scholarly journals Effluent Markers Related to Epithelial Mesenchymal Transition with Adjusted Values for Effluent Cancer Antigen 125 in Peritoneal Dialysis Patients

2011 ◽  
Vol 2011 ◽  
pp. 1-5 ◽  
Author(s):  
Sonoo Mizuiri ◽  
Hiromichi Hemmi ◽  
Michitsune Arita ◽  
Reibin Tai ◽  
Yoshinari Hattori ◽  
...  
Keyword(s):  
Peritoneal Dialysis ◽  
Growth Factor ◽  
Epithelial Mesenchymal Transition ◽  
Compensatory Mechanism ◽  
Vascular Endothelial ◽  
Cancer Antigen 125 ◽  
Cancer Antigen ◽  
Mesenchymal Transition ◽  
Endothelial Growth Factor ◽  
Hepatocyte Growth

Objectives. Epithelial mesenchymal transition (EMT) is important for peritoneal deterioration. We evaluated the association between peritoneal solute transport rate (PSTR) and effluent markers related to EMT with adjusted values for effluent cancer antigen 125 (CA125).Methods. One hundred five incident peritoneal dialysis (PD) patients on PD for 25 (12–68) months with biocompatible solutions were included in the study. Fast peritoneal equilibration test was used to evaluate PSTR. Effluent hepatocyte growth factor (HGF), bone morphogenic protein-7 (BMP-7), vascular endothelial growth factor (VEGF), interleukin-6 (IL-6), and CA125 at 4 h were measured.Results. Patients with dialysate/plasma creatinine ≧0.82 showed significantly higher effluent HGF (240 versus 133 pg/mL, ), VEGF, IL-6, and IL6/CA125 levels than the others but no significant differences in effluent HGF/CA125, BMP-7, and BMP7/CA125 were observed.Conclusion. Increase in the effluent HGF levels as a compensatory mechanism is a marker of peritoneal deterioration, but controversy remains regarding adjusted value for CA125.

The Association between the Vascular Endothelial Growth Factor–to–Cancer Antigen 125 Ratio in Peritoneal Dialysis Effluent and the Epithelial-to-Mesenchymal Transition in Continuous Ambulatory Peritoneal Dialysis

2008 ◽  
Vol 28 (3_suppl) ◽  
pp. 101-106 ◽  
Author(s):  
Jun-Young Do ◽  
Yong-Lim Kim ◽  
Jong-Won Park ◽  
Kyung-Ae Chang ◽  
Seung-Hyun Lee ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Peritoneal Dialysis ◽  
Growth Factors ◽  
Growth Factor ◽  
Epithelial To Mesenchymal Transition ◽  
Vascular Endothelial ◽  
Cancer Antigen 125 ◽  
Cancer Antigen ◽  
Mesenchymal Transition ◽  
Endothelial Growth Factor

We examined peritoneal growth factors, mesothelial mass, and epithelial-to-mesenchymal transition (EMT) in response to peritoneal exposure to peritoneal dialysate with standard and low concentrations of glucose degradation products (GDPs). We randomized 56 incident continuous ambulatory peritoneal dialysis (CAPD) patients to receive either low-GDP (30 patients) or high-GDP (standard) peritoneal dialysis (PD) solution (26 patients). The effects of the PD solutions on EMT and peritoneal growth factors in overnight dialysate effluent were compared at 1, 6, and 12 months. Assessment of EMT was performed after human peritoneal mesothelial cells (HPMCs) were cultured from overnight effluent. The low-GDP solution group showed significantly higher dialysate levels of cancer antigen 125 (CA125), fibronectin, transforming growth factor β(TGFβ)–induced gene product (βig-h3), and interleukin-6 (IL-6), but the rate of EMT was significantly lower in the low-GDP solution group during the initial 12 months of CAPD treatment. After adjusting peritoneal growth factors for dialysate CA125 concentration, the low-GDP solution group showed significantly lower ratios of fibronectin/CA125, βig-h3/CA125, IL-6/CA125, TGFβ/CA125, and vascular endothelial growth factor (VEGF)/CA125 than did patients in the high-GDP (standard) solution group. Factors associated with higher EMT were the type of solution (high in GDPs), the mass of HPMCs (low CA125), and higher VEGF/CA125. Adjustment of dialysate VEGF for effluent CA125 revealed a significant association with EMT. It suggests that fibroblastoid transition from HPMCs could be affected by the intraperitoneal VEGF per unit mass of HPMCs.

scholarly journals Immunohistochemical Features of Epithelial-Mesenchymal Transition in Feline Oral Squamous Cell Carcinoma

2019 ◽  
Vol 56 (6) ◽  
pp. 826-839 ◽  
Author(s):  
Krystal Harris ◽  
Howard B. Gelberg ◽  
Matti Kiupel ◽  
Stuart C. Helfand
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Squamous Cell Carcinoma ◽  
Growth Factor ◽  
Cell Lines ◽  
Epithelial Mesenchymal Transition ◽  
Vascular Endothelial ◽  
Programmed Death Ligand 1 ◽  
Mesenchymal Transition ◽  
Programmed Death ◽  
Endothelial Growth Factor

Feline oral squamous cell carcinoma (FOSCC) is an aggressive malignancy with invasive and metastatic behavior. It is poorly responsive to chemotherapy and radiation. Neoplastic epithelial-mesenchymal transition (EMT) portends highly malignant behavior and enhances resistance to therapy. In transitioning to a more malignant phenotype, carcinoma stem cells undergo transformation mediated by expression of proteins, endowing them with mesenchymal properties advantageous to cell survival. The goal of the current study was to identify proteins associated with EMT in FOSCC. This study documents protein expression patterns in 10 FOSCC biopsies and 3 FOSCC cell lines (SCCF1, SCCF2, SCCF3), compatible with an EMT phenotype. As markers of EMT, P-cadherin, N-cadherin, vimentin, nuclear transcription factors Twist and Snail, hypoxia inducible factor 1α (HIF-1α), programmed death ligand 1, and vascular endothelial growth factor D, as well as E-cadherin, were examined using immunohistochemistry, Western blot, and enzyme-linked immunosorbent assay. P-cadherin, Twist, HIF-1α, and programmed death ligand 1 were commonly expressed in biopsies and cell lines. N-cadherin, classically associated with EMT, was not highly expressed, and E-cadherin was coexpressed along with proteins characteristic of EMT in all specimens. Production of vascular endothelial growth factor A by cell lines, a process regulated by HIF-1α expression, was suppressed by the small-molecule inhibitor dasatinib. These data are consistent with EMT in FOSCC and shed light on cellular changes that could contribute to the aggressive behavior of FOSCC.

scholarly journals Endometrial Stromal Decidualization Responds Reversibly to Hormone Stimulation and Withdrawal

Endocrinology ◽  
2016 ◽  
Vol 157 (6) ◽  
pp. 2432-2446 ◽  
Author(s):  
Jie Yu ◽  
Sarah L. Berga ◽  
Erika B. Johnston-MacAnanny ◽  
Neil Sidell ◽  
Indrani C. Bagchi ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Gap Junctions ◽  
Epithelial Mesenchymal Transition ◽  
Morphological Changes ◽  
Vascular Endothelial ◽  
Ovulatory Cycle ◽  
Cx43 Expression ◽  
Mesenchymal Transition ◽  
Endothelial Growth Factor

Human endometrial stromal decidualization is required for embryo receptivity, angiogenesis, and placentation. Previous studies from our laboratories established that connexin (Cx)-43 critically regulates endometrial stromal cell (ESC) differentiation, whereas gap junction blockade prevents it. The current study evaluated the plasticity of ESC morphology and Cx43 expression, as well as other biochemical markers of cell differentiation, in response to decidualizing hormones. Primary human ESC cultures were exposed to 10 nM estradiol, 100 nM progesterone, and 0.5 mM cAMP for up to 14 days, followed by hormone withdrawal for 14 days, mimicking a biphasic ovulatory cycle. Reversible differentiation was documented by characteristic changes in cell shape. Cx43 was reversibly up- and down-regulated after the estradiol, progesterone, and cAMP treatment and withdrawal, respectively, paralleled by fluctuations in prolactin, vascular endothelial growth factor, IL-11, and glycodelin secretion. Markers of mesenchymal-epithelial transition (MET), and its counterpart epithelial-mesenchymal transition, followed reciprocal patterns corresponding to the morphological changes. Incubation in the presence of 18α-glycyrrhetinic acid, an inhibitor of gap junctions, partially reversed the expression of decidualization and MET markers. In the absence of hormones, Cx43 overexpression promoted increases in vascular endothelial growth factor and IL-11 secretion, up-regulated MET markers, and reduced N-cadherin, an epithelial-mesenchymal transition marker. The combined results support the hypothesis that Cx43-containing gap junctions and endocrine factors cooperate to regulate selected biomarkers of stromal decidualization and MET and suggest roles for both phenomena in endometrial preparation for embryonic receptivity.

scholarly journals Cbl-transforming Variants Trigger a Cascade of Molecular Alterations That Lead to Epithelial Mesenchymal Conversion

2000 ◽  
Vol 11 (10) ◽  
pp. 3397-3410 ◽  
Author(s):  
Tanya M. Fournier ◽  
Louie Lamorte ◽  
Christiane R. Maroun ◽  
Mark Lupher ◽  
Hamid Band ◽  
...  
Keyword(s):  
Growth Factor ◽  
Epithelial Cells ◽  
Hepatocyte Growth Factor ◽  
Epithelial Mesenchymal Transition ◽  
Morphological Changes ◽  
Cell Spreading ◽  
Mesenchymal Transition ◽  
Amino Terminal ◽  
Src Homology ◽  
Hepatocyte Growth

Dispersal of epithelial cells is an important aspect of tumorigenesis, and invasion. Factors such as hepatocyte growth factor induce the breakdown of cell junctions and promote cell spreading and the dispersal of colonies of epithelial cells, providing a model system to investigate the biochemical signals that regulate these events. Multiple signaling proteins are phosphorylated in epithelial cells during hepatocyte growth factor–induced cell dispersal, including c-Cbl, a protooncogene docking protein with ubiquitin ligase activity. We have examined the role of c-Cbl and a transforming variant (70z-Cbl) in epithelial cell dispersal. We show that the expression of 70z-Cbl in Madin-Darby canine kidney epithelial cells resulted in the breakdown of cell–cell contacts and alterations in cell morphology characteristic of epithelial–mesenchymal transition. Structure–function studies revealed that the amino-terminal portion of c-Cbl, which corresponds to the Cbl phosphotyrosine-binding/Src homology domain 2 , is sufficient to promote the morphological changes in cell shape. Moreover, a point mutation at Gly-306 abrogates the ability of the Cbl Src homology domain 2 to induce these morphological changes. Our results identify a role for Cbl in the regulation of epithelial–mesenchymal transition, including loss of adherens junctions, cell spreading, and the initiation of cell dispersal.

scholarly journals Macrophage-Derived Inflammation Induces a Transcriptome Makeover in Mesenchymal Stromal Cells Enhancing Their Potential for Tissue Repair

2021 ◽  
Vol 22 (2) ◽  
pp. 781
Author(s):  
Inés Maldonado-Lasunción ◽  
Nick O’Neill ◽  
Oliver Umland ◽  
Joost Verhaagen ◽  
Martin Oudega
Keyword(s):  
Growth Factor ◽  
Tissue Repair ◽  
Therapeutic Potential ◽  
Vascular Endothelial ◽  
Glial Derived Neurotrophic Factor ◽  
Transcriptomic Changes ◽  
Endothelial Growth Factor ◽  
Cellular Components ◽  
Hepatocyte Growth ◽  
Go Terms

Pre-clinical and clinical studies revealed that mesenchymal stromal cell (MSC) transplants elicit tissue repair. Conditioning MSC prior to transplantation may boost their ability to support repair. We investigated macrophage-derived inflammation as a means to condition MSC by comprehensively analyzing their transcriptome and secretome. Conditioning MSC with macrophage-derived inflammation resulted in 3208 differentially expressed genes, which were annotated with significantly enriched GO terms for 1085 biological processes, 85 cellular components, and 79 molecular functions. Inflammation-mediated conditioning increased the secretion of growth factors that are key for tissue repair, including vascular endothelial growth factor, hepatocyte growth factor, nerve growth factor and glial-derived neurotrophic factor. Furthermore, we found that inflammation-mediated conditioning induces transcriptomic changes that challenge the viability and mobility of MSC. Our data support the notion that macrophage-derived inflammation stimulates MSC to augment their paracrine repair-supporting activity. The results suggest that inflammatory pre-conditioning enhances the therapeutic potential of MSC transplants.

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