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#22652544   2012/08/21 Save this To Up

Serum angiopoietin-like protein 3 concentrations in rheumatic diseases.

Angiopoietin-like protein 3 (Angptl3) is one of the angiogenic cytokines that stimulates endothelial cell adhesion, migration, and neovascularization. No link has been established between Angptl3 and rheumatic diseases such as systemic sclerosis or dermatomyositis (DM). In this study, we determined the serum Angptl3 levels in patients with various rheumatic diseases, and tried to evaluate the possibility that serum levels of Angptl3 can be a useful disease marker. Serum samples were collected from 21 SSc patients, 10 systemic lupus erythematosus (SLE) patients, 21 DM patients, 5 polymyositis (PM) patients and 11 patients with clinically amyopathic DM (CADM) as well as 12 healthy volunteers. Levels of serum Angptl3 were measured with a specific ELISA kit. There was a significant increase of serum Angptl3 levels in patients with SSc or DM (p<0.05). Levels of serum Angptl3 were also slightly higher in patients with ADM, PM or SLE compared with healthy controls, but not statistically significant. Myoglobin levels were significantly higher in DM patients with increased serum Angptl3 levels than those with normal levels (p<0.05). In addition, among patients with SSc, the prevalence of cutaneous ulcers was significantly greater in patients with elevated Angptl3 levels than those with normal levels (p<0.05). Serum Angptl3 levels may be associated with the pathogenesis of muscle involvement in DM patients and microangiopathy in SSc patients. Clarifying the role of Angptl3 in each rheumatic disease may lead to further understanding of the pathogenesis and new therapeutic approaches.

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#18382669   2008/04/02 Save this To Up

Paracrine factors of mesenchymal stem cells recruit macrophages and endothelial lineage cells and enhance wound healing.

Bone marrow derived mesenchymal stem cells (BM-MSCs) have been shown to enhance wound healing; however, the mechanisms involved are barely understood. In this study, we examined paracrine factors released by BM-MSCs and their effects on the cells participating in wound healing compared to those released by dermal fibroblasts. Analyses of BM-MSCs with Real-Time PCR and of BM-MSC-conditioned medium by antibody-based protein array and ELISA indicated that BM-MSCs secreted distinctively different cytokines and chemokines, such as greater amounts of VEGF-alpha, IGF-1, EGF, keratinocyte growth factor, angiopoietin-1, stromal derived factor-1, macrophage inflammatory protein-1alpha and beta and erythropoietin, compared to dermal fibroblasts. These molecules are known to be important in normal wound healing. BM-MSC-conditioned medium significantly enhanced migration of macrophages, keratinocytes and endothelial cells and proliferation of keratinocytes and endothelial cells compared to fibroblast-conditioned medium. Moreover, in a mouse model of excisional wound healing, where concentrated BM-MSC-conditioned medium was applied, accelerated wound healing occurred compared to administration of pre-conditioned or fibroblast-conditioned medium. Analysis of cell suspensions derived from the wound by FACS showed that wounds treated with BM-MSC-conditioned medium had increased proportions of CD4/80-positive macrophages and Flk-1-, CD34- or c-kit-positive endothelial (progenitor) cells compared to wounds treated with pre-conditioned medium or fibroblast-conditioned medium. Consistent with the above findings, immunohistochemical analysis of wound sections showed that wounds treated with BM-MSC-conditioned medium had increased abundance of macrophages. Our results suggest that factors released by BM-MSCs recruit macrophages and endothelial lineage cells into the wound thus enhancing wound healing.

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#17828495   2007/09/10 Save this To Up

Effects of meloxicam on vascular endothelial growth factor and angiopoietin-2 expression in colon carcinoma cell line HT-29.

To investigate the effect of meloxicam, a selected NSAIDs, on cell growth, expression of VEGF and angiopointin-2 (Ang-2) protein in HT-29 cell line, cultured HT-29 cells were treated with meloxicam of various concentrations for various lengths of time. The proliferation of HT-29 was detected by cell counting kit-8 (CCK-8), the cell cycle was determined by flow cytometer and the levels of VEGF and Ang-2 protein in supernatants were examined by enzyme linked immunosorbent assay (ELISA). The mRNA expressions of VEGF and Ang-2 in cultured HT-29 were determined by real-time quantitative reverse-transcription polymerase chain reaction. Our results showed that treatment of meloxicam of different concentrations and for various lengths of time had a cytotoxicic effect on the cell proliferation of HT-29 cells in a concentration-dependant and time-dependant manner. Cell cycle analysis showed that the cells were mainly blocked in G0/G1 phase. The VEGF and Ang-2 protein levels in supernatants of the culture medium were decreased gradually in a concentration-dependent or time-dependent fashion. The mRNA expression of cox-2, VEGF and Ang-2 showed a gradual and concentration-dependent reduction. It is concluded that meloxicam can reduce the expression of VEGF and Ang-2 at the protein and mRNA level in colon carcinoma cell line.

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