 7782-7790, 2001. link
Li Y., Adachi T., Bolotina V.M., Knowles C., Ault K.A. Cohen R.A. Abnormal platelet function and calcium handling in Dahl salt-hypertensive rats. Hypertention 37: 1129-1135, 2001.
Trepakova E.S., Bolotina V.M. Comparison of the store-operated channels and the effects of nitric oxide on capacitative Ca2+ influx in platelets, smooth muscle cells and Jurkat cells. Membr.Cell Biology (Biol.Membr)19: 49-56, 2002.
Zakharov S.I., Smani T., Leno E., Macianskiene R., Mubagwa K., Bolotina V.M. Monovalent cation (MC) current in cardiac myocytes and smooth muscle cells: regulation by intracellular Mg2+ and inhibition by extracellular polycations. Br.J.Pharmacol. 138: 234-244, 2003. link
Birk A.V., Leno E., Robertson H.D., Bolotina V.M., Szeto H.H. Interaction between ATP and catecholamines in stimulation of platelet aggregation. Am.J.Physiol. 284: H619-H625, 2003.
Smani T., Zakharov S.I., Leno E., Csutora P., Trepakova E.S. and Bolotina V.M. Ca2+-independent phospholipase A2 is a novel determinant of store-operated Ca2+ influx. J.Biol.Chem.278:11909- 11915,
Smani T., Zakharov S.I., Csutora P., Leno E., Trepakova E.S. and Bolotina V.M. Novel mechanism of Ca2+ influx pathway Nature Cell Biol 6: 113-120, 2004. link
Zakharov S.I., Smani T., Dobryndneva Y., Blackmore,P.F., Bolotina V.M. Diethylstilbestrol is a potent inhibitor of CRAC channels and capacitative Ca2+ influx. Molecular Pharmacology 66: 702-707, 2004
Gwanyanya A., Amuzescu B., Macianskiene R., Zakharov S.I., Sipido K., Bolotina V.M, Vereecke J., Mubagwa K. Magnesium-inhibited, TRPM6/7-like channel in cardiac myocytes: Permeation of divalent cations and pH-mediated regulation. J Physiol. 559: 761-76, 2004.
Bolotina V.M. Store-operated calcium influx channels: Diversity and activation mechanisms. Science STKE, 2004 link
Bolotina V.M. Calcium Influx Factor and other mysteries of the store-operated Ca2+ influx pathway. TiBS, 30:378-387, 2005. link
Csutora P., Zarayskiy V., Peter K., Monje F., Smani T., Zakharov S.I., Litvinov D., and Bolotina V.M. Activation mechanism for CRAC current and store-operated Ca2+ entry: calcium influx factor and iPLA2β-dependent pathway, J.Biol.Chem 281:34926-34935, 2006. link
Zarayskiy V., Monje F., Peter K., Csutora P., Khodorov B.I., Bolotina V.M. Store-operated Orai1 and IP3 receptor-operated TRPC1: separation of Siamese twins. Channels 1(4):246-252, 2007. link
Park K., Trucillo M., Serban D.N., Cohen R.A., Bolotina V.M. The role of iPLA2 and store-operated channels in agonist-induced constriction of small resistant vessels. Am.J.Physiol. 294:H1183-H1187, 2008. link
Csutora P., Peter K., Kilic H., Park K., Zarayskiy V., Gwozdz T., and Bolotina V.M. Novel role of STIM1 as a trigger for Calcium Influx Factor (CIF) production. J Biol Chem 283: 14524-14531, 2008. link
Smani T., Patel T., Bolotina V.M. The complex role of PKCε in iPLA2-induced activation of store-operated channels and capacitative Ca2+ influx. Am J Physiol (Cell Physiol.) 294(6): C1499-508, 2008. link
Gwozdz T., Dutko-Gwozdz J., Zarayskiy V., and Bolotina V.M. How strict is the correlation between STIM1 and Orai1 expression, puncta formation and ICRAC activation. Am.J.Phys. (Cell Physiol) 295: C1133-1140, 2008. link
Bolotina VM. Orai1, STIM1 and iPLA2β : a view from a different perspective. J Physiol 586(13):3035-42, 2008. link
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