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We presently demonstrate that aqueous ATX may be a prognostic factor affecting the fibrotic response in human conjunctiva fibroblast and bleb formation, and inhibition of ATX could be a therapeutic target after trabeculectomy.
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Serum Autotaxin Is a Useful Disease Progression Marker in Patients with Primary Biliary Cholangitis
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High Autotaxin exacerbates tumor progression by enhancing MEK1 and overriding the function of miR-489-3p.
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ATX-LPA signaling-related proteins are highly expressed in breast cancer with adipose stroma, with associated macrophage infiltration.
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ENPP2 was in silico discovered to be genetically altered in some patients with lung cancer, whereas increased autotaxin (ATX) staining and activity were detected in patients and mouse models, accompanied by a downregulation of PLPP3 expression. Most importantly, genetic deletion of Enpp2 or Lpar1 in mice resulted in disease attenuation, thus confirming a pro-carcinogenic role of ATX/LPA in the lung.
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AUTOTAXIN (ATX) represents a non-invasive biomarker for liver fibrosis in HCV-infected patients.
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High autotaxin expression in hepatocellular carcinoma (HCC) is detected in patients with histological grade II and III. Patients with elevated expression levels were found to possess an eight-fold higher risk of death
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mRNA expression analyses revealed that ADSCs and MES largely expressed LPA receptor 1 (LPAR1) while epithelial cells mainly expressed LPAR6. LPA 18:1 activated all the cell populations and cell lines by rise in cytosolic free calcium concentrations. MES and ADSCs expressed ATX whereas epithelial cells did not.
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Small intestinal ATX expression by enteroendocrine cells might represent an important source of cholestasis-induced serum ATX activity in men.
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In the presence of LPC, the cell motile activity of PANC-R9 cells was markedly stimulated. In contrast, LPC did not affect the cell motile activity of PANC-1 cells. PANC-R9 cell motility was inhibited by an ATX inhibitor, PF-8380. These results suggest that LPA signaling via LPA1 is a potent molecular target for the regulation of tumor progression in PANC-1 cells.
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increase in serum autotaxin concentrations is fairly specific for liver fibrosis, and the serum autotaxin concentrations can be analysed without consideration of food intake before blood collection
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High ATX gene expression is associated with type I endometrial cancer.
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These results suggest functional interactions among ATX, VEGFR-2, and VEGFR-3 in the modulation of hemovascular and lymphovascular cell activation during vascular development.
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LPAR mRNA and ATX protein levels are anatomic site-dependent in high-grade serous carcinoma and the former are informative of disease outcome.
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Study revealed that serum total ATX and ATX isoforms were significantly associated with the clinical stages of female subjects with melanoma.
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Serum ATX levels may at least partially reflect histological severity in non-alcoholic fatty liver disease.
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ATX-LPA axis facilitates estrogen-induced endometrial cancer cell proliferation via MAPK/ERK signaling pathway.
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Significant suppression of these aforementioned changes was observed after ATX/LPA-receptor/ROCK inhibition as well as suppression of fibrotic changes and MLC and cofilin phosphorylation in HTM cells.
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Autotaxin levels were significantly higher in early-onset preeclampsia group compared with late-onset preeclampsia group. Autotaxin levels were found to be significantly higher in preeclamptic patients compared with control group. Serum autotaxin levels showed a significant positive correlation with maternal systolic, diastolic blood pressures and uric acid levels.
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Results demonstrated, for the first time, that increased serum ATX activity and protein levels are associated with several aspects of quality of life in cholestatic patients as well as with markers of cholestatic liver injury and higher risks of death and transplantation. The study provides novel clinical evidence of the pruritogenic role of the ATX/lysophosphatidic acid axis in the pathogenesis of cholestatic itch.