Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA245232 | ENA |
REPOSITORIES: ENA
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Project description:In MTN-007, a phase 1, randomized, double-blinded rectal microbicide trial, we used systems genomics/proteomics to determine the effect of tenofovir 1% gel, nonoxynol-9 2% gel, placebo gel or no treatment on rectal biopsies taken at baseline, after one application or after seven daily applications (15 subjects/arm). Experiments were repeated using primary vaginal epithelial cells from four healthy women. 36 Arrays (3 primary vaginal epithelial cell lines from healthy women donors, cultured with or without 50uM or 500 uM Tenofovir for 1,4,7, or 14 days per donor cell line. A no treatment, culture media only control was included for each donor cell line and for each time point.
2015-02-23 | E-GEOD-57026 | biostudies-arrayexpress
Project description:In MTN-007, a phase 1, randomized, double-blinded rectal microbicide trial, we used systems genomics/proteomics to determine the effect of tenofovir 1% gel, nonoxynol-9 2% gel, placebo gel or no treatment on rectal biopsies taken at baseline, after one application or after seven daily applications (15 subjects/arm). Experiments were repeated using primary vaginal epithelial cells from four healthy women.
2015-02-23 | GSE57026 | GEO
Project description:In MTN-007, a phase 1, randomized, double-blinded rectal microbicide trial, we used systems genomics/proteomics to determine the effect of tenofovir 1% gel, nonoxynol-9 2% gel, placebo gel or no treatment on rectal biopsies taken at baseline, after one application or after seven daily applications (15 subjects/arm). Experiments were repeated using primary vaginal epithelial cells from four healthy women.
2015-02-23 | GSE57025 | GEO
Project description:In MTN-007, a phase 1, randomized, double-blinded rectal microbicide trial, we used systems genomics/proteomics to determine the effect of tenofovir 1% gel, nonoxynol-9 2% gel, placebo gel or no treatment on rectal biopsies taken at baseline, after one application or after seven daily applications (15 subjects/arm). Experiments were repeated using primary vaginal epithelial cells from four healthy women. 192 Arrays (8 donors per treatment group, 2 biopsy sites per donor (9cm and 15 cm), biopsies taken at baseline, after a single application, and after 7 daily applications)
2015-02-23 | E-GEOD-57025 | biostudies-arrayexpress
Project description:We report the HIV-1 induced gene signature of vaginal tissues (EpiVaginalTM, MatTek Corporation, Ashland, MA) using a customised ex vivo model that mimics the vaginal transmission of HIV-1. Importantly, we demonstrate that recombinant fragment of human Surfactant Protein D (rhSP-D) (Mahajan et al., 2008) treated EpiVaginal tissues exhibited a remarkable but selective reversal of HIV-1 specific gene signature suggesting that epithelial behaviour significantly influences transmission events.
2018-11-29 | GSE107478 | GEO
Project description:AIM Vitamin D deficiency is associated with risk of several common cancers, including colorectal cancer (CRC). We investigated the effects of vitamin D on in vitro and ex vivo epithelial cell gene expression and assessed dysregulation of pathways involved in anti-tumour effects. METHODS We performed in vitro and ex vivo intervention studies using established CRC cell lines and patient-derived epithelial organoids developed from normal human colonic (resectional colorectal surgery) and rectal mucosa (rectal biopsy). RNA and protein were harvested after 16-24 hours’ calcitriol treatment. Gene expression was assessed by qRT-PCR, microarray and RNA-sequencing, and protein expression by immunoblotting and mass-spectrometry. Gene Ontology enrichment analysis was performed using GOrilla and Gene Set Enrichment Analysis. RESULTS Calcitriol increased the expression of the tumour suppressor gene CDH1 in CRC cell lines (SW480; FC=3.60, 95%CI 2.17-5.03) and patient-derived epithelial cell organoids (n=6, FC=1.64, 95%CI 1.49-1.80), with associated in vitro E-cadherin protein induction. Significant differential expression of a further 6 common genes was observed on microarray analysis of in vitro and ex vivo experiments, including genes with established links to carcinogenesis GADD45, EFTUD1 and KIAA1199. Numerous ontologies relevant to carcinogenesis were enriched (e.g. ‘regulation of Wnt signaling pathway’, ‘regulation of cell death’), with common enriched processes across in vitro and ex vivo cultures including ‘negative regulation of cell proliferation’, ‘regulation of cell migration’ and ‘regulation of cell differentiation’. CONCLUSIONS We report for the first time, common genes and pathways modulated by calcitriol treatment in both in vitro and ex vivo models, with several differentially expressed genes strongly linked to CRC tumourigenesis. Enrichment of biological pathways after calcitriol treatment provides further evidence of anti-tumour effects. These findings support epidemiological data and provide strong rationale for well-designed trials of vitamin D supplementation as a novel CRC chemopreventive and chemotherapeutic agent. see above
2022-06-01 | GSE181644 | GEO
Project description:The female menopause, characterised by reduced estrogen associates with an increased risk of recurrent UTIs caused by uropathogenic Escherichia coli (UPEC). Clinically such infections can be countered by topical vaginal estrogen treatment and the aim of this study was to investigate, in vitro, the effects of topical estrogen treatment on vaginal epithelial responses following challenge with E.coli flagellin used to mimic UPEC. Immortalised vaginal epithelial cells (VK2 E6/E7), modelling the vaginal epithelium were treated with either 4nM 17β-estradiol (E) for seven days, 50ng/ml E.coli flagellin (F) for 12h, or 4nM 17β-estradiol plus 50ng/ml flagellin (E + F(12h)). RNA was analysed by microarray gene profiling using the Illumina HumanHT-12 v 4 Expression Beadchip. Following E + F treatments expression of genes encoding host defence molecules including DEFβ4A, DEFB103A, LCN2 as well as those associated with keratinisation e.g. CNFN and SPRR family genes were significantly enhanced (P<0.05) compared to either E or F treatments alone. Mutation of EREs identified in the DEFβ4 gene promoter abolished the augmented gene expression suggesting estrogen functioned directly through a transcriptional regulatory mechanism involving ESR1/2. Ingenuity pathway analyses also suggested the pro-inflammatory cytokine IL-17A to regulate the vaginal host defences during infection. Pre-treating VK2 E6/E7 cells with estrogen (4nM) and challenging with 1L-17A & F (12h) significantly enhanced DEFβ4, DEF103A and S100A7 expression (P<0.05). Origins of vaginal IL-17 in vivo remain unclear, but vaginal biopsy material suggests gd T cells located within the vaginal epithelium. These data suggest that the vaginal antimicrobial response induced by flagellin activation of TLR5 cell signalling is augmented significantly by topical estrogen treatment.
2020-01-01 | GSE135583 | GEO
Project description:During sexual transmission of HIV-1 from male to female partners, the vagina is the initial site of contact with HIV infected semen. The mechanism of HIV traversing the CD4 negative multi-layered stratified squamous epithelial barrier of the vagina to infect sub-epithelial susceptible immune cells, is hitherto unknown. HIV gp120 binds to several host proteins on vaginal epithelial cells. To gain an insight into the physiologic changes that may occur in vaginal epithelial cells in response to interactions with HIV gp120, and obtain an understanding of the molecular mechanisms by which HIV breaches the vaginal epithelium, a global snap shot of gene expression profiles in the vaginal epithelial cell line Vk2/E6E7, treated with HIV gp120 was determined. The vaginal epithelial cell line Vk2/E6E7 was treated with HIV gp120 (83nM) for 24 hr, and Agilent one colour, microarrays were performed.
2014-03-01 | GSE44914 | GEO
Project description:HIV-1 infections of women are mainly acquired through female reproductive tract where cervical and vaginal epithelial cells are the first line of defense. Although HIV-1 does not directly infect epithelial cells, HIV-1 obligatorily interacts with and crosses over epithelial layer to infect susceptible target cells, mainly CD4+ T cells, in the lamina propria to initiate an infection. However, the mechanism and ramification of the interaction of HIV-1 and epithelial cells in vaginal transmission of HIV-1 remain to be elucidated. We hypothesized that cervical epithelial cells are not a passive barrier, but actively respond to HIV-1 to change mucosal milieu and facilitate HIV-1 transmission. We tested this hypothesis by studying the responses of cervical epithelial cells to HIV-1 through profiling genome-wide transcription. We found 1) cervical epithelial cells actively respond to HIV-1. Five hundred forty-three transcripts/genes in cervical epithelial cells were significantly altered in expression at four hours post exposure to HIV-1, of which many relate to important signaling pathways, such as innate immune responses, pattern recognition receptors, apoptosis, biosynthesis, and energy production, 2) HIV-1 increases the expression of CXC Chemokines (IL-8, CXCL1 and CXCL3) in cervical epithelial cells. IL-8 and CXCL1 are potent chemotactic for multinuclear neutrophils (MNP), monocytes and a minority of lymphocytes, and CXCL3 is predominant chemotactic for monocytes, 3) HIV-1 increases the expression of key inflammatory enzymes-COX-1 and COX-2. COX-1 is responsible for the production of prostaglandins that are important for homeostatic functions, and COX-2 is a key enzyme to convert arachidonic acid to prostaglandins, key inflammatory mediators, and 4) the increased expression of IL-8 and COX-2 revealed using microarray analysis was mapped into the endocervical epithelial cells of macaques inoculated with inactivated SIV in vivo. Our date lead to a role model of epithelial cells in HIV-1 vaginal transmission, that is the axis of HIV-1, epithelial cells, proinflammatory molecules (IL-8, CXCL1, CXCL3, COX-1 and COX-2), cell recruitment (MNP, monocytes and T cells), and inflammation. This model implies that moderating epithelial proinflammatory response to HIV-1 may be utilized in prevention of HIV vaginal transmission. Human endocervical epithelial cell line, CRL-2615, was inoculated with HIV-1 ME1 and collected 4hrs post exposure. Biologically duplicated mRNAs were prepared after exposure.
2013-02-01 | E-GEOD-42291 | biostudies-arrayexpress
Project description:During sexual transmission of HIV-1 from male to female partners, the vagina is the initial site of contact with HIV infected semen. The mechanism of HIV traversing the CD4 negative multi-layered stratified squamous epithelial barrier of the vagina to infect sub-epithelial susceptible immune cells, is hitherto unknown. HIV gp120 binds to several host proteins on vaginal epithelial cells. To gain an insight into the physiologic changes that may occur in vaginal epithelial cells in response to interactions with HIV gp120, and obtain an understanding of the molecular mechanisms by which HIV breaches the vaginal epithelium, a global snap shot of gene expression profiles in the vaginal epithelial cell line Vk2/E6E7, treated with HIV gp120 was determined. The vaginal epithelial cell line Vk2/E6E7 was treated with HIV gp120 (83nM) for 24 hr, and Agilent one colour, microarrays were performed. Agilent one-color experiment,Organism: Human ,Agilent-Custom Whole Genome Human 8x60k designed by Genotypic Technology Pvt. Ltd. (AMADID: 027114), Labeling kit: Agilent Quick-Amp labeling Kit (p/n5190-0442)
2014-03-01 | E-GEOD-44914 | biostudies-arrayexpress