• Publications
  • Influence
Mechanisms underlying acute protection from cardiac ischemia-reperfusion injury.
Preconditioning activates a number of signaling pathways that reduce Ca(2+) overload and reduce activation of the mitochondrial permeability transition pore, and reducing ROS have both been reported to reduce ischemic injury. Expand
The physiological role of mitochondrial calcium revealed by mice lacking the mitochondrial calcium uniporter (MCU)
The characterize of a mouse model that lacks expression of the recently discovered mitochondrial calcium uniporter (MCU) and mitochondria derived from MCU−/− mice have no apparent capacity to rapidly uptake calcium clarify how acute alterations in mitochondrial matrix calcium can regulate mammalian physiology. Expand
A fluorescent indicator for measuring cytosolic free magnesium.
The previously developed chelator O-aminophenol-N,N,O-triacetic acid (APTRA) has been modified to yield a fluorescent analogue which can be utilized as an intracellular probe for ionized Mg2+. Expand
Preconditioning Results in S-Nitrosylation of Proteins Involved in Regulation of Mitochondrial Energetics and Calcium Transport
IPC and GSNO produced a similar pattern of S-nitrosylation modification and cardiac protection against ischemia/reperfusion injury, suggesting that protein S- nitrogen oxide may play an important cardioprotective role in heart. Expand
Ischemic Preconditioning Activates Phosphatidylinositol-3-Kinase Upstream of Protein Kinase C
PC induced phosphorylation of protein kinase B and translocation of PKC&egr; and it increased NO production, and these effects were blocked by WM, which suggests a role for PI3-kinase in PC upstream ofPKC and NO. Expand
Deoxymyoglobin Is a Nitrite Reductase That Generates Nitric Oxide and Regulates Mitochondrial Respiration
The nitrite reductase activity of deoxymyoglobin is characterized, which reduces nitrite approximately 36 times faster than deoxyhemoglobin because of its lower heme redox potential, and it is demonstrated that NO generation from nitrite reduction can escape heme autocapture to regulate NO-dependent signaling. Expand
Diazoxide-Induced Cardioprotection Requires Signaling Through a Redox-Sensitive Mechanism
Using 31P NMR spectroscopy, diazoxide significantly attenuated ischemia-induced intracellular acidification and enhanced post-ischemic recovery of phosphocreatine levels, both of which were blocked by cotreatment with NAC. Expand
Activation of a novel estrogen receptor, GPER, is cardioprotective in male and female rats.
G-1 activation of GPER improves functional recovery and reduces infarct size in isolated rat hearts following I/R through a PI3K-dependent, gender-independent mechanism, and shown to be cardioprotective in rats. Expand
Phosphorylation of Glycogen Synthase Kinase-3&bgr; During Preconditioning Through a Phosphatidylinositol-3-Kinase–Dependent Pathway Is Cardioprotective
Findings indicate that inhibition of GSK-3-bgr; is protective and that this PI3-kinase–dependent signaling pathway may play an important role in ischemic preconditioning. Expand
Estrogen signaling and cardiovascular disease.
  • E. Murphy
  • Chemistry, Medicine
  • Circulation research
  • 2 September 2011
The different estrogen receptors and their signaling mechanisms are reviewed, mechanisms that regulate estrogen receptor levels and locations are discussed, and the cardiovascular effects of estrogen signaling are considered. Expand