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#27590242   2016/09/03 Save this To Up

The role of serum levels of microRNA-21 and matrix metalloproteinase-9 in patients with acute coronary syndrome.

Acute coronary syndrome (ACS) is one of the leading causes of cardiovascular death. It seems that microRNA-21 and matrix metalloproteinase-9 implicated in the pathogenesis of cardiovascular diseases. The aim of this study was to investigate the role of circulating miR-21 and MMP-9 as biomarkers for ACS. Based on coronary angiography and electrocardiography results, 50 patients with ACS and 50 patients with stable coronary artery disease (stable CAD) were enrolled in this study. Samples were collected from patients and stored at -80 °C. Serum miR-21 gene expression was measured by quantitative real-time PCR method. Serum total MMP-9 was measured by enzyme-linked immunosorbent assay kit. Also, the activity of MMP-9 was measured by gelatin zymography. Patients with ACS had a significantly higher miR-21 level compared to the stable CAD ([Formula: see text] = 0.88 ± 0.06 and 0.31 ± 0.08 respectively, P < 0.001). At the same time, the serum levels and activity of MMP-9 were significantly higher in ACS patients compared to those with stable CAD (324.01 ± 17.57 and 204.6 ± 12.39 ng/mL, P < 0.001, and 2524.5 ± 131.3 and 1280.8 ± 19.6 units, P < 0.001, respectively). miR-21 expression levels were correlated positively with MMP-9, hs-CRP, and age and negatively with HDL-cholesterol (r = 0.33, P < 0.001, r = 0.22, P < 0.031, r = 0.26, P < 0.008, r = -0.32, P < 0.001, respectively). We concluded that increased serum expression of miR-21 and higher serum activity of MMP-9 may be useful indicators for ACS. However, we suggest further studies to be performed.

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#26722450   2016/01/01 Save this To Up

Molecular biological characteristics of the recruitment of hematopoietic stem cells from bone marrow niche in chronic myeloid leukemia.

Chronic myeloid leukemia (CML) can be contextualized as a disease of unregulated self-renewal of stem cells which exist in a quiescent state and are instructed to differentiate and mobilize to circulation under pathologic circumstances leading to tumor invasion and metastasis. Here we found that matrix metalloproteinase-9 (MMP-9), induced by TGF-β1, upregulated s-KitL and s-ICAM-1, permitting the transfer of c-kit(+) hematopoietic stem cells (HSCs) from the quiescent to proliferative niche in CML. Further study showed that this MMP-9 production was raised by CML specific BCR/ABL(+) oncogene mediated TGF-β1. Besides, phosphatidylinositol-3 kinase (PI3K)/Akt/nuclear factor (NF)-κB signaling pathway was evidenced to govern this stem cell recruitment in CML pathogenesis. Overall, our observations defined a novel critical role for TGF-β1 induced PI3K/Akt/NF-κB signaling pathway in the recruitment of the malignant cells in CML by releasing s-KitL and s-ICAM-1 and this was through a distinct PI3K/Akt/NF-κB signaling pathway.

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#25945502   2015/05/07 Save this To Up

Adiponectin attenuates lung fibroblasts activation and pulmonary fibrosis induced by paraquat.

Pulmonary fibrosis is one of the most common complications of paraquat (PQ) poisoning, which demands for more effective therapies. Accumulating evidence suggests adiponectin (APN) may be a promising therapy against fibrotic diseases. In the current study, we determine whether the exogenous globular APN isoform protects against pulmonary fibrosis in PQ-treated mice and human lung fibroblasts, and dissect the responsible underlying mechanisms. BALB/C mice were divided into control group, PQ group, PQ + low-dose APN group, and PQ + high-dose APN group. Mice were sacrificed 3, 7, 14, and 21 days after PQ treatment. We compared pulmonary histopathological changes among different groups on the basis of fibrosis scores, TGF-β1, CTGF and α-SMA pulmonary content via Western blot and real-time quantitative fluorescence-PCR (RT-PCR). Blood levels of MMP-9 and TIMP-1 were determined by ELISA. Human lung fibroblasts WI-38 were divided into control group, PQ group, APN group, and APN receptor (AdipoR) 1 small-interfering RNA (siRNA) group. Fibroblasts were collected 24, 48, and 72 hours after PQ exposure for assay. Cell viability and apoptosis were determined via Kit-8 (CCK-8) and fluorescein Annexin V-FITC/PI double labeling. The protein and mRNA expression level of collagen type III, AdipoR1, and AdipoR2 were measured by Western blot and RT-PCR. APN treatment significantly decreased the lung fibrosis scores, protein and mRNA expression of pulmonary TGF-β1, CTGF and α-SMA content, and blood MMP-9 and TIMP-1 in a dose-dependent manner (p<0.05). Pretreatment with APN significantly attenuated the reduced cell viability and up-regulated collagen type III expression induced by PQ in lung fibroblasts, (p<0.05). APN pretreatment up-regulated AdipoR1, but not AdipoR2, expression in WI-38 fibroblasts. AdipoR1 siRNA abrogated APN-mediated protective effects in PQ-exposed fibroblasts. Taken together, our data suggests APN protects against PQ-induced pulmonary fibrosis in a dose-dependent manner, via suppression of lung fibroblast activation. Functional AdipoR1 are expressed by human WI-38 lung fibroblasts, suggesting potential future clinical applicability of APN against pulmonary fibrosis.

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#24330623   2014/01/01 Save this To Up

Plasma levels of the MMP-9:TIMP-1 complex as prognostic biomarker in breast cancer: a retrospective study.

Worldwide more than one million women are annually diagnosed with breast cancer. A considerable fraction of these women receive systemic adjuvant therapy; however, some are cured by primary surgery and radiotherapy alone. Prognostic biomarkers guide stratification of patients into different risk groups and hence improve management of breast cancer patients. Plasma levels of Matrix Metalloproteinase-9 (MMP-9) and its natural inhibitor Tissue inhibitor of metalloproteinase-1 (TIMP-1) have previously been associated with poor patient outcome and resistance to certain forms of chemotherapy. To pursue additional prognostic information from MMP-9 and TIMP-1, the level of the MMP-9 and TIMP-1 complex (MMP-9:TIMP-1) was investigated in plasma from breast cancer patients.

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#23755818   2013/06/12 Save this To Up

[Role of PI3K-AKT signaling pathway in CD40-mediated proliferation and invasiveness of lung cancer cell].

To analyze the CD40-mediated in vitro proliferation and invasiveness of lung cancer cell H1299, and explore the role of phosphatidylinositol-3-kinase-protein kinase B (PI3K-AKT) signaling pathway in the above-mentioned process.

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#23478276   2013/05/22 Save this To Up

Urinary MMP-9/NGAL ratio as a potential marker of FSGS in nephrotic children.

The study was undertaken to develop a potential new markers for distinguishing minimal change nephrotic syndrome (MCNS) and focal segmental glomerulosclerosis (FSGS) in children. We hypothesized that matrix metalloproteinase-9/neutrophil gelatinase-associated lipocalin (MMP-9/NGAL) is a better marker of focal sclerosis in the glomerulus then matrix metalloproteinase-9/tissue inhibitor of metalloproteinase-1 (MMP-9/TIMP-1) and matrix metalloproteinase-2/tissue inhibitor of metalloproteinase-2 MMP2/TIMP-2.

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#20195229   2010/03/02 Save this To Up

Altered pattern of circulating matrix metalloproteinases -2,- 9 and tissue inhibitor of metalloproteinase-2 in patients with HCV-related chronic hepatitis. Relationship to histological features.

The aim of this paper was to assess circulating levels of metalloprotease2 (MMP2), metalloprotease9 (MMP9) and tissue inhibitor of metalloprotease2 (TIMP2) in patients with HCV-related chronic hepatitis to verify whether there was a relationship between these molecules and biochemical and histological features.

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