Muniswamy Madesh

Summary

Affiliation: Temple University
Country: USA

Publications

  1. ncbi Execution of superoxide-induced cell death by the proapoptotic Bcl-2-related proteins Bid and Bak
    Muniswamy Madesh
    Department of Biochemistry, Temple University, Philadelphia, PA 19140, USA
    Mol Cell Biol 29:3099-112. 2009
  2. ncbi Caveolae are an essential component of the pathway for endothelial cell signaling associated with abrupt reduction of shear stress
    Tatyana Milovanova
    Institute for Environmental Medicine, University of Pennsylvania Medical Center, One John Morgan Building, Philadelphia, PA 19104 6068, USA
    Biochim Biophys Acta 1783:1866-75. 2008
  3. ncbi G protein-coupled receptor Ca2+-linked mitochondrial reactive oxygen species are essential for endothelial/leukocyte adherence
    Brian J Hawkins
    Institute for Environmental Medicine, University of Pennsylvania, Philadelphia, PA 19104 6068, USA
    Mol Cell Biol 27:7582-93. 2007
  4. ncbi Selective role for superoxide in InsP3 receptor-mediated mitochondrial dysfunction and endothelial apoptosis
    Muniswamy Madesh
    Institute for Environmental Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA
    J Cell Biol 170:1079-90. 2005
  5. ncbi STIM proteins: dynamic calcium signal transducers
    Jonathan Soboloff
    Department of Biochemistry, Temple University School of Medicine, 3400 North Broad Street, Philadelphia, Pennsylvania 19140, USA
    Nat Rev Mol Cell Biol 13:549-65. 2012
  6. ncbi The proapoptotic factors Bax and Bak regulate T Cell proliferation through control of endoplasmic reticulum Ca(2+) homeostasis
    Russell G Jones
    Department of Cancer Biology, Abramson Family Cancer Research Institute, University of Pennsylvania, Philadelphia, PA 19104, USA
    Immunity 27:268-80. 2007
  7. ncbi Requirement of FADD, NEMO, and BAX/BAK for aberrant mitochondrial function in tumor necrosis factor alpha-induced necrosis
    Krishna M Irrinki
    Department of Biochemistry, Temple University, Philadelphia, PA 19140, USA
    Mol Cell Biol 31:3745-58. 2011
  8. ncbi Superoxide flux in endothelial cells via the chloride channel-3 mediates intracellular signaling
    Brian J Hawkins
    Institute for Environmental Medicine, University of Pennsylvania, Philadelphia, PA 19104 6068, USA
    Mol Biol Cell 18:2002-12. 2007
  9. ncbi Nitration of the mitochondrial complex I subunit NDUFB8 elicits RIP1- and RIP3-mediated necrosis
    Christiana W Davis
    Institute for Environmental Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA
    Free Radic Biol Med 48:306-17. 2010
  10. ncbi Mitochondrial complex II prevents hypoxic but not calcium- and proapoptotic Bcl-2 protein-induced mitochondrial membrane potential loss
    Brian J Hawkins
    Department of Biochemistry, Temple University, Philadelphia, Pennsylvania 19140, USA
    J Biol Chem 285:26494-505. 2010

Research Grants

  1. Coordination of Pathophysiologic Endothelial Cell Signaling by ROS
    Madesh Muniswamy; Fiscal Year: 2009
  2. Coordination of Pathophysiologic Endothelial Cell Signaling by ROS
    Madesh Muniswamy; Fiscal Year: 2009
  3. Coordination of Pathophysiologic Endothelial Cell Signaling by ROS
    Madesh Muniswamy; Fiscal Year: 2010

Collaborators

Detail Information

Publications38

  1. ncbi Execution of superoxide-induced cell death by the proapoptotic Bcl-2-related proteins Bid and Bak
    Muniswamy Madesh
    Department of Biochemistry, Temple University, Philadelphia, PA 19140, USA
    Mol Cell Biol 29:3099-112. 2009
    ....
  2. ncbi Caveolae are an essential component of the pathway for endothelial cell signaling associated with abrupt reduction of shear stress
    Tatyana Milovanova
    Institute for Environmental Medicine, University of Pennsylvania Medical Center, One John Morgan Building, Philadelphia, PA 19104 6068, USA
    Biochim Biophys Acta 1783:1866-75. 2008
    ..These studies indicate that caveolin-1 functions as a shear sensor in flow-adapted EC resulting in ROS-mediated cell signaling and endothelial cell proliferation following the abrupt reduction in flow...
  3. ncbi G protein-coupled receptor Ca2+-linked mitochondrial reactive oxygen species are essential for endothelial/leukocyte adherence
    Brian J Hawkins
    Institute for Environmental Medicine, University of Pennsylvania, Philadelphia, PA 19104 6068, USA
    Mol Cell Biol 27:7582-93. 2007
    ..These results demonstrate that mROS is the downstream effector molecule that translates receptor-mediated Ca(2+) signals into proinflammatory signaling and leukocyte/EC firm adhesion...
  4. ncbi Selective role for superoxide in InsP3 receptor-mediated mitochondrial dysfunction and endothelial apoptosis
    Muniswamy Madesh
    Institute for Environmental Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA
    J Cell Biol 170:1079-90. 2005
    ..This study provides evidence that O2*- facilitates an InsP3R-linked apoptotic cascade and may serve a critical function in I/R injury and inflammation...
  5. ncbi STIM proteins: dynamic calcium signal transducers
    Jonathan Soboloff
    Department of Biochemistry, Temple University School of Medicine, 3400 North Broad Street, Philadelphia, Pennsylvania 19140, USA
    Nat Rev Mol Cell Biol 13:549-65. 2012
    ..Details are emerging on the remarkable organization within these STIM-induced junctional microdomains and the identification of new regulators and alternative target proteins for STIM...
  6. ncbi The proapoptotic factors Bax and Bak regulate T Cell proliferation through control of endoplasmic reticulum Ca(2+) homeostasis
    Russell G Jones
    Department of Cancer Biology, Abramson Family Cancer Research Institute, University of Pennsylvania, Philadelphia, PA 19104, USA
    Immunity 27:268-80. 2007
    ..Together, the data establish that Bax and Bak play an essential role in the control of T cell proliferation by modulating ER Ca(2+) release...
  7. ncbi Requirement of FADD, NEMO, and BAX/BAK for aberrant mitochondrial function in tumor necrosis factor alpha-induced necrosis
    Krishna M Irrinki
    Department of Biochemistry, Temple University, Philadelphia, PA 19140, USA
    Mol Cell Biol 31:3745-58. 2011
    ..Finally, elimination of BAX and BAK or overexpression of Bcl-x(L) protects cells from necroptosis at a later step. These findings provide evidence that mitochondria play an amplifying role in inflammation-induced necroptosis...
  8. ncbi Superoxide flux in endothelial cells via the chloride channel-3 mediates intracellular signaling
    Brian J Hawkins
    Institute for Environmental Medicine, University of Pennsylvania, Philadelphia, PA 19104 6068, USA
    Mol Biol Cell 18:2002-12. 2007
    ..This study demonstrates that O(2)(.-) flux across the endothelial cell plasma membrane occurs through ClC-3 channels and induces intracellular Ca(2+) release, which activates mitochondrial O(2)(.-) generation...
  9. ncbi Nitration of the mitochondrial complex I subunit NDUFB8 elicits RIP1- and RIP3-mediated necrosis
    Christiana W Davis
    Institute for Environmental Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA
    Free Radic Biol Med 48:306-17. 2010
    ....
  10. ncbi Mitochondrial complex II prevents hypoxic but not calcium- and proapoptotic Bcl-2 protein-induced mitochondrial membrane potential loss
    Brian J Hawkins
    Department of Biochemistry, Temple University, Philadelphia, Pennsylvania 19140, USA
    J Biol Chem 285:26494-505. 2010
    ..This finding is important as it sets the stage for complex II functional preservation as an attractive therapy to maintain mitochondrial function during hypoxia...
  11. ncbi PECAM-targeted delivery of SOD inhibits endothelial inflammatory response
    Vladimir V Shuvaev
    Institute for Environmental Medicine, Department of Pharmacology, University of Pennsylvania School of Medicine, 1 John Morgan Bldg, 3620 Hamilton Walk, Philadelphia, PA 19104 6068, USA
    FASEB J 25:348-57. 2011
    ....
  12. ncbi NF-kappaB protects cells from gamma interferon-induced RIP1-dependent necroptosis
    Roshan J Thapa
    Immune Cell Development and Host Defense Program, Fox Chase Cancer Center, Philadelphia, Pennsylvania 19111, USA
    Mol Cell Biol 31:2934-46. 2011
    ..Together, these studies demonstrate that NF-κB protects cells from IFN-γ-mediated necroptosis by transcriptionally activating a survival response that quenches ROS to preserve mitochondrial integrity...
  13. ncbi Bad targets the permeability transition pore independent of Bax or Bak to switch between Ca2+-dependent cell survival and death
    Soumya Sinha Roy
    Department of Pathology, Anatomy and Cell Biology, Thomas Jefferson University, Philadelphia, PA 19107, USA
    Mol Cell 33:377-88. 2009
    ..Thus, phospho-regulatory mechanisms converge on Bad to switch between the survival and apoptotic functions of mitochondrial calcium signaling by activating a mechanism whereby a BH3-only protein bypasses Bax/Bak and engages the PTP...
  14. ncbi MICU1 is an essential gatekeeper for MCU-mediated mitochondrial Ca(2+) uptake that regulates cell survival
    Karthik Mallilankaraman
    Department of Biochemistry, Temple University, Philadelphia, PA 19140, USA
    Cell 151:630-44. 2012
    ..Thus, MICU1 is a gatekeeper of MCU-mediated Ca(2+)(m) uptake that is essential to prevent [Ca(2+)](m) overload and associated stress...
  15. ncbi Sensing cellular stress through STIM proteins
    Jonathan Soboloff
    Department of Biochemistry, Temple University School of Medicine, Philadelphia, Pennsylvania, USA
    Nat Chem Biol 7:488-92. 2011
    ..In addition to Ca2+-related endoplasmic reticulum stress, STIM proteins are emerging as general stress sensors that react to multiple stress signals to orchestrate Ca2+ signaling and homeostasis...
  16. ncbi ABCA3 is critical for lamellar body biogenesis in vivo
    NaEun Cheong
    Department of Physiology, University of Pennsylvania School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA
    J Biol Chem 282:23811-7. 2007
    ..Collectively, these findings strongly suggest that ABCA3 is necessary for lamellar body biogenesis, surfactant protein-B processing, and lung development late in gestation...
  17. ncbi MCUR1 is an essential component of mitochondrial Ca2+ uptake that regulates cellular metabolism
    Karthik Mallilankaraman
    Department of Biochemistry, Temple University, Philadelphia, Pennsylvania 19140, USA
    Nat Cell Biol 14:1336-43. 2012
    ..Thus, MCUR1 is a critical component of a mitochondrial uniporter channel complex required for mitochondrial Ca(2+) uptake and maintenance of normal cellular bioenergetics...
  18. ncbi Hypoxia-induced acidosis uncouples the STIM-Orai calcium signaling complex
    Salvatore Mancarella
    Department of Biochemistry, Temple University School of Medicine, Philadelphia, Pennsylvania 19140, USA
    J Biol Chem 286:44788-98. 2011
    ....
  19. ncbi Carcinoembryonic cell adhesion molecule 6 in human lung: regulated expression of a multifunctional type II cell protein
    Venkatadri Kolla
    Department of Pediatrics, Children s Hospital of Philadelphia, University of Pennsylvania, Philadelphia, Pennsylvania, USA
    Am J Physiol Lung Cell Mol Physiol 296:L1019-30. 2009
    ..Because CEACAM6 acts as an antiapoptotic factor and stabilizes surfactant function, in addition to a putative role in innate defense against bacteria, we propose that it is a multifunctional alveolar protein...
  20. ncbi S-glutathionylation activates STIM1 and alters mitochondrial homeostasis
    Brian J Hawkins
    Department of Biochemistry, Temple University, Philadelphia, PA 19140, USA
    J Cell Biol 190:391-405. 2010
    ..These experiments reveal that cysteine 56 is a sensor for oxidant-dependent activation of STIM1 and demonstrate a molecular link between oxidant stress and Ca(2+) signaling via the CRAC channel...
  21. ncbi The HIV-1 Vpr and glucocorticoid receptor complex is a gain-of-function interaction that prevents the nuclear localization of PARP-1
    Karuppiah Muthumani
    Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA
    Nat Cell Biol 8:170-9. 2006
    ..These data provide important insights into Vpr biology and its role in HIV pathogenesis...
  22. ncbi Calcium signaling and apoptosis
    Gyorgy Hajnoczky
    Department of Pathology, Anatomy, and Cell Biology, Thomas Jefferson University, Philadelphia, PA 19107, USA
    Biochem Biophys Res Commun 304:445-54. 2003
    ..In this paper, the recent progress of research on the mechanisms mediating the apoptosis-regulating effects of Ca(2+) and the interactions of Bcl-2 family proteins with the Ca(2+) storage organelles are discussed...
  23. ncbi Membrane-tethered MUC1 mucin is phosphorylated by epidermal growth factor receptor in airway epithelial cells and associates with TLR5 to inhibit recruitment of MyD88
    Kosuke Kato
    Department of Physiology, Center for Inflammation, Translational and Clinical Lung Research, Temple University School of Medicine, Philadelphia, PA 19140, USA
    J Immunol 188:2014-22. 2012
    ..This unique ability of MUC1 to control TLR5 signaling suggests its potential role in the pathogenesis of chronic inflammatory lung diseases...
  24. ncbi Functional and trafficking defects in ATP binding cassette A3 mutants associated with respiratory distress syndrome
    NaEun Cheong
    Department of Physiology, Institute for Environmental Medicine, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104 6068, USA
    J Biol Chem 281:9791-800. 2006
    ..We conclude that ABCA3 is required for lysosomal loading of phosphatidylcholine and conversion of lysosomes to lamellar body-like structures...
  25. ncbi The endoplasmic reticulum gateway to apoptosis by Bcl-X(L) modulation of the InsP3R
    Carl White
    Department of Physiology, Abramson Family Cancer Research Institute, Philadelphia, PA 19104, USA
    Nat Cell Biol 7:1021-8. 2005
    ..As a consequence, cells are protected against apoptosis by a more sensitive and dynamic coupling of ER to mitochondria through Ca(2+)-dependent signal transduction that enhances cellular bioenergetics and preserves survival...
  26. ncbi Involvement of transforming growth factor-beta in regulation of calcium transients in diabetic vascular smooth muscle cells
    Kumar Sharma
    Dorrance Hamilton Research Laboratories, Division of Nephrology, Department of Medicine, Thomas Jefferson University, Suite 353, Jeff Alumni Hall, 1020 Locust Street, Philadelphia, PA 19107, USA
    Am J Physiol Renal Physiol 285:F1258-70. 2003
    ..We conclude that TGF-beta plays an important role in the vascular dysfunction of early diabetes by inhibiting calcium transients in vascular smooth muscle cells...
  27. ncbi Acidic NAADP-sensitive calcium stores in the endothelium: agonist-specific recruitment and role in regulating blood pressure
    G Cristina Brailoiu
    Departments of Pharmacology, University School of Medicine, Philadelphia, Pennsylvania 19140, USA
    J Biol Chem 285:37133-7. 2010
    ..Our data extend the actions of NAADP to the endothelium both in vitro and in vivo, pointing to a previously unrecognized role for this messenger in controlling blood pressure...
  28. ncbi Proliferative signaling by store-operated calcium channels opposes colon cancer cell cytostasis induced by bacterial enterotoxins
    Shiva Kazerounian
    Division of Clinical Pharmacology, Department of Medicine, Thomas Jefferson University, Philadelphia, PA 19107, USA
    J Pharmacol Exp Ther 314:1013-22. 2005
    ..They suggest that combining guanylyl cyclase C agonists and SOC inhibitors offers a novel paradigm for cGMP-directed therapy and prevention for colorectal tumors...
  29. ncbi Endothelial targeting of semi-permeable polymer nanocarriers for enzyme therapies
    Thomas D Dziubla
    Institute for Environmental Medicine, University of Pennsylvania Medical Center, 1 John Morgan Building, 36th Street and Hamilton Walk, Philadelphia, PA 19104 6068, USA
    Biomaterials 29:215-27. 2008
    ..Vascular targeting of PNC-loaded detoxifying enzymes may find wide medical applications including management of oxidative stress and other toxicities...
  30. ncbi Lung endothelial cell proliferation with decreased shear stress is mediated by reactive oxygen species
    Tatyana Milovanova
    Institute for Environmental Medicine, Univ of Pennsylvania Medical Center, One John Morgan Bldg, Philadelphia, PA 19104 6068, USA
    Am J Physiol Cell Physiol 290:C66-76. 2006
    ..Thus loss of shear stress in flow-adapted mPMVECs results in cell division associated with ROS generated by NADPH oxidase. This effect requires a functioning cell membrane KATP channel...
  31. ncbi Hyperhomocysteinemia impairs endothelium-derived hyperpolarizing factor-mediated vasorelaxation in transgenic cystathionine beta synthase-deficient mice
    Zhongjian Cheng
    Department of Pharmacology, Temple University School of Medicine, Philadelphia, PA 19140, USA
    Blood 118:1998-2006. 2011
    ..Our results suggest that HHcy impairs EDHF relaxation in SMAs by inhibiting SK/IK activities via oxidation- and tyrosine nitration-related mechanisms...
  32. ncbi The polypeptide chain-releasing factor GSPT1/eRF3 is proteolytically processed into an IAP-binding protein
    Ramesh Hegde
    Center for Apoptosis Research and the Department of Microbiology and Immunology, Kimmel Cancer Institute, Thomas Jefferson University, Philadelphia, Pennsylvania 19107, USA
    J Biol Chem 278:38699-706. 2003
    ....
  33. ncbi Melanocyte-like cells in the heart and pulmonary veins contribute to atrial arrhythmia triggers
    Mark D Levin
    Penn Cardiovascular Institute and University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA
    J Clin Invest 119:3420-36. 2009
    ..These data suggest that dysfunction of melanocyte-like cells in the atrium and pulmonary veins may contribute to atrial arrhythmias...
  34. ncbi Inflammasomes: sensors of metabolic stresses for vascular inflammation
    Ying Yin
    Department of Pharmacology and Cardiovascular Research Center, Temple University School of Medicine, 3500 North Broad Street, MERB 1059, Philadelphia, PA 19140, USA
    Front Biosci 18:638-49. 2013
    ....
  35. ncbi The common inhalational anesthetic isoflurane induces apoptosis via activation of inositol 1,4,5-trisphosphate receptors
    Huafeng Wei
    Department of Anesthesiology and Critical Care, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104, USA
    Anesthesiology 108:251-60. 2008
    ..The authors hypothesized that isoflurane activates inositol 1,4,5-trisphosphate (IP3) receptors on the endoplasmic reticulum (ER) membrane, causing excessive calcium release, triggering apoptosis...
  36. ncbi tcBid promotes Ca(2+) signal propagation to the mitochondria: control of Ca(2+) permeation through the outer mitochondrial membrane
    György Csordás
    Department of Pathology, Anatomy and Cell Biology, Thomas Jefferson University, Philadelphia, PA 19107, USA
    EMBO J 21:2198-206. 2002
    ..Facilitation of Ca(2+) delivery to the mitochondria by tcBid may also support recruitment of mitochondria to the cell death machinery...
  37. ncbi TGF-beta-induced Ca(2+) influx involves the type III IP(3) receptor and regulates actin cytoskeleton
    Tracy A McGowan
    Dorrance Hamilton Laboratory, Division of Nephrology, Department of Medicine, Thomas Jefferson University, Philadelphia, Pennsylvania 19107, USA
    Am J Physiol Renal Physiol 282:F910-20. 2002
    ..The alterations in the actin cytoskeleton by TGF-beta are dependent on TGF-beta-induced Ca(2+) influx. These studies identify a novel pathway by which TGF-beta regulates Ca(2+) influx and induces cytoskeletal alterations...
  38. ncbi Rapid kinetics of tBid-induced cytochrome c and Smac/DIABLO release and mitochondrial depolarization
    Muniswamy Madesh
    Department of Pathology, Thomas Jefferson University, Philadelphia, Pennsylvania 19107, USA
    J Biol Chem 277:5651-9. 2002
    ..The tBid-induced loss of DeltaPsi(m) occurs after cytochrome c release and reflects impairment of oxidative metabolism...

Research Grants4

  1. Coordination of Pathophysiologic Endothelial Cell Signaling by ROS
    Madesh Muniswamy; Fiscal Year: 2009
    ....
  2. Coordination of Pathophysiologic Endothelial Cell Signaling by ROS
    Madesh Muniswamy; Fiscal Year: 2009
    ....
  3. Coordination of Pathophysiologic Endothelial Cell Signaling by ROS
    Madesh Muniswamy; Fiscal Year: 2010
    ....