Strikingly, cytokine induction by chemotherapy was not observed in macrophages isolated from heparanase-knockout mice, suggesting macrophage activation by chemotherapy is heparanase dependent. paclitaxel-treated macrophages enhanced the growth of Lewis lung carcinoma tumors that was attenuated by a CXCR2 inhibitor.
This, in turn, is determined by the combinatorial action of enzymes for biosynthesis and modification of HS such as exostosis (EXTs), sulfotransferases (NDSTs), and heparanase 1 (HPSE1).
This study suggests that the automated structure-function report combining results from the SD-OCT and the HEP may assist in the evaluation and management of glaucoma.
Our data suggest that the mechanisms that underlie the role of heparanase in promoting cell survival could be uniquely beneficial to the heart by providing protection against cellular stresses, and could be useful for exploitation as a therapeutic target for the treatment of heart disease.
This, in turn, is determined by the combinatorial action of enzymes for biosynthesis and modification of HS such as exostosis (EXTs), sulfotransferases (NDSTs), and heparanase 1 (HPSE1).
Most notably, expression profiles of Sdcs, EXTs, NDSTs, and HPSE1 differentially correlate with the presence of inflammatory infiltrate in healthy and diseased periodontal tissue, which might imply that these factors could also be involved in modulation of inflammatory response in periodontitis.
HPA polymorphism has been associated with HCV presence and fibrosis progression in chronic hepatitis C. However, it is unknown if there is an association between HPA-1 polymorphism and hepatocellular carcinoma (HCC).
This behavior seems specific to FaDu cells, and could be linked to previously reported overexpression of T5, heparanase splice variants that produces protein lacking enzymatic activity of heparanase.
This, in turn, is determined by the combinatorial action of enzymes for biosynthesis and modification of HS such as exostosis (EXTs), sulfotransferases (NDSTs), and heparanase 1 (HPSE1).
Importantly, significant shorter patient survival was found in heparanase-high/CD24-high tumors vs. heparanase-high/CD24-low tumors for both high-grade and low-grade glioma (p = 0.02).
These nanoparticles bonded to the HPA overexpressed on the surface of TNBC cells and were taken up by these cells, resulting in remarkably enhanced cellular toxicity compared with non-targeted PTX-NP that lack the HPA aptamer (P < 0.01).
These nanoparticles bonded to the HPA overexpressed on the surface of TNBC cells and were taken up by these cells, resulting in remarkably enhanced cellular toxicity compared with non-targeted PTX-NP that lack the HPA aptamer (P < 0.01).
The relations between stress, HPA-axis, and the immune system have been extensively studied; however, no study to date addressed the joint contribution of immune and HPA biomarkers to the development of anxiety in youth exposed to chronic trauma as mediated by mother-child interaction patterns.
The relations between stress, HPA-axis, and the immune system have been extensively studied; however, no study to date addressed the joint contribution of immune and HPA biomarkers to the development of anxiety in youth exposed to chronic trauma as mediated by mother-child interaction patterns.
Collectively, these findings suggest that heparanase blockade is highly effective in slowing atherosclerosis formation and progression, and decreasing liver steatosis.
In this study, we examined the potential use of our human 3D myoma disc and Myogel models in in vitro chemoradiation studies by analysing the effects of ionizing radiation (IR) and the combined effect of heparanase I (HPSE1) inhibitors and IR on OTSCC cell proliferation, invasion and MMP-2 and - 9 production.
These findings provide a strong preclinical rationale for developing drug regimens combining heparanase inhibitors/HS mimetics with IGF1R antagonists for treatment of metastatic SS.
These findings provide a strong preclinical rationale for developing drug regimens combining heparanase inhibitors/HS mimetics with IGF1R antagonists for treatment of metastatic SS.