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The complement system plays a major role in systemic lupus erythematosus (SLE). At present, complement component 3(C3) and component 4(C4) are the diagnostic markers in the internationally recognized standard of SLE classification. Complement C3 and C4 can play a role in the diagnosis of SLE patients, but they are not very specific diagnostic markers. Therefore, it is important to find more better biomarkers of SLE. In this review, the latest findings in complement-focused research in SLE were explored. Complement level, cell-bound complement activation products and membrane-bound complement regulatory proteins are associated with the pathogenesis of SLE. They may become SLE biomarkers and aid the diagnosis and monitoring of patients with this disease.
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Atherosclerosis(AS) is the basic pathological process of many cardiovascular and cerebrovascular diseases. Particularly, the rupture of vulnerable plaques is a major cause of disability and death among middle-aged and elderly people. It's crucial to find out some reliable serummarkers for diagnosis, treatment and prognosis of AS. This study aims to summarize some newly reported miRNAs which can control the development of AS by regulating the biological function of endothelial cells, smooth muscle cells and macrophages.We also enumerated some target genes and signal pathways that they may act on, and thus provide some new ideas for the treatment of AS and to provide theoretical basis for finding serum biomarkers which can evaluate the occurrence and stability of AS plaque.
ABSTRACT
The complement system plays a major role in systemic lupus erythematosus (SLE). At present, complement component 3(C3) and component 4(C4) are the diagnostic markers in the internationally recognized standard of SLE classification. Complement C3 and C4 can play a role in the diagnosis of SLE patients, but they are not very specific diagnostic markers. Therefore, it is important to find more better biomarkers of SLE. In this review, the latest findings in complement-focused research in SLE were explored. Complement level, cell-bound complement activation products and membrane-bound complement regulatory proteins are associated with the pathogenesis of SLE. They may become SLE biomarkers and aid the diagnosis and monitoring of patients with this disease.
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Aquaporin (AQP)is a molecular weight of about 28 kD of the four polymer structure membrane channel protein. In mammals,there are 1 3 different AQP,expressed in different tissues and organs,regulating waterand glycerol and urea and other small molecules transmembrane transport of major proteins.AQP-1 is mainly expressed in the renal proximal tubule and Henle’s loop drop bronchiole epithelial cell apical membrane and basement membrane,is responsible for the reabsorption of renal tubular water molecules.The expression of AQP-1 can be changed when the kidney is damaged or damaged,so it is very important to study the mechanism of AQP-1 for understanding the pathogenesis of water metabolism and the treatment of clinical water metabolism.
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Objective To investigate the effects of TLR7 on imiquimod induced apoptosis of THP-1 derived macrophages.Methods Three cell lines ( THP-1 derived macrophages, MDCK cell line and HUVEC cell line) with different capabilities of expressing TLR7 were selected.The survival rates of cells af-ter the treatment with different concentrations of imiquimod were detected by MTT assay.The levels of IL-6 in the supernatants of TLR7 inhibitor chloroquine or TLR7-siRNA treated cells were detected by enzyme-linked immunosorbent assay.The apoptosis of cells was detected by flow cytometry after inhibiting the ex-pression of TLR7.Results Imiquimod induced the apoptosis of THP-1 derived macrophages, MDCK cell lines and HUVEC cell lines.The levels of IL-6 were significantly decreased as the expression of TLR7 was inhibited by treating THP-1 derived macrophages with chloroquine or TLR7-siRNA.Treating THP-1 derived macrophages with chloroquine or TLR7-siRNA did not affect the cell apoptosis induced by imiquimod.Con-clusion Imiquimod could induce the apoptosis of THP-1 derived macrophages through TLR7 independent pathway.
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Objective To study the effects of Toll-like receptor 4(TLR4) on oxidized low density lipoprotein ( ox-LDL) induced macrophage apoptosis and its possible mechanism .Methods THP-1 derived macrophages were divided into four groups including untreated control group , ox-LDL treated group , ox-LDL+LPS treated group and tunicamycin treated group .MTT assay and flow cytometry analysis were performed to measure cell vitality and cell apoptosis , respectively .Oil red O staining was used to observe the phagocytosis of lipids by macrophages .The persistent and intense endoplasmic reticulum ( ER) stress markers were de-tected by analyzing the expression of glucose-regulated protein 78 ( GRP78 ) and CCAAT/enhancer-binding protein homologous protein ( CHOP) at mRNA and protein levels by q-RT-PCR and Western blot .Small in-terfering RNA ( siRNA) was used to silence the expression of TLR 4 to further elucidate its possible mecha-nism.Results Flow cytomotry and MTT assay showed that the number of apoptotic cells in ox-LDL+LPS treated group were increased more significantly than that in ox-LDL treated group (P<0.01), and cell apop-tosis in both two groups were greater than that in control group (P<0.01).Compared with control group, the expression of GRP78 and CHOP at mRNA and protein levels were up-regulated in ox-LDL+LPS treated group and ox-LDL treated group (P<0.01), and the expression of GRP78 and CHOP in ox-LDL+LPS treated group was significantly higher than that in ox-LDL treated group (P<0.01).Silenced expression of TLR4 al-leviated the endoplasmic reticulum stress (P<0.05).Conclusion Increased expression of CHOP contribu-ted to cell apoptosis .TLR4 might promote ox-LDL induced macrophage apoptosis through accelerating endo-plasmic reticulum stress .
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Objective To research the influenza virus infection on rat vascular smooth cells number,proliferation,apoptosis,the amount of IL-6,sFas,platelet-derived growth factor(PDGF) and the mechanism of atherosclerosis.Methods Flow cytometry,enzyme-linked immunosorbent assay and cell count experiments were used to detect these indicators at 0 h,6 h,12 h,24 h,48 h.Results After influenza virus infected at 0 h,proliferation,apoptosis condition were 10.39％,0.44％,respectively; at 6 h,proliferation,apoptosis respectively increased to 12.68％,0.73％ ; proliferation reached the peak at 12 h (18.01％),instead apoptosis decreased to 0.14％ ; at 24 h,proliferation decreased to 12.89％ and apoptosis markedly increased to 1.09％ ; at 48 h,proliferation further reduced to 7.07％ and apoptosis reached the peak(4.61％).The number of cells and the cytokine secretion were statistically significant to control group (P＜0.05).Conclusion Influenza virus infection might lead to change of cell proliferation and apoptosis and involve the atherosclerosis form and development,and cytokines played an important role in them.
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Objective:The research was performed to understand the expression of CD80,CD86 and its ligand CD28 on peripheral lymphocytes in patients suffered from idiopathic thrombocytopenic purpura(ITP).Methods:The expression of co-stimulatory molecules(CD80,CD86 and its ligand CD28)on peripheral lymphocytes from 34 ITP patient samples and 34 normal samples was detected by immunofluorescence and flow cytometry.Results:The expression of CD80 and CD86 on peripheral lymphocytes from ITP patients(4.21?2.27%,7.19?5.16%) was higher than that of the normal samples as control(2.34?0.87%,4.08?1.96%,p