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Article: Structural, Functional, and Metabolic Alterations in Human Cerebrovascular Endothelial Cells during

Al-Sandaqchi, Alaa T / Marsh, Victoria / Williams, Huw E L / Stevenson, Carl W / Elsheikha, Hany M

2020 Volume 8, Issue 9

Abstract: Toxoplasma ... ...

Abstract	Toxoplasma gondii
Language	English
Publishing date	2020-09-10
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2720891-6
ISSN	2076-2607
ISSN	2076-2607
DOI	10.3390/microorganisms8091386
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Article ; Online: Effects of Toxoplasma gondii infection on the function and integrity of human cerebrovascular endothelial cells and the influence of verapamil treatment in vitro.

Harun, M S R / Marsh, Victoria / Elsaied, Nashwa A / Webb, Kevin F / Elsheikha, Hany M

Brain research

2020 Volume 1746, Page(s) 147002

Abstract: Toxoplasma gondii can cause parasitic encephalitis, a life-threatening infection that predominately occurs in immunocompromised individuals. T. gondii has the ability to invade the brain, but the mechanisms by which this parasite crosses the blood-brain- ... ...

Abstract	Toxoplasma gondii can cause parasitic encephalitis, a life-threatening infection that predominately occurs in immunocompromised individuals. T. gondii has the ability to invade the brain, but the mechanisms by which this parasite crosses the blood-brain-barrier (BBB) remain incompletely understood. The present study reports the changes associated with infection and replication of T. gondii within human brain microvascular endothelial cells (BMECs) in vitro. Our results indicated that exposure to T. gondii had an adverse impact on the function and integrity of the BMECs - through induction of cell cycle arrest, disruption of the BMEC barrier integrity, reduction of cellular viability and vitality, depolarization of the mitochondrial membrane potential, increase of the DNA fragmentation, and alteration of the expression of immune response and tight junction genes. The calcium channel/P-glycoprotein transporter inhibitor verapamil was effective in inhibiting T. gondii crossing the BMECs in a dose-dependent manner. The present study showed that T. gondii can compromise several functions of BMECs and demonstrated the ability of verapamil to inhibit T. gondii crossing of the BMECs in vitro.
MeSH term(s)	Blood-Brain Barrier/drug effects ; Blood-Brain Barrier/metabolism ; Blood-Brain Barrier/physiopathology ; Brain/drug effects ; Brain/metabolism ; Brain/physiopathology ; Calcium Channel Blockers/pharmacology ; Cells, Cultured ; Endothelial Cells/drug effects ; Endothelial Cells/metabolism ; Endothelial Cells/pathology ; Humans ; Toxoplasmosis/metabolism ; Toxoplasmosis/pathology ; Toxoplasmosis/physiopathology ; Verapamil/pharmacology
Chemical Substances	Calcium Channel Blockers ; Verapamil (CJ0O37KU29)
Language	English
Publishing date	2020-06-24
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1200-2
ISSN	1872-6240 ; 0006-8993
ISSN (online)	1872-6240
ISSN	0006-8993
DOI	10.1016/j.brainres.2020.147002
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Article: Structural, Functional, and Metabolic Alterations in Human Cerebrovascular Endothelial Cells during Toxoplasma gondii Infection and Amelioration by Verapamil In Vitro

Al-sandaqchi, Alaa T. / Marsh, Victoria / Williams, Huw E. L. / Stevenson, Carl W. / Elsheikha, Hany M.

Microorganisms. 2020 Sept. 10, v. 8, no. 9

2020

Abstract: Toxoplasma gondii (T. gondii), the causative agent of toxoplasmosis, is a frequent cause of brain infection. Despite its known ability to invade the brain, there is still a dire need to better understand the mechanisms by which this parasite interacts ... ...

Abstract	Toxoplasma gondii (T. gondii), the causative agent of toxoplasmosis, is a frequent cause of brain infection. Despite its known ability to invade the brain, there is still a dire need to better understand the mechanisms by which this parasite interacts with and crosses the blood–brain barrier (BBB). The present study revealed structural and functional changes associated with infection and replication of T. gondii within human brain microvascular endothelial cells (BMECs) in vitro. T. gondii proliferated within the BMECs and disrupted the integrity of the cerebrovascular barrier through diminishing the cellular viability, disruption of the intercellular junctions and increasing permeability of the BMEC monolayer, as well as altering lipid homeostasis. Proton nuclear magnetic resonance (¹H NMR)-based metabolomics combined with multivariate data analysis revealed profiles that can be attributed to infection and variations in the amounts of certain metabolites (e.g., amino acids, fatty acids) in the extracts of infected compared to control cells. Notably, treatment with the Ca²⁺ channel blocker verapamil rescued BMEC barrier integrity and restricted intracellular replication of the tachyzoites regardless of the time of treatment application (i.e., prior to infection, early- and late-infection). This study provides new insights into the structural and functional changes that accompany T. gondii infection of the BMECs, and sheds light upon the ability of verapamil to inhibit the parasite proliferation and to ameliorate the adverse effects caused by T. gondii infection.
Keywords	Toxoplasma gondii ; blood-brain barrier ; brain ; calcium ; cell viability ; etiological agents ; homeostasis ; humans ; metabolites ; metabolomics ; multivariate analysis ; nuclear magnetic resonance spectroscopy ; parasites ; permeability ; tachyzoites ; toxoplasmosis ; verapamil
Language	English
Dates of publication	2020-0910
Publishing place	Multidisciplinary Digital Publishing Institute
Document type	Article
ZDB-ID	2720891-6
ISSN	2076-2607
ISSN	2076-2607
DOI	10.3390/microorganisms8091386
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Intestinal homeostasis and neoplasia studied using conditional transgenesis.

Marsh, Victoria / Clarke, Alan

Expert review of anticancer therapy

2007 Volume 7, Issue 4, Page(s) 519–531

Abstract: Constitutive mouse models of intestinal neoplasia, such as the Apc(min/+) (multiple intestinal neoplasia) mouse have proven valuable tools both for furthering our understanding of tumorigenesis and for the development of therapeutic strategies. However, ... ...

Abstract	Constitutive mouse models of intestinal neoplasia, such as the Apc(min/+) (multiple intestinal neoplasia) mouse have proven valuable tools both for furthering our understanding of tumorigenesis and for the development of therapeutic strategies. However, the in vivo study of a number of genes has been precluded by their absolute requirement during embryonic development. This has led to the development of conditional strategies that allow gene regulation in vivo. This review describes the principal techniques used to achieve conditional transgenesis within the mouse intestine, with a particular focus upon the Cre-Lox and Tet-regulable systems. Further, we discuss how these techniques are being used to dissect the mechanisms governing both normal homeostasis and neoplastic development within the intestine.
MeSH term(s)	Animals ; Disease Models, Animal ; Gene Transfer Techniques ; Homeostasis/genetics ; Humans ; Intestinal Neoplasms/genetics ; Intestinal Neoplasms/metabolism ; Mice ; Signal Transduction/genetics ; Wnt Proteins/biosynthesis ; Wnt Proteins/genetics
Chemical Substances	Wnt Proteins
Language	English
Publishing date	2007-04-11
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	2112544-2
ISSN	1744-8328 ; 1473-7140
ISSN (online)	1744-8328
ISSN	1473-7140
DOI	10.1586/14737140.7.4.519
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Zs.A 5907: Show issues

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Article ; Online: Origin and maintenance of the intestinal cancer stem cell.

Davies, Emma J / Marsh, Victoria / Clarke, Alan R

Molecular carcinogenesis

2011 Volume 50, Issue 4, Page(s) 254–263

Abstract: Colorectal cancer is one of the most common cancers in the western world and its incidence is steadily increasing. Understanding the basic biology of both the normal intestine and of intestinal tumorigenesis is vital for developing appropriate and ... ...

Abstract	Colorectal cancer is one of the most common cancers in the western world and its incidence is steadily increasing. Understanding the basic biology of both the normal intestine and of intestinal tumorigenesis is vital for developing appropriate and effective cancer therapies. However, relatively little is known about the normal intestinal stem cell or the hypothetical intestinal cancer stem cell, and there is much debate surrounding these areas. This review briefly describes our current understanding of the properties of both the intestinal stem cell and the intestinal cancer stem cell. We also discuss recent theories regarding the origin of the intestinal cancer stem cell, and the signals required for its maintenance and proliferation. Finally, we place the relevance of cancer stem cell research into context by discussing potential clinical applications of targeting the intestinal cancer stem cell.
MeSH term(s)	Animals ; Cell Differentiation ; Cell Lineage ; Colorectal Neoplasms/pathology ; Humans ; Intestines/cytology ; Neoplastic Stem Cells/pathology ; Signal Transduction ; Stem Cells/cytology
Language	English
Publishing date	2011-04
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	1004029-8
ISSN	1098-2744 ; 0899-1987
ISSN (online)	1098-2744
ISSN	0899-1987
DOI	10.1002/mc.20631
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Zs.A 2664: Show issues

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Article ; Online: PTEN loss and KRAS activation cooperate in murine biliary tract malignancies.

Marsh, Victoria / Davies, Emma J / Williams, Geraint T / Clarke, Alan R

The Journal of pathology

2013 Volume 230, Issue 2, Page(s) 165–173

Abstract: Carcinomas of the biliary tract are aggressive malignancies in humans. Loss of the tumour suppressor PTEN has previously been associated with cholangiocarcinoma development in a murine model. Activation of KRAS is reported in up to one-third of human ... ...

Abstract	Carcinomas of the biliary tract are aggressive malignancies in humans. Loss of the tumour suppressor PTEN has previously been associated with cholangiocarcinoma development in a murine model. Activation of KRAS is reported in up to one-third of human cholangiocarcinomas and 50% of gall bladder carcinomas. In this study we aimed to test the potential interaction between PTEN and KRAS mutation in biliary tract malignancy. We used an inducible Cre-LoxP-based approach to coordinately delete PTEN and activate KRAS within the adult mouse biliary epithelium. We found that activation of KRAS alone has little effect upon biliary epithelium. Loss of PTEN alone results in the development of low-grade neoplastic lesions, following long latency and at low incidence. Combination of both mutations causes rapid development of biliary epithelial proliferative lesions, which progress through dysplasia to invasive carcinoma. We conclude that activation of the PI3'K pathway following loss of PTEN is sufficient to drive slow development of low-grade biliary lesions in mice. In contrast, mutational activation of KRAS does not result in a similar phenotype, despite a prediction that this should activate both the RAF-MEK-ERK and PI3'-kinase pathways. However, mutation of both genes results in rapid tumourigenesis, arguing that PTEN normally functions as a 'brake' on the PI3'-kinase pathway, limiting the influence of KRAS activation. Mutation of both genes creates a 'permissive' environment, allowing the full effects of both mutations to be manifested. These data reveal an in vivo synergy between these mutations and provides a new mouse model of biliary tract malignancy.
MeSH term(s)	Animals ; Animals, Outbred Strains ; Bile Duct Neoplasms/genetics ; Bile Duct Neoplasms/metabolism ; Bile Duct Neoplasms/mortality ; Biliary Tract/cytology ; Biliary Tract/metabolism ; Cholangiocarcinoma/genetics ; Cholangiocarcinoma/metabolism ; Cholangiocarcinoma/mortality ; Epithelial Cells/metabolism ; Extracellular Signal-Regulated MAP Kinases/genetics ; Female ; Gene Deletion ; Gene Expression Regulation, Neoplastic ; Kaplan-Meier Estimate ; Male ; Mice ; Mitogen-Activated Protein Kinase Kinases/genetics ; Mutation ; PTEN Phosphohydrolase/deficiency ; PTEN Phosphohydrolase/genetics ; PTEN Phosphohydrolase/metabolism ; Phosphatidylinositol 3-Kinases/genetics ; Phosphatidylinositol 3-Kinases/metabolism ; Proto-Oncogene Proteins B-raf/genetics ; Proto-Oncogene Proteins p21(ras)/biosynthesis ; Proto-Oncogene Proteins p21(ras)/genetics ; Survival Rate
Chemical Substances	Proto-Oncogene Proteins B-raf (EC 2.7.11.1) ; Extracellular Signal-Regulated MAP Kinases (EC 2.7.11.24) ; Mitogen-Activated Protein Kinase Kinases (EC 2.7.12.2) ; PTEN Phosphohydrolase (EC 3.1.3.67) ; Pten protein, mouse (EC 3.1.3.67) ; Hras protein, mouse (EC 3.6.5.2) ; Proto-Oncogene Proteins p21(ras) (EC 3.6.5.2)
Language	English
Publishing date	2013-03-06
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	3119-7
ISSN	1096-9896 ; 0022-3417
ISSN (online)	1096-9896
ISSN	0022-3417
DOI	10.1002/path.4189
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Article ; Online: DNA evidence for global dispersal and probable endemicity of protozoa

Matthai Lena / Richards Thomas A / Bass David / Marsh Victoria / Cavalier-Smith Thomas

BMC Evolutionary Biology, Vol 7, Iss 1, p

2007 Volume 162

Abstract: Abstract Background It is much debated whether microbes are easily dispersed globally or whether they, like many macro-organisms, have historical biogeographies. The ubiquitous dispersal hypothesis states that microbes are so numerous and so easily ... ...

Abstract	Abstract Background It is much debated whether microbes are easily dispersed globally or whether they, like many macro-organisms, have historical biogeographies. The ubiquitous dispersal hypothesis states that microbes are so numerous and so easily dispersed worldwide that all should be globally distributed and found wherever growing conditions suit them. This has been broadly upheld for protists (microbial eukaryotes) by most morphological and some molecular analyses. However, morphology and most previously used evolutionary markers evolve too slowly to test this important hypothesis adequately. Results Here we use a fast-evolving marker (ITS1 rDNA) to map global diversity and distribution of three different clades of cercomonad Protozoa ( Eocercomonas and Paracercomonas : phylum Cercozoa) by sequencing multiple environmental gene libraries constructed from 47–80 globally-dispersed samples per group. Even with this enhanced resolution, identical ITS sequences (ITS-types) were retrieved from widely separated sites and on all continents for several genotypes, implying relatively rapid global dispersal. Some identical ITS-types were even recovered from both marine and non-marine samples, habitats that generally harbour significantly different protist communities. Conversely, other ITS-types had either patchy or restricted distributions. Conclusion Our results strongly suggest that geographic dispersal in macro-organisms and microbes is not fundamentally different: some taxa show restricted and/or patchy distributions while others are clearly cosmopolitan. These results are concordant with the 'moderate endemicity model' of microbial biogeography. Rare or continentally endemic microbes may be ecologically significant and potentially of conservational concern. We also demonstrate that strains with identical 18S but different ITS1 rDNA sequences can differ significantly in terms of morphological and important physiological characteristics, providing strong additional support for global protist biodiversity being significantly higher than previously thought.
Keywords	Biology (General) ; QH301-705.5 ; Science ; Q ; DOAJ:Biology ; DOAJ:Biology and Life Sciences ; Evolution ; QH359-425
Language	English
Publishing date	2007-09-01T00:00:00Z
Publisher	BioMed Central
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Mutationally activated PIK3CA(H1047R) cooperates with BRAF(V600E) to promote lung cancer progression.

Trejo, Christy L / Green, Shon / Marsh, Victoria / Collisson, Eric A / Iezza, Gioia / Phillips, Wayne A / McMahon, Martin

Cancer research

2013 Volume 73, Issue 21, Page(s) 6448–6461

Abstract: Adenocarcinoma of the lung, a leading cause of cancer death, frequently displays mutational activation of the KRAS proto-oncogene but, unlike lung cancers expressing mutated EGFR, ROS1, or ALK, there is no pathway-targeted therapy for patients with KRAS- ... ...

Abstract	Adenocarcinoma of the lung, a leading cause of cancer death, frequently displays mutational activation of the KRAS proto-oncogene but, unlike lung cancers expressing mutated EGFR, ROS1, or ALK, there is no pathway-targeted therapy for patients with KRAS-mutated lung cancer. In preclinical models, expression of oncogenic KRAS(G12D) in the lung epithelium of adult mice initiates development of lung adenocarcinoma through activation of downstream signaling pathways. In contrast, mutationally activated BRAF(V600E), a KRAS effector, fails to initiate lung carcinogenesis despite highly efficient induction of benign lung tumorigenesis. To test if phosphoinositide 3-kinase (PI3K)-α (PIK3CA), another KRAS effector, might cooperate with oncogenic BRAF(V600E) to promote lung cancer progression, we used mice carrying a conditional allele of Pik3ca that allows conversion of the wild-type catalytic subunit of PIK3CA to mutationally activated PIK3CA(H1047R). Although expression of PIK3CA(H1047R) in the lung epithelium, either alone or in combination with PTEN silencing, was without phenotype, concomitant expression of BRAF(V600E) and PIK3CA(H1047R) led to dramatically decreased tumor latency and increased tumor burden compared with BRAF(V600E) alone. Most notably, coexpression of BRAF(V600E) and PIK3CA(H1047R) elicited lung adenocarcinomas in a manner reminiscent of the effects of KRAS(G12D). These data emphasize a role for PI3K signaling, not in lung tumor initiation per se, but in both the rate of tumor growth and the propensity of benign lung tumors to progress to a malignant phenotype. Finally, biologic and biochemical analysis of BRAF(V600E)/PIK3CA(H1047R)-expressing mouse lung cancer cells revealed mechanistic clues about cooperative regulation of the cell-division cycle and apoptosis by these oncogenes.
MeSH term(s)	Adenocarcinoma/genetics ; Adenocarcinoma/mortality ; Adenocarcinoma/pathology ; Animals ; Apoptosis ; Blotting, Western ; Cell Movement ; Cell Proliferation ; Cell Transformation, Neoplastic/pathology ; Class I Phosphatidylinositol 3-Kinases ; Disease Progression ; Immunoenzyme Techniques ; Lung Neoplasms/genetics ; Lung Neoplasms/mortality ; Lung Neoplasms/pathology ; Mice ; Mice, Knockout ; Mutation/genetics ; PTEN Phosphohydrolase/physiology ; Phosphatidylinositol 3-Kinases/physiology ; Proto-Oncogene Proteins B-raf/physiology ; Signal Transduction ; Survival Rate
Chemical Substances	Class I Phosphatidylinositol 3-Kinases (EC 2.7.1.137) ; Pik3ca protein, mouse (EC 2.7.1.137) ; Braf protein, mouse (EC 2.7.11.1) ; Proto-Oncogene Proteins B-raf (EC 2.7.11.1) ; PTEN Phosphohydrolase (EC 3.1.3.67) ; Pten protein, mouse (EC 3.1.3.67)
Language	English
Publishing date	2013-09-09
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1432-1
ISSN	1538-7445 ; 0008-5472
ISSN (online)	1538-7445
ISSN	0008-5472
DOI	10.1158/0008-5472.CAN-13-0681
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Article: Influence of chromatin and single strand binding proteins on the activity of an archaeal MCM.

Marsh, Victoria L / McGeoch, Adam T / Bell, Stephen D

Journal of molecular biology

2006 Volume 357, Issue 5, Page(s) 1345–1350

Abstract: The mini-chromosome maintenance (MCM) complex is the presumptive replicative helicase in archaea and eukaryotes. In archaea, the MCM is a homo-multimer, in eukaryotes a heterohexamer composed of six related subunits, MCM 2-7. Biochemical studies using ... ...

Abstract	The mini-chromosome maintenance (MCM) complex is the presumptive replicative helicase in archaea and eukaryotes. In archaea, the MCM is a homo-multimer, in eukaryotes a heterohexamer composed of six related subunits, MCM 2-7. Biochemical studies using naked DNA templates have revealed that archaeal MCMs and a sub-complex of eukaryotic MCM 4, 6 and 7 have 3' to 5' helicase activity. Here, we investigate the influence of the major chromatin proteins, Alba and Sul7d, of Sulfolobus solfataricus (Sso) on the ability of the MCM complex to melt partial duplex DNA substrates. In addition, we test the effect of Sso SSB on MCM activity. We reveal that Alba represents a formidable barrier to MCM activity and further demonstrate that acetylation of Alba alleviates repression of MCM activity.
MeSH term(s)	Acetylation ; Archaeal Proteins/metabolism ; Chromatin/metabolism ; DNA Helicases/metabolism ; DNA-Binding Proteins/metabolism ; Multiprotein Complexes/metabolism ; Nucleic Acid Denaturation ; Sulfolobus solfataricus/genetics ; Sulfolobus solfataricus/metabolism
Chemical Substances	Archaeal Proteins ; Chromatin ; DNA-Binding Proteins ; Multiprotein Complexes ; Sso10b protein, Sulfolobus solfataricus ; DNA Helicases (EC 3.6.4.-)
Language	English
Publishing date	2006-04-14
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80229-3
ISSN	1089-8638 ; 0022-2836
ISSN (online)	1089-8638
ISSN	0022-2836
DOI	10.1016/j.jmb.2006.01.074
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Article: Sir2 and the acetyltransferase, Pat, regulate the archaeal chromatin protein, Alba.

Marsh, Victoria L / Peak-Chew, Sew Yeu / Bell, Stephen D

The Journal of biological chemistry

2005 Volume 280, Issue 22, Page(s) 21122–21128

Abstract: The DNA binding affinity of Alba, a chromatin protein of the archaeon Sulfolobus solfataricus P2, is regulated by acetylation of lysine 16. Here we identify an acetyltransferase that specifically acetylates Alba on this residue. The effect of acetylation ...

Abstract	The DNA binding affinity of Alba, a chromatin protein of the archaeon Sulfolobus solfataricus P2, is regulated by acetylation of lysine 16. Here we identify an acetyltransferase that specifically acetylates Alba on this residue. The effect of acetylation is to lower the affinity of Alba for DNA. Remarkably, the acetyltransferase is conserved not only in archaea but also in bacteria where it appears to play a role in metabolic regulation. Therefore, our data suggest that S. solfataricus has co-opted this bacterial regulatory system to generate a rudimentary form of chromatin regulation.
MeSH term(s)	Acetyltransferases/chemistry ; Acetyltransferases/metabolism ; Acetyltransferases/physiology ; Amino Acid Motifs ; Amino Acid Sequence ; Archaeal Proteins/chemistry ; Archaeal Proteins/metabolism ; Chromatin/chemistry ; Chromatin/metabolism ; Chromatin Immunoprecipitation ; Cloning, Molecular ; DNA/chemistry ; DNA/metabolism ; DNA-Binding Proteins/chemistry ; DNA-Binding Proteins/metabolism ; Gene Expression Regulation ; Gene Expression Regulation, Archaeal ; Lysine/chemistry ; Mass Spectrometry ; Molecular Sequence Data ; Open Reading Frames ; Sirtuins/chemistry ; Sirtuins/metabolism ; Sulfolobus solfataricus/metabolism ; Temperature
Chemical Substances	Archaeal Proteins ; Chromatin ; DNA-Binding Proteins ; Sso10b protein, Sulfolobus solfataricus ; DNA (9007-49-2) ; Acetyltransferases (EC 2.3.1.-) ; Sirtuins (EC 3.5.1.-) ; Lysine (K3Z4F929H6)
Language	English
Publishing date	2005-04-11
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2997-x
ISSN	1083-351X ; 0021-9258
ISSN (online)	1083-351X
ISSN	0021-9258
DOI	10.1074/jbc.M501280200
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