MIR HOSSAIN

Summary

Affiliation: Kennedy Krieger Institute
Country: USA

Publications

  1. doi request reprint Sex differences in mitochondrial biogenesis determine neuronal death and survival in response to oxygen glucose deprivation and reoxygenation
    Jaswinder Sharma
    Department of Neurology, The Hugo W, Moser Research Institute at Kennedy Krieger, Baltimore, MD, USA
    BMC Neurosci 15:9. 2014
  2. pmc Hypoxic-ischemic injury in neonatal brain: involvement of a novel neuronal molecule in neuronal cell death and potential target for neuroprotection
    Mir Ahamed Hossain
    Department of Neurology, The Johns Hopkins University School of Medicine and The Kennedy Krieger Research Institute, Baltimore, MD 21205, USA
    Int J Dev Neurosci 26:93-101. 2008
  3. ncbi request reprint Molecular mediators of hypoxic-ischemic injury and implications for epilepsy in the developing brain
    Mir Ahamed Hossain
    Department of Neurology, The Johns Hopkins University School of Medicine and The Kennedy Krieger Research Institute, Baltimore, MD 21205, USA
    Epilepsy Behav 7:204-13. 2005
  4. ncbi request reprint Neuronal pentraxin 1: a novel mediator of hypoxic-ischemic injury in neonatal brain
    Mir Ahamed Hossain
    Department of Neurology, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA
    J Neurosci 24:4187-96. 2004
  5. ncbi request reprint Neuroprotection by scatter factor/hepatocyte growth factor and FGF-1 in cerebellar granule neurons is phosphatidylinositol 3-kinase/akt-dependent and MAPK/CREB-independent
    Mir Ahamed Hossain
    Department of Neurology, The Johns Hopkins University School of Medicine, Baltimore, Maryland, USA
    J Neurochem 81:365-78. 2002
  6. ncbi request reprint Induction of vascular endothelial growth factor in human astrocytes by lead. Involvement of a protein kinase C/activator protein-1 complex-dependent and hypoxia-inducible factor 1-independent signaling pathway
    M A Hossain
    Departments of Neurology, Neuroscience, and Oncology, The Johns Hopkins University School of Medicine and The Kennedy Krieger Research Institute, Baltimore, Maryland 21205, USA
    J Biol Chem 275:27874-82. 2000
  7. ncbi request reprint Human FGF-1 gene delivery protects against quinolinate-induced striatal and hippocampal injury in neonatal rats
    M A Hossain
    1Department of Neurology, The Johns Hopkins University School of Medicine, USA 2The Kennedy Krieger Research Institute, Baltimore, MD 21205, USA
    Eur J Neurosci 10:2490-9. 1998
  8. ncbi request reprint Microarray analysis of differential gene expression in lead-exposed astrocytes
    C M Bouton
    Department of Neuroscience, Johns Hopkins University, Baltimore, Maryland 21205, USA
    Toxicol Appl Pharmacol 176:34-53. 2001
  9. pmc Akt as a mediator of cell death
    Hongbo R Luo
    Department of Neuroscience, Johns Hopkins University School of Medicine, 725 North Wolfe Street, Baltimore, MD 21205, USA
    Proc Natl Acad Sci U S A 100:11712-7. 2003
  10. ncbi request reprint Transgenic expression of human FGF-1 protects against hypoxic-ischemic injury in perinatal brain by intervening at caspase-XIAP signaling cascades
    Juliet C Russell
    The Kennedy Krieger Research Institute, Baltimore, MD 21205, USA
    Neurobiol Dis 22:677-90. 2006

Research Grants

Collaborators

Detail Information

Publications13

  1. doi request reprint Sex differences in mitochondrial biogenesis determine neuronal death and survival in response to oxygen glucose deprivation and reoxygenation
    Jaswinder Sharma
    Department of Neurology, The Hugo W, Moser Research Institute at Kennedy Krieger, Baltimore, MD, USA
    BMC Neurosci 15:9. 2014
    ..However, the role of mitochondrial biogenesis in hypoxic-ischemic brain injury between male vs. female has not been studied yet...
  2. pmc Hypoxic-ischemic injury in neonatal brain: involvement of a novel neuronal molecule in neuronal cell death and potential target for neuroprotection
    Mir Ahamed Hossain
    Department of Neurology, The Johns Hopkins University School of Medicine and The Kennedy Krieger Research Institute, Baltimore, MD 21205, USA
    Int J Dev Neurosci 26:93-101. 2008
    ..These very novel results could lead to more effective neuroprotective strategies against hypoxic-ischemic brain injury in neonates...
  3. ncbi request reprint Molecular mediators of hypoxic-ischemic injury and implications for epilepsy in the developing brain
    Mir Ahamed Hossain
    Department of Neurology, The Johns Hopkins University School of Medicine and The Kennedy Krieger Research Institute, Baltimore, MD 21205, USA
    Epilepsy Behav 7:204-13. 2005
    ....
  4. ncbi request reprint Neuronal pentraxin 1: a novel mediator of hypoxic-ischemic injury in neonatal brain
    Mir Ahamed Hossain
    Department of Neurology, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA
    J Neurosci 24:4187-96. 2004
    ..05), implicating a role for NP1 in the excitotoxic cascade. Our results show that NP1 induction mediates hypoxic-ischemic injury probably by interacting with and modulating GluR1 and potentially other excitatory glutamate receptors...
  5. ncbi request reprint Neuroprotection by scatter factor/hepatocyte growth factor and FGF-1 in cerebellar granule neurons is phosphatidylinositol 3-kinase/akt-dependent and MAPK/CREB-independent
    Mir Ahamed Hossain
    Department of Neurology, The Johns Hopkins University School of Medicine, Baltimore, Maryland, USA
    J Neurochem 81:365-78. 2002
    ..These data show that both SF/HGF and FGF-1 protect cerebellar granule neurons against excitotoxicity with similar potency in a P13-K/Akt-dependent and MAP-kinase/CREB-independent manner...
  6. ncbi request reprint Induction of vascular endothelial growth factor in human astrocytes by lead. Involvement of a protein kinase C/activator protein-1 complex-dependent and hypoxia-inducible factor 1-independent signaling pathway
    M A Hossain
    Departments of Neurology, Neuroscience, and Oncology, The Johns Hopkins University School of Medicine and The Kennedy Krieger Research Institute, Baltimore, Maryland 21205, USA
    J Biol Chem 275:27874-82. 2000
    ..These findings indicate that lead induces VEGF expression in SV-FHAs via a PKC/AP-1-dependent and HIF-1-independent signaling pathway...
  7. ncbi request reprint Human FGF-1 gene delivery protects against quinolinate-induced striatal and hippocampal injury in neonatal rats
    M A Hossain
    1Department of Neurology, The Johns Hopkins University School of Medicine, USA 2The Kennedy Krieger Research Institute, Baltimore, MD 21205, USA
    Eur J Neurosci 10:2490-9. 1998
    ..Our results show that intracerebral FGF-1 gene expression within the developing brain can protect striatum and hippocampus from quinolinate-mediated injury...
  8. ncbi request reprint Microarray analysis of differential gene expression in lead-exposed astrocytes
    C M Bouton
    Department of Neuroscience, Johns Hopkins University, Baltimore, Maryland 21205, USA
    Toxicol Appl Pharmacol 176:34-53. 2001
    ..We conclude that microarray technology is an effective tool for the identification of lead-induced patterns of gene expression and molecular targets of lead...
  9. pmc Akt as a mediator of cell death
    Hongbo R Luo
    Department of Neuroscience, Johns Hopkins University School of Medicine, 725 North Wolfe Street, Baltimore, MD 21205, USA
    Proc Natl Acad Sci U S A 100:11712-7. 2003
    ..Infection of neurons with adenovirus expressing constitutively active Akt prevents excitotoxicity, whereas phosphatidylinositol 3-kinase inhibitors or infection with dominant negative Akt induce death of untreated neuronal cells...
  10. ncbi request reprint Transgenic expression of human FGF-1 protects against hypoxic-ischemic injury in perinatal brain by intervening at caspase-XIAP signaling cascades
    Juliet C Russell
    The Kennedy Krieger Research Institute, Baltimore, MD 21205, USA
    Neurobiol Dis 22:677-90. 2006
    ....
  11. doi request reprint Nuclear translocation of X-linked inhibitor of apoptosis (XIAP) determines cell fate after hypoxia ischemia in neonatal brain
    Juliet C Russell
    The Hugo W Moser Research Institute at Kennedy Krieger, Baltimore, Maryland, USA
    J Neurochem 106:1357-70. 2008
    ..This is evidenced by the enhanced caspase 3 activity and neuronal death. Our findings implicate XIAP nuclear translocation in neuronal death and point to a novel mechanism in the regulation of hypoxic-ischemic brain injury...
  12. pmc Scatter factor/hepatocyte growth factor stimulation of glioblastoma cell cycle progression through G(1) is c-Myc dependent and independent of p27 suppression, Cdk2 activation, or E2F1-dependent transcription
    Kevin A Walter
    Department of Neurosurgery, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA
    Mol Cell Biol 22:2703-15. 2002
    ..We conclude that SF/HGF prevents G(1)/G(0) arrest in glioma cell lines by a c-myc-dependent mechanism that is independent of p27, Cdk2, or E2F1...
  13. ncbi request reprint Vascular endothelial growth factor mediates vasogenic edema in acute lead encephalopathy
    Mir Ahamed Hossain
    Department of Neurology, The Johns Hopkins University School of Medicine, Baltimore, Maryland, USA
    Ann Neurol 55:660-7. 2004
    ..This establishes that Pb(2+)-induced vasogenic edema formation develops via a Flk-1-dependent mechanism and suggests that the vascular permeability caused by Pb(2+) is Flk-1 independent...

Research Grants6

  1. Neurotrophin Protection of Hypoxic Ischemic Brain Injury
    MIR HOSSAIN; Fiscal Year: 2007
    ..Our findings will contribute to the development of therapeutic strategies for treating hypoxic ischemic neonatal brain injury. ..
  2. Neurotrophin Protection of Hypoxic Ischemic Brain Injury
    Mir Ahamed Hossain; Fiscal Year: 2010
    ..Our findings will contribute towards the development of preventive or therapeutic interventions for this major human health problem in the United States and in the world. ..