Role of adhesion molecules in cholestatic liver disease
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PROVIDER: PRJEB82426 | ENA |
REPOSITORIES: ENA
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Project description:Systemic mastocytosis (SM) is an incurable neoplasm characterized by abnormal accumulation of neoplastic mast cells (MC) in vascularized organs. In indolent SM, MC express several different adhesion-molecules including CD2 and CD58, and form focal tissue-aggregates, whereas in advanced SM, MC often lack CD2 and produce a more diffuse infiltration-pattern. To explore the functional role of CD2 in the pathology of SM, stable CD2+ and CD2− subclones of the human MC-leukemia cell line HMC-1 were generated and injected intraperitoneally into pfp/rag2 mice. CD2+ HMC-1 cells formed solid mastocytomas in the peritoneum and lungs, whereas CD2− cells produced diffuse infiltration. CD2+ and CD2− HMC-1 subclones all displayed the driver-mutant KIT D816V, exhibited the same growth-kinetics, and displayed identical adhesion-receptors including CD44 and selectin-ligands. To explore the mechanism of organ invasion, E- and P-selectin-deficient scid mice (scid-select) were employed. While massive HMC-1 infiltrates were detected in the lungs of control mice, infiltration was markedly reduced or absent in scid-select mice. The invasion-receptor CD44 was detectable in all MC infiltrates, with most abundant expression in the invasion-front. Together, our data show that selectins mediate organ-invasion of MC and CD2-CD58 interactions contribute to a more focal infiltration-pattern which is lost during progression to MC leukemia. HMC1 cells were sorted by FACS for expression of CD2 surface expression. 2 subclones were obtained (CD2+ or CD2-) and compared by gene expression profiling using U133 plus 2.0 GeneChips
2013-01-01 | E-GEOD-33504 | biostudies-arrayexpress
Project description:Systemic mastocytosis (SM) is an incurable neoplasm characterized by abnormal accumulation of neoplastic mast cells (MC) in vascularized organs. In indolent SM, MC express several different adhesion-molecules including CD2 and CD58, and form focal tissue-aggregates, whereas in advanced SM, MC often lack CD2 and produce a more diffuse infiltration-pattern. To explore the functional role of CD2 in the pathology of SM, stable CD2+ and CD2− subclones of the human MC-leukemia cell line HMC-1 were generated and injected intraperitoneally into pfp/rag2 mice. CD2+ HMC-1 cells formed solid mastocytomas in the peritoneum and lungs, whereas CD2− cells produced diffuse infiltration. CD2+ and CD2− HMC-1 subclones all displayed the driver-mutant KIT D816V, exhibited the same growth-kinetics, and displayed identical adhesion-receptors including CD44 and selectin-ligands. To explore the mechanism of organ invasion, E- and P-selectin-deficient scid mice (scid-select) were employed. While massive HMC-1 infiltrates were detected in the lungs of control mice, infiltration was markedly reduced or absent in scid-select mice. The invasion-receptor CD44 was detectable in all MC infiltrates, with most abundant expression in the invasion-front. Together, our data show that selectins mediate organ-invasion of MC and CD2-CD58 interactions contribute to a more focal infiltration-pattern which is lost during progression to MC leukemia.
2013-01-01 | GSE33504 | GEO
Project description:Accumulated research has suggested the importance of the adhesion molecules modulation as therapeutic approach for bronchial asthma. Adhesion molecules expression alteration contributes to the pathogenesis of asthma. In order to probe the relationship between expression imbalance of adhesion molecules and asthma pathogenesis, expression profiling of adhesion molecules was performed using cDNA microarray. The results showed that there were various adhesion molecules with abnormal expressions in peripheral blood leucocytes of asthma patients.
2014-02-01 | GSE54605 | GEO
Project description:Accumulated research has suggested the importance of the adhesion molecules modulation as therapeutic approach for bronchial asthma. Adhesion molecules expression alteration contributes to the pathogenesis of asthma. In order to probe the relationship between expression imbalance of adhesion molecules and asthma pathogenesis, expression profiling of adhesion molecules was performed using cDNA microarray. The results showed that there were various adhesion molecules with abnormal expressions in peripheral blood leucocytes of asthma patients. RNA was extracted from leucocytes in peripheral blood of 4 normal adults and 6 asthma patients by using TRIzol Reagent. Microarray expression studies were performed using the GEArray Q Series Human Extracellular Matrix & Adhesion Molecules Gene Array (SABiosciences Corporation, USA). This microarray profiles the expression of 96 genes key to the functions of cell adhesion. A negative control (PUC18DNA and blank), and the housekeeping genes including β-actin, GAPDH, Cyclophilin A and ribose body protein L13a were spread on each chip.
2014-02-01 | E-GEOD-54605 | biostudies-arrayexpress
Project description:Tumor cell extravasation takes place, similar to leukocytes, in a multi-step process by which cells emigrate from the blood stream through the vascular endothelium into the tissue. Selectins are regarded as the most important molecules for the first capturing step of the cascade. Whether all tumor cells employ selectin dependent adhesion to metastasize or there is an alternative mechanism still is an open question. Comparative transcriptomic analysis of OVCAR8 and SKOV3 cultured cells and revealed that one third of genes encoding proteins involved in the selectin dependent leukocyte like adhesion cascade show lower expression levels in OVCAR8 cultured cells in comparison to that in SKOV3 cultured cells. In contrast to SKOV3 cells, c-Fos overexpression in OVCAR8 cells does not significantly influence expression of the leukocyte like adhesion cascade genes leaving them at similar levels as in control OVCAR8 cells. The intraperitoneal xenograft model of OVCAR8 cells demonstrated that aggressiveness of OVCAR8-derived tumors is not dependent of c-Fos expression level and comparable with that for SKOV3 control tumors. Based on transcriptome array data we analyzed in details expression of genes encoding proteins involved in the leukocyte like adhesion cascade, E- and P-selectin ligands, as well as glycosylation enzymes in both type of tumors. Our results suggest that selectin-dependent mechanism is not the only for adhesion of OVCAR8 ovarian cancer cells. There is at least one additional mechanism of extravasation that does not rely on selectins.
2017-03-31 | GSE97226 | GEO
Project description:The adhesion of monocytic cells to the M-^SdysfunctionalM-^T endothelium constitutes a critical step in the initiation of atherosclerotic plaque formation. Cigarette smoke (CS) has been shown to contribute to the monocyte-endothelial adhesion process. Yet, the complex mechanisms underlying this event remain to be discovered. In the systemic compartment, monocytes and endothelial cells are exposed primarily to soluble constituents originating from the inhaled CS and absorbed through the lung alveolar epithelium and the adjacent microvascular endothelium. Considering this rationale, we developed an in vitro adhesion assay, intending to mimic the in vivo situation, to deeply investigate the impact of CS on the adhesion of monocytic cell to the endothelium. Using a transcriptomics approach followed by confirmation experiments, we were able to identify a key mechanism by which aqueous extract of CS (smoke-bubbled Phosphate Buffered Saline, sbPBS) promotes the adhesion of monocytic Mono Mac 6 (MM6) cells to the human umbilical vein endothelial cells (HUVECs). While CS-derived constituents directly provoke a strong oxidative stress response in both cell types, the induced expression of E-selectin, VCAM-1 and ICAM-1 adhesion molecules, responsible for the binding of MM6 cells to HUVECs, occurs through a proinflammatory paracrine effect. We demonstrate that this effect is mainly driven by TNF? produced by MM6 cells exposed to sbPBS. In conclusion, the development of our in vitro adhesion assay, intending to mimic the in vivo conditions, enabled to show that the adhesion of monocytic cells to endothelial cells is promoted through an indirect effect of the sbPBS.
2014-04-24 | E-MTAB-1173 | biostudies-arrayexpress
Project description:The acute lymphoblastic leukemia cells lines JM-1, REH, Nalm-27, and SUP-B15 were analyzed for baseline expression of extacellular matrix and adhesion molecules using a pathway focused cDNA microarray (SABiosciences). RNA isolated from the ALL cell lines JM-1, REH, Nalm-27, and SUP-B15 was analyzed using the Extracellular Matrix and Adhesion Molecules Oligo GEArray (SABIosciences).
2010-05-01 | E-GEOD-18516 | biostudies-arrayexpress
Project description:A Whole-Cell Screening Platform for Discovering Cell Adhesion Molecules Enabling Programmable Bacterial Cell-Cell Adhesion
| PRJNA1047165 | ENA
Project description:The acute lymphoblastic leukemia cells lines JM-1, REH, Nalm-27, and SUP-B15 were analyzed for baseline expression of extacellular matrix and adhesion molecules using a pathway focused cDNA microarray (SABiosciences).
2010-05-01 | GSE18516 | GEO
Project description:To identify cell adhesion molecules (CAMs) targeting bacterial membrane proteins within a synthetic bacteria-displayed nanobody library, we present a comprehensive whole-cell screening platform. This involves targeted amplicon sequencing to discover nanobodies targeting the natural adhesin, TraN. Furthermore, we employ deep mutational engineering to enhance the binding affinity of these nanobodies toward TraN.
2023-12-18 | GSE249103 | GEO