Background/aims: Serum concentrations of the hepatokine fibroblast growth factor (FGF) 21 are elevated in obesity, type2 diabetes, and the metabolic syndrome. We asked whether FGF21 levels differ between subjects with metabolically healthy vs. unhealthy obesity (MHO vs. MUHO) opening the possibility that FGF21 is a crosstalker between liver and adipose tissue in MUHO. Furthermore, we studied the effects of chronic FGF21 treatment on adipocyte differentiation, lipid storage, and adipokine secretion.
Fibroblast growth factor 21 is elevated in metabolically unhealthy obesity and affects lipid deposition, adipogenesis, and adipokine secretion of human abdominal subcutaneous adipocytes.
Specimen part, Treatment, SubjectView Samples
In this randomised placebo-controlled trial, irritable bowel syndrome (IBS) patients were treated with faecal material from a healthy donor (n=8, allogenic FMT) or with their own faecal microbiota (n=8, autologous FMT). The faecal transplant was administered by whole colonoscopy into the caecum (30 g of stool in 150 ml sterile saline). Two weeks before the FMT (baseline) as well as two and eight weeks after the FMT, the participants underwent a sigmoidoscopy, and biopsies were collected at a standardised location (20-25 cm from the anal verge at the crossing with the arteria iliaca communis) from an uncleansed sigmoid. In patients treated with allogenic FMT, predominantly immune response-related genes sets were induced, with the strongest response two weeks after FMT. In patients treated with autologous FMT, predominantly metabolism-related gene sets were affected.
Allogenic Faecal Microbiota Transfer Induces Immune-Related Gene Sets in the Colon Mucosa of Patients with Irritable Bowel Syndrome.
Age, Specimen part, SubjectView Samples
Pericytes are integral components of the tissue vasculature and have essential functions in tumour angiogenesis. Endosialin (CD248) is a type I transmembrane glycoprotein highly expressed on pericytes in the tumour vasculature of most solid tumours, however it is low or negligibly expressed on normal tissue pericytes. Experiments using wild-type and endosialin-knockout mice has revealed that stromal endosialin expression facilitates intravasation of tumor cells from the primary tumor into the circulation, thereby promoting metastatic dissemination.
Endosialin-Expressing Pericytes Promote Metastatic Dissemination.
Sex, Specimen part, DiseaseView Samples
Wildtype mice were given saline or bleomycin by oropharyngeal instillation. After 14 days, during the fibrotic phase of the response, lungs were dissected and total RNA was extracted and used for gene expression profiling. The aim was to identify those genes regulated during the development of fibrosis in this animal model of bleomycin-induced lung fibrosis.
Increased local expression of coagulation factor X contributes to the fibrotic response in human and murine lung injury.
Sex, Specimen part, TreatmentView Samples
To identify genes that are regulated from the lncRNA ANRIL (EXON 13), we designed inducible short hairpin RNA constructs and stable integrated them into HEK cells
The large non-coding RNA ANRIL, which is associated with atherosclerosis, periodontitis and several forms of cancer, regulates ADIPOR1, VAMP3 and C11ORF10.
Mesenchymal stromal cells (MSC) are multipotent cells that potentially promote angiogenesis. Especially MSC derived from the amnionic membrane of human term placentas (hAMSC) are promising candidates for a therapeutic use in vascular diseases, as cells can be isolated using non-invasive methods and are immunologically tolerated in vivo. In this study, we wanted to evaluate the endothelial differentiation potential of hAMSC.
Amnion-derived mesenchymal stromal cells show angiogenic properties but resist differentiation into mature endothelial cells.
Specimen partView Samples
Transient siRNA-mediated knockdown of hnRNP L, followed by cycloheximide treatment to eliminate NMD.
Crosslinking-immunoprecipitation (iCLIP) analysis reveals global regulatory roles of hnRNP L.
Cell line, TreatmentView Samples
Histidine-rich glycoprotein (HRG) is a 75 kDa heparin-binding plasma protein which has been implicated in regulation of tumor angiogenesis and growth. To exert some of its biological functions, HRG acts on macrophages.This study was performed to assess changes in gene expression in peritoneal macrophages treated with HRG using oligonucleotide microarrays
Genetic deficiency in plasma protein HRG enhances tumor growth and metastasis by exacerbating immune escape and vessel abnormalization.
Specimen part, Disease, Treatment, TimeView Samples
Constitutive low level DNA damage is linked to innate immune activation. Hierarchical clustering of over 9000 transcripts revealed remarkably similar profiles in a patient with lupus erythematosus and a patient with AGS with up-regulation of genes involved in DNA damage signaling, p53-inducible genes, senescence-associated genes as well as up-regulation of interferon-stimulated genes. Transcriptional profiling of fibroblasts exposed to oxidative stress showed a marked up-regulation of genes involved in DNA replication/repair and replication licensing in TREX1-deficient cells compared to wild type cells suggesting massive replication stress. Overall design: Comparison of transcriptional profiles of unstressed patient fibroblasts with wild type cells as well as fibroblasts exposed to oxidative stress
RPA and Rad51 constitute a cell intrinsic mechanism to protect the cytosol from self DNA.
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