10 results match your criteria: "Medical College of Georgia and Veterans Affairs Medical Center[Affiliation]"
Am J Physiol Renal Physiol
March 2008
Department of Cellular Biology and Anatomy, Medical College of Georgia and Veterans Affairs Medical Center, 1459 Laney Walker Blvd., Augusta, GA 30912, USA.
Bcl-2 family proteins are central regulators of apoptosis. As the prototypic member, Bcl-2 protects various types of cells against apoptotic insults. In mammalian cells, Bcl-2 has a dual subcellular localization, in mitochondria and endoplasmic reticulum (ER).
View Article and Find Full Text PDFCell Cycle
December 2007
Department of Cellular Biology and Anatomy, Medical College of Georgia and Veterans Affairs Medical Center, Augusta, Georgia 30912, USA.
Early during apoptosis, the mitochondrial network collapses into short punctuate fragments. The seemingly morphological change, called mitochondrial fragmentation, contributes to mitochondrial injury. Mitochondrial morphology is dictated by two opposing processes, fission and fusion.
View Article and Find Full Text PDFRen Fail
March 2008
Department of Cellular Biology and Anatomy, Medical College of Georgia and Veterans Affairs Medical Center, Augusta, Georgia 30912, USA.
Bid, a BH3-only member of the Bcl-2 family proteins, is most abundantly expressed in the kidneys. Recent research has shown Bid activation in renal tubular cells in vitro following ATP-depletion and hypoxic injury, and also in vivo during renal ischemia-reperfusion in rats and mice. Importantly, Bid-deficient mice are resistant to ischemic kidney injury.
View Article and Find Full Text PDFProc Natl Acad Sci U S A
July 2007
Department of Cellular Biology and Anatomy, Medical College of Georgia and Veterans Affairs Medical Center, Augusta, GA 30912, USA.
Mitochondrial injury, characterized by outer membrane permeabilization and consequent release of apoptogenic factors, is a key to apoptosis of mammalian cells. Bax and Bak, two multidomain Bcl-2 family proteins, provide a requisite gateway to mitochondrial injury. However it is unclear how Bax and Bak cooperate to provoke mitochondrial injury and whether their roles are redundant.
View Article and Find Full Text PDFKidney Int
July 2007
Department of Cellular Biology and Anatomy, Medical College of Georgia and Veterans Affairs Medical Center, Augusta, Georgia 30912, USA.
A robust inflammatory response involving tumor necrosis factor-alpha (TNF-alpha) is induced during cisplatin nephrotoxicity. Using chimeric models, Reeves and colleagues now demonstrate that resident kidney cells, rather than infiltrating immune cells, are the major producers of TNF-alpha. Blockade of TNF-alpha attenuates inflammation and associated kidney injury.
View Article and Find Full Text PDFKidney Int
July 2007
Department of Cellular Biology and Anatomy, Medical College of Georgia and Veterans Affairs Medical Center, Augusta, Georgia 30912, USA.
Nephrotoxicity induced by cisplatin involves tubular cell necrosis and apoptosis; the latter of which may be initiated by multiple mechanisms including activation of the intrinsic mitochondrial pathway. In cultured tubular epithelial cells, cisplatin can activate the proapoptotic protein Bax resulting in cytochrome c release, caspase activation, and apoptosis. Definitive evidence for the involvement of Bax in cisplatin nephrotoxicity in vivo, however, is lacking.
View Article and Find Full Text PDFBiochem Pharmacol
May 2007
Department of Cellular Biology and Anatomy, Medical College of Georgia and Veterans Affairs Medical Center, 1459 Laney Walker Blvd., Augusta, GA 30912, United States.
Nephrotoxicity is a major side effect of cisplatin, a widely used cancer therapy drug. Recent work has suggested a role of p53 in renal cell injury by cisplatin. However, the mechanism of p53 activation by cisplatin is unclear.
View Article and Find Full Text PDFJ Biol Chem
January 2007
Department of Cellular Biology and Anatomy, Medical College of Georgia and Veterans Affairs Medical Center, Augusta, Georgia 30912, USA.
Nutlins, the newly developed small molecule antagonists of MDM2, activate p53 and induce apoptosis in cancer cells, offering a novel strategy of chemotherapy. Recent studies have further suggested synergistic effects of nutlins with other chemotherapeutic drugs. However, it is unclear whether nutlins increase or decrease the side effects of these drugs in normal non-malignant cells or tissues.
View Article and Find Full Text PDFNeurology
February 2000
Department of Neurology, Medical College of Georgia and Veterans Affairs Medical Center, Augusta 30904, USA.
Statins represent a promising class of agents to prevent stroke. In randomized trials of middle-aged patients with coronary artery disease, statins reduce the incidence of stroke. The reduction in stroke may not be solely related to cholesterol or low-density lipoprotein reduction but may involve nonsterol mechanisms effects on endothelial cells, macrophages, platelets, and smooth muscle cells.
View Article and Find Full Text PDFJ Neurophysiol
December 1997
Department of Pharmacology and Toxicology, Medical College of Georgia and Veterans Affairs Medical Center, Augusta, Georgia 30912-2300, USA.
Gi proteins inhibit voltage-gated calcium channels and activate inwardly rectifying K+ channels in hippocampal pyramidal neurons. The effect of activation of G-protein-coupled receptors on action potential-evoked calcium influx was examined in pyramidal neuron dendrites with optical and extracellular voltage recording. We tested the hypotheses that 1) activation of these receptors would inhibit calcium channels in dendrites; 2) hyperpolarization resulting from K+ channel activation would deinactivate low-threshold, T-type calcium channels on dendrites, increasing calcium influx mediated by these channels; and 3) activation of these receptors would inhibit propagation of action potentials into dendrites, and thus indirectly decrease calcium influx.
View Article and Find Full Text PDF