Topics (27) View all

Questions and Answers (4) View all

  • Answer added in Neuroinflammation
    18 Microglial staining with Iba1 is displaying a lot of background.
    By Kanchan Bisht · ETH Zurich
    Ganta Chaitanya · Louisiana State University Health Sciences Center Shreveport
    I recently found out that some antibodies doesnt like blocking step. For example, I was using similar steps in the immunostaining protocol described b... [more]
  • Answer added in Neurobiology
    9 Does anyone know of an antibody to demonstrate changes in neuronal dendrites following ischemic damage?
    By James Bourne · Monash University
    Ganta Chaitanya · Louisiana State University Health Sciences Center Shreveport
    Synaptophysin or neuronal filament antibodies might also be useful markers. If you have expertise, I consider Golgi staining as one of the best metho... [more]
  • Answer added in Angiogenesis
    10 Is there a way to grow HUVECs on a matrigel coated permeable insert to form a confluent monolayer as opposed to differentiate into tubes?
    By Yavor Denchev · University of Victoria
    Ganta Chaitanya · Louisiana State University Health Sciences Center Shreveport
    Hi Yavor, In my experiments, we perform TEER measurements and matrigel separately. I think once the cells are plated on matrigel, since they try to f... [more]
  • Answer added in Cell Culture
    4 Will 3D matrix (matrigel, cultrex, etc) help?
    By Bernard Okere · Università degli Studi di Modena e Reggio Emilia
    Ganta Chaitanya · Louisiana State University Health Sciences Center Shreveport
    Extracellular matrix proteins can influence the characters of epithelial/endothelial cells. I used matrigel not for growing or differentiation of epit... [more]

Publications (22) View all

  • Source
    Article: Focus on carbon monoxide: a modulator of neutrophil oxidants and elastase spatial localization?
    V C Ganta, J S Alexander
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    ABSTRACT: The protective roles of CO in various patho-physiological conditions are rapidly expanding. We are only beginning to understand how this gaseous signal molecule exerts such diverse cell and model specific effects. CO interacts in NO signaling, and is an activator of guanylate cyclase/PKG. However several downstream molecular signals mediated by CO (p38-MAPK, ERK1/2) may be oxidant dependent. How CO affects these and other signaling pathways in PMN is not well understood, but is of immense clinical interest. The present study by Mizoguchi et al. describes cell-specific roles of CORM-3 derived CO in protecting the lung against neutrophil dependent septic injury. Importantly, CO donors appear to only affect neutrophils and may involve a novel mechanism whereby CO induces the shedding of neutrophil elastase from the active front of the neutrophil. Shedding of this protease, and neutrophil rolling and adhesion were also inhibited by CO in a novel fashion involving elevation of ROS species. The involvement of various cellular ROS production sites (especially mitochondria); their mechanisms and the potential therapeutic benefit of CO donors like CORM-3 are discussed. Key words: elastase, hemoxygenase, lung injury, CO.
    AJP Heart and Circulatory Physiology 08/2009; 297(3):H902-4. · 3.71 Impact Factor
  • Source
    Article: Discovery of transcriptional programs in cerebral ischemia by in silico promoter analysis.
    [show abstract] [hide abstract]
    ABSTRACT: In stroke, gene transcription plays a central role in processes such as neuroinflammation and neuroregeneration. To predict new transcriptional regulatory mechanisms in cerebral ischemia, we applied a computational approach combining two kinds of information: the results of a microarray analysis in a mouse model of stroke and in silico detection of transcription factor (TF) binding sites in promoter regions of the genes on the array. By using a discriminative logistic regression model, we identified binding sites significantly associated with the up-regulation of genes. Out of 356 TF binding sites defined in TRANSFAC, we could link 32 to gene up-regulation in cerebral ischemia. These sites bind both TFs with an established and a so far unknown role in cerebral ischemia. To evaluate the results further we investigated whether two TFs, CCAAT/enhancer binding protein beta (C/EBP beta) and vitamin D receptor (VDR), are activated as predicted. Immunohistochemistry demonstrated that C/EBP beta and VDR translocated to the nucleus in cerebral ischemia. Chromatin immunoprecipitation revealed increased binding of C/EBP beta to the promoter of its target gene saa3. In addition, we found evidence for the up-regulation of VDR in brain samples from human stroke patients. These results confirm the activation of C/EBP beta and VDR in cerebral ischemia. Thus, our in silico analysis may provide additional information on transcriptional regulation in stroke and suggests several novel transcriptional programs for further exploration.
    Brain research 04/2009; 1272:3-13. · 2.46 Impact Factor
  • Source
    Article: Granzyme-b mediated cell death in the spinal cord-injured rat model.
    Ganta Vijay Chaitanya, Mayuri Kolli, Phanithi Prakash Babu
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    ABSTRACT: Spinal cord injury initiates a complex series of inflammatory and immune responses including the influx of monocytes, macrophages, T-cells, NK cells and so on, into the injured area. In the present study, we found a significant increase in the levels of granzyme-b (gra-b) from the first day after the transection until the third day, with decrease in intensity thereafter. The chemokine IP-10/CXCL10 was also found to be elevated along with gra-b correlating with the infiltration of CD-8(+) cytotoxic T lymphocytes (CTLs) into the injured spinal cord. We observed an increase in the levels of the 64 kDa poly ADP ribose polymerase fragment, known to be a signature fragment produced by gra-b. Localization of gra-b in TUNEL positive neurons indicates that gra-b might play a crucial role in neuronal death and contributes to the pathophysiology of spinal cord injury.
    Neuropathology 01/2009; 29(3):270-9. · 2.02 Impact Factor
  • Article: Expanding roles of glutamate receptors in neurovascular regulation.
    J S Alexander, Chaitanya V Ganta
    Vascular Pharmacology 03/2012; 57(1):1-2. · 1.99 Impact Factor
  • Source
    Article: Multiple apoptogenic proteins are involved in the nuclear translocation of Apoptosis Inducing Factor during transient focal cerebral ischemia in rat.
    Ganta Vijay Chaitanya, Phanithi Prakash Babu
    [show abstract] [hide abstract]
    ABSTRACT: Apoptosis Inducing Factor is a mitochondrial protein which upon translocation to nucleus causes large scale DNA fragmentation. The stimulus for the cytosolic release and nuclear translocation for this protein still remains to be understood. The role of calpains, cathepsin-b, Poly ADP (ribose) Polymerase and granzyme-b in the nuclear translocation of AIF has been investigated in the pathology of cerebral ischemia. Calpains, cathepsin-b and PARP-1 which were mostly confined to cytosol, lysosomes and nucleus respectively were found to be elevated in the mitochondrial fraction interacting with AIF in the western blot analysis and double immunofluorescence analysis. Western blot and immunohistochemical analysis revealed elevated levels of granzyme-b secreted by cytotoxic T lymphocytes and natural killer cells in the infarct of ischemic mouse brain. Co-immunoprecipitation revealed and western blot analysis the interaction and break down of Heat Shock Protein-70 an endogenous inhibitor of AIF into signature fragments by granzyme-b facilitating the nuclear translocation of AIF. Break down of HSP-70 correlated with the nuclear translocation of AIF observed in western and immunohistochemical analysis. These results indicate that multiple proteases were involved in the nuclear translocation of AIF during the pathology of cerebral ischemia.
    Brain research 11/2008; 1246:178-90. · 2.46 Impact Factor

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