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Guiling Zhao Ph.D.

Academic Title: Assistant Professor
Primary Appointment: Physiology
gzhao@umaryland.edu
Location: BIOTECH, S220
Phone: (410) 706-2663

Personal History:

07/2012-present: Assistant Professor, Center for Biomedical Engineering and Technology & Department of Physiology, University of Maryland School of Medicine, Baltimore, MD, USA.
01/2010-06/2012: Research Associate, Center for Biomedical Engineering and Technology, University of Maryland, School of Medicine, Baltimore, MD, USA.
06/2009-12/2009: Research Associate, Medical Biotechnology Center, University of Maryland Biotechnology Institute, Baltimore, MD, USA.
04/2005-05/2009: Postdoctoral Research Fellow, Department of Physiology, University of Tennessee Health Science Center, Memphis, Tennessee, USA.


Grants & Contracts:

July 2010 - June 2014: National Scientist Development Grant

Publications:

Lederer WJ, Hagen B, and Guiling Zhao. Cell biology. Superresolution subspace signaling. Science. (2012) :336 (6081): 546-7.   "PMC in Process"

Zhao G, Neeb ZP, Leo MD, Pachuau J, Adebiyi A, Ouyang K, Chen J, and Jaggar JH (2010). Type 1 IP3 receptors activate BKCa channels via local molecular coupling in arterial smooth muscle cells. J Gen Physiol. 36(3):283-91.  PMCID: PMC2931145

Adebiyi A, Zhao G, Narayanan D, Thomas CM, Bannister J, and Jaggar JH (2010). Isoform-selective physical coupling of TRPC3 channels to IP3 receptors in smooth muscle cells regulates arterial contractility. Circ Res. 106 (10):1603-12.  PMCID: PMC3050672

Xi Q, Umstot E, Zhao G, Narayanan D, Leffler CW, and Jaggar JH (2010). Glutamate regulates Ca2+ signals in smooth muscle cells of newborn piglet brain slice arterioles through astrocyte- and heme oxygenase-dependent mechanisms. Am J Physiol Heart Circ Physiol. 298(2): H562-9.  PMCID: PMC2822590

Bannister JP, Adebiyi A, Zhao G, Narayanan D, Thomas CM, Feng J, and Jaggar JH (2009). α2δ-1 controls arterial diameter through acute and chronic regulation of smooth muscle cell CaV1.2 α1 subunits. Circ Res. 105: 948-955.

Zhao G, Adebiyi A, Blaskova E, Xi Q, and Jaggar JH (2008). Type 1 inositol 1,4,5-trisphosphate receptors mediate UTP-induced cation currents, Ca2+ signals, and vasoconstriction in cerebral arteries. Am J Physiol Cell Physiol. 295(5):C1376-84.  PMCID: PMC2585000

Xi Q, Adebiyi A, Zhao G, Chapman KE, Waters CM, Hassid A, and Jaggar JH (2008). IP3 constricts cerebral arteries via IP3 receptor-mediated TRPC3 channel activation and independently of sarcoplasmic reticulum Ca2+ release. Circ Res. 102: 1118-1126.  PMCID: PMC2430658

Zhao G, Zhao Y, Pan B, Liu J, Huang X, Zhang X, Cao C, Hou N, Wu C, Zhao KS, and Cheng H (2007). Hypersensitivity of BKCa to Ca2+ Sparks underlies vascular hyporeactivity in arterial smooth muscle. Circ Res. 101(5): 493-502.

Zhao G, Adebiyi A, Xi Q, and Jaggar, JH (2007). Hypoxia reduces KCa channel activity by inducing Ca2+ spark uncoupling in cerebral artery smooth muscle cells. Am J Physiol Cell Physiol. 292(6):C2122-8.  PMCID: PMC2241735

Adebiyi A, Zhao G, Cheranov SY, Ahmed A, and Jaggar, JH (2007). Caveolin-1 abolishment attenuates the myogenic response in murine cerebral arteries. Am J Physiol Heart Circ Physiol. 292(3):H1584-92.  PMCID: PMC2241733

Pan BX, Zhao GL, Huang XL, Zhao KS (2004). Calcium mobilization is required for peroxynitrite-mediated enhancement of spontaneous transient outward currents in arteriolar smooth muscle cells. Free Radical Biology & Medicine. 37(6):823-838.

Pan BX, Zhao GL, Huang XL, Zhao KS (2004). Mobilization of intracellular calcium by peroxynitrite in arteriolar smooth muscle cells from rats. Redox Report. 9(1): 49-55.

Pan BX, Zhao GL, Huang XL, Jin JQ, Zhao KS (2004). Peroxynitrite induces arteriolar smooth muscle cells membrane hyperpolarization with arteriolar hyporeactivity in rats. Life Sciences. 74 (10): 1199-1210.

Wang SH, Wei C, Zhao G, Brochet DXP, Shen J, Song LS, Wang W, Yang D and Cheng H (2004). Imaging Microdomain Ca2+ in muscle cell. Circ Res. 94(8):1011-22 (review).

Zhao KS, Huang X, Liu J, Huang Q, Jin C, Jiang Y, Jin J, Zhao G (2002). New approach to treatment of shock--restitution of vasoreactivity. Shock. 18(2):189-92.