The Experts below are selected from a list of 10248 Experts worldwide ranked by ideXlab platform

Judy M. Teale - One of the best experts on this subject based on the ideXlab platform.

  • Changes in gene expression of pial vessels of the blood brain barrier during murine neurocysticercosis.
    PLoS neglected tropical diseases, 2013
    Co-Authors: Pramod Kumar Mishra, Judy M. Teale
    Abstract:

    In murine neurocysticercosis (NCC), caused by infection with the parasite Mesocestoides corti, the breakdown of the Blood Brain Barrier (BBB) and associated leukocyte infiltration into the CNS is dependent on the anatomical location and type of vascular bed. Prior studies of NCC show that the BBB comprised of pial vessels are most affected in comparison to the BBB associated with the vasculature of other compartments, particularly parenchymal vessels. Herein, we describe a comprehensive study to characterize infection-induced changes in the genome wide gene expression of pial vessels using laser capture microdissection microscopy (LCM) combined with microarray analyses. Of the 380 genes that were found to be affected, 285 were upregulated and 95 were downregulated. Ingenuity Pathway Analysis (IPA) software was then used to assess the biological significance of differentially expressed genes. The most significantly affected networks of genes were “inflammatory response, cell-to-cell signaling and interaction, cellular movement”, “cellular movement, Hematological System development and function, immune cell trafficking, and “antimicrobial response, cell-to-cell signaling and interaction embryonic development”. RT-PCR analyses validated the pattern of gene expression obtained from microarray analysis. In addition, chemokines CCL5 and CCL9 were confirmed at the protein level by immunofluorescence (IF) microscopy. Our data show altered gene expression related to immune and physiological functions and collectively provide insight into changes in BBB disruption and associated leukocyte infiltration during murine NCC.

  • Changes in Gene Expression of Pial Vessels of the Blood
    2013
    Co-Authors: Brain Barrier, Murine Neurocysticercosis, Pramod Kumar Mishra, Judy M. Teale
    Abstract:

    In murine neurocysticercosis (NCC), caused by infection with the parasite Mesocestoides corti, the breakdown of the Blood Brain Barrier (BBB) and associated leukocyte infiltration into the CNS is dependent on the anatomical location and type of vascular bed. Prior studies of NCC show that the BBB comprised of pial vessels are most affected in comparison to the BBB associated with the vasculature of other compartments, particularly parenchymal vessels. Herein, we describe a comprehensive study to characterize infection-induced changes in the genome wide gene expression of pial vessels using laser capture microdissection microscopy (LCM) combined with microarray analyses. Of the 380 genes that were found to be affected, 285 were upregulated and 95 were downregulated. Ingenuity Pathway Analysis (IPA) software was then used to assess the biological significance of differentially expressed genes. The most significantly affected networks of genes were ‘‘inflammatory response, cell-to-cell signaling and interaction, cellular movement’’, ‘‘cellular movement, Hematological System development and function, immune cell trafficking, and ‘‘antimicrobial response, cell-to-cell signaling and interaction embryonic development’’. RT-PCR analyses validated the pattern of gene expression obtained from microarray analysis. In addition, chemokines CCL5 and CCL9 were confirmed at the protein level by immunofluorescence (IF) microscopy. Our data show altered gene expression related to immune and physiological functions and collectively provid

Pramod Kumar Mishra - One of the best experts on this subject based on the ideXlab platform.

  • Changes in gene expression of pial vessels of the blood brain barrier during murine neurocysticercosis.
    PLoS neglected tropical diseases, 2013
    Co-Authors: Pramod Kumar Mishra, Judy M. Teale
    Abstract:

    In murine neurocysticercosis (NCC), caused by infection with the parasite Mesocestoides corti, the breakdown of the Blood Brain Barrier (BBB) and associated leukocyte infiltration into the CNS is dependent on the anatomical location and type of vascular bed. Prior studies of NCC show that the BBB comprised of pial vessels are most affected in comparison to the BBB associated with the vasculature of other compartments, particularly parenchymal vessels. Herein, we describe a comprehensive study to characterize infection-induced changes in the genome wide gene expression of pial vessels using laser capture microdissection microscopy (LCM) combined with microarray analyses. Of the 380 genes that were found to be affected, 285 were upregulated and 95 were downregulated. Ingenuity Pathway Analysis (IPA) software was then used to assess the biological significance of differentially expressed genes. The most significantly affected networks of genes were “inflammatory response, cell-to-cell signaling and interaction, cellular movement”, “cellular movement, Hematological System development and function, immune cell trafficking, and “antimicrobial response, cell-to-cell signaling and interaction embryonic development”. RT-PCR analyses validated the pattern of gene expression obtained from microarray analysis. In addition, chemokines CCL5 and CCL9 were confirmed at the protein level by immunofluorescence (IF) microscopy. Our data show altered gene expression related to immune and physiological functions and collectively provide insight into changes in BBB disruption and associated leukocyte infiltration during murine NCC.

  • Changes in Gene Expression of Pial Vessels of the Blood
    2013
    Co-Authors: Brain Barrier, Murine Neurocysticercosis, Pramod Kumar Mishra, Judy M. Teale
    Abstract:

    In murine neurocysticercosis (NCC), caused by infection with the parasite Mesocestoides corti, the breakdown of the Blood Brain Barrier (BBB) and associated leukocyte infiltration into the CNS is dependent on the anatomical location and type of vascular bed. Prior studies of NCC show that the BBB comprised of pial vessels are most affected in comparison to the BBB associated with the vasculature of other compartments, particularly parenchymal vessels. Herein, we describe a comprehensive study to characterize infection-induced changes in the genome wide gene expression of pial vessels using laser capture microdissection microscopy (LCM) combined with microarray analyses. Of the 380 genes that were found to be affected, 285 were upregulated and 95 were downregulated. Ingenuity Pathway Analysis (IPA) software was then used to assess the biological significance of differentially expressed genes. The most significantly affected networks of genes were ‘‘inflammatory response, cell-to-cell signaling and interaction, cellular movement’’, ‘‘cellular movement, Hematological System development and function, immune cell trafficking, and ‘‘antimicrobial response, cell-to-cell signaling and interaction embryonic development’’. RT-PCR analyses validated the pattern of gene expression obtained from microarray analysis. In addition, chemokines CCL5 and CCL9 were confirmed at the protein level by immunofluorescence (IF) microscopy. Our data show altered gene expression related to immune and physiological functions and collectively provid

Thomas A Gasiewicz - One of the best experts on this subject based on the ideXlab platform.

  • aryl hydrocarbon receptor activation in hematopoietic stem progenitor cells alters cell function and pathway specific gene modulation reflecting changes in cellular trafficking and migration
    Molecular Pharmacology, 2011
    Co-Authors: Fanny L Casado, K P Singh, Thomas A Gasiewicz
    Abstract:

    The aryl hydrocarbon receptor (AhR) is a transcription factor belonging to the Per-ARNT-Sim family of proteins. These proteins sense molecules and stimuli from the cellular/tissue environment and initiate signaling cascades to elicit appropriate cellular responses. Recent literature reports suggest an important function of AhR in hematopoietic stem cell (HSC) biology. However, the molecular mechanisms by which AhR signaling regulates HSC functions are unknown. In previous studies, we and others reported that treatment of mice with the AhR agonist 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) compromises the competitive reconstitution of bone marrow (BM) cells into irradiated host animals. Additional studies indicated a requirement for AhR in hematopoietic cells and not marrow microenvironment cells. In this study, we tested the hypothesis that TCDD-mediated phenotypic and functional changes of HSCs are a result of changes in gene expression that disrupt stem cell numbers and/or their migration. TCDD treatment to mice increased the numbers of phenotypically defined HSCs in BM. These cells showed compromised migration to the BM in vivo and to the chemokine CXCL12 in vitro, as well as increased expression of the leukemia-associated receptors CD184 (CXCR4) and CD44. Gene expression profiles at 6 and 12 h after exposure were consistent with the phenotypic and functional changes observed. The expressions of Scin, Nqo1, Flnb, Mmp8, Ilf9, and Slamf7 were consistently altered. TCDD also disrupted expression of other genes involved in Hematological System development and function including Fos, JunB, Egr1, Ptgs2 (Cox2), and Cxcl2. These data support a molecular mechanism for an AhR ligand to disrupt the homeostatic cell signaling of HSCs that may promote altered HSC function.

Fanny L Casado - One of the best experts on this subject based on the ideXlab platform.

  • aryl hydrocarbon receptor activation in hematopoietic stem progenitor cells alters cell function and pathway specific gene modulation reflecting changes in cellular trafficking and migration
    Molecular Pharmacology, 2011
    Co-Authors: Fanny L Casado, K P Singh, Thomas A Gasiewicz
    Abstract:

    The aryl hydrocarbon receptor (AhR) is a transcription factor belonging to the Per-ARNT-Sim family of proteins. These proteins sense molecules and stimuli from the cellular/tissue environment and initiate signaling cascades to elicit appropriate cellular responses. Recent literature reports suggest an important function of AhR in hematopoietic stem cell (HSC) biology. However, the molecular mechanisms by which AhR signaling regulates HSC functions are unknown. In previous studies, we and others reported that treatment of mice with the AhR agonist 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) compromises the competitive reconstitution of bone marrow (BM) cells into irradiated host animals. Additional studies indicated a requirement for AhR in hematopoietic cells and not marrow microenvironment cells. In this study, we tested the hypothesis that TCDD-mediated phenotypic and functional changes of HSCs are a result of changes in gene expression that disrupt stem cell numbers and/or their migration. TCDD treatment to mice increased the numbers of phenotypically defined HSCs in BM. These cells showed compromised migration to the BM in vivo and to the chemokine CXCL12 in vitro, as well as increased expression of the leukemia-associated receptors CD184 (CXCR4) and CD44. Gene expression profiles at 6 and 12 h after exposure were consistent with the phenotypic and functional changes observed. The expressions of Scin, Nqo1, Flnb, Mmp8, Ilf9, and Slamf7 were consistently altered. TCDD also disrupted expression of other genes involved in Hematological System development and function including Fos, JunB, Egr1, Ptgs2 (Cox2), and Cxcl2. These data support a molecular mechanism for an AhR ligand to disrupt the homeostatic cell signaling of HSCs that may promote altered HSC function.

Etheresia Pretorius - One of the best experts on this subject based on the ideXlab platform.

  • iron dysregulation and dormant microbes as causative agents for impaired blood rheology and pathological clotting in alzheimer s type dementia
    Frontiers in Neuroscience, 2018
    Co-Authors: Lesha Pretorius, Douglas B Kell, Etheresia Pretorius
    Abstract:

    : Alzheimer's disease and other similar dementias are debilitating neurodegenerative disorders whose etiology and pathogenesis remain largely unknown, even after decades of research. With the anticipated increase in prevalence of Alzheimer's type dementias among the more susceptible aging population, the need for disease-modifying treatments is urgent. While various hypotheses have been put forward over the last few decades, we suggest that Alzheimer's type dementias are triggered by external environmental factors, co-expressing in individuals with specific genetic susceptibilities. These external stressors are defined in the Iron Dysregulation and Dormant Microbes (IDDM) hypothesis, previously put forward. This hypothesis is consistent with current literature in which serum ferritin levels of individuals diagnosed with Alzheimer's disease are significantly higher compared those of age- and gender-matched controls. While iron dysregulation contributes to oxidative stress, it also causes microbial reactivation and virulence of the so-called dormant blood (and tissue) microbiome. Dysbiosis (changes in the microbiome) or previous infections can contribute to the dormant blood microbiome (atopobiosis), and also directly promotes Systemic inflammation via the amyloidogenic formation and shedding of potent inflammagens such as lipopolysaccharides. The simultaneous iron dysregulation and microbial aberrations affect the Hematological System, promoting fibrin amylodiogenesis, and pathological clotting. Systemic inflammation and oxidative stress can contribute to blood brain barrier permeability and the ensuing neuro-inflammation, characteristic of Alzheimer's type dementias. While large inter-individual variability exists, especially concerning disease pathogenesis, the IDDM hypothesis acknowledges primary causative factors which can be targeted for early diagnosis and/or for prevention of disease progression.

  • the stabilizing effect of an oligomeric proanthocyanidin on red blood cell membrane structure of poorly controlled type ii diabetes
    Nutrition & Diabetes, 2017
    Co-Authors: J Visser, P Van Staden, Prashilla Soma, Antoinette V Buys, Etheresia Pretorius
    Abstract:

    Type II diabetes (T2D) is a pandemic characterized by pathological circulating inflammatory markers, high-glucose levels and oxidative stress. The Hematological System is especially vulnerable to these aberrant circulating molecules, and erythrocytes (RBCs) show aberrant rheology properties, owing to the direct contact with these molecules. Pathological levels of circulating inflammatory markers in T2D therefore have a direct effect on the molecular and cellular structure of RBCs. Previous research has suggested that antioxidants may reduce oxidative stress that results from the pathological inflammatory markers. Particularly, polyphenol antioxidants like oligomeric proanthocyanidins (OPCs) may act as a hydroxyl mopping agent, and may have a positive effect on the deformability and membrane protein structure of RBCs from T2D. In this paper, we look at the effect of one such agent, Pinus massoniana bark extract (standardized to 95% oligomeric proanthicyanidins), on the RBC membrane structures and RBC shape changes of T2D, after laboratory exposure at physiological levels. Our methods of choice were atomic force microscopy and scanning electron microscopy to study RBC elasticity and ultrastructure. Results showed that in our hands, this OPC could change both the eryptotic nature of the RBCs, as viewed with scanning electron microscopy, as well as the elasticity. We found a significant difference in variation between the elasticity measurement values between the RBCs before and after OPC exposure (P-value <0.0001). In conclusion, the data from both these techniques therefore suggest that OPC usage might contribute to the improvement of RBC functioning.