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ELISA Kit for Monocyte Chemotactic Protein 1 (MCP1) Organism: Rhesus monkey (Simian)

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[#E90087Si] ELISA Kit for Monocyte Chemotactic Protein 1 (MCP1) Organism: Rhesus monkey (Simian)

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E90087Si | ELISA Kit for Monocyte Chemotactic Protein 1 (MCP1) Organism: Rhesus monkey (Simian), 96T
More informations about ELISA Kit for Monocyte Chemotactic Protein 1 (MCP1) Organism: Rhesus monkey (Simian) in Antibody-antibodies.com

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(1) Direct Effect of Septic Plasma in Human Cell Lines Viability.[TOP]

Pubmed ID :30522094
Publication Date : //
Sepsis is a life-threatening condition often associated with a high incidence of multiple organs injury. Several papers suggested the immune response by itself, with the production of humoral inflammatory mediators, is crucial in determining organ injury. However, little is known of how sepsis directly induces organ injury at the cellular levels. To assess this point, we set up an in vitro study to investigate the response of renal tubular cells (RTCs), monocytes (U937) and hepatocytes (HepG2) after 24 h-incubation with septic patients' plasma.

Authors : Virzì Grazia Maria, Borga Chiara, Pasqualin Chiara, Pastori Silvia, Brocca Alessandra, de Cal Massimo, Nalesso Federico, Zanella Monica, Brendolan Alessandra, Ronco Claudio,



(2) Anti-neuroinflammatory effects of GPR55 antagonists in LPS-activated primary microglial cells.[TOP]

Pubmed ID :30453998
Publication Date : //
Neuroinflammation plays a vital role in Alzheimer's disease and other neurodegenerative conditions. Microglia are the resident mononuclear immune cells of the central nervous system, and they play essential roles in the maintenance of homeostasis and responses to neuroinflammation. The orphan G-protein-coupled receptor 55 (GPR55) has been reported to modulate inflammation and is expressed in immune cells such as monocytes and microglia. However, its effects on neuroinflammation, mainly on the production of members of the arachidonic acid pathway in activated microglia, have not been elucidated in detail.

Authors : Saliba Soraya Wilke, Jauch Hannah, Gargouri Brahim, Keil Albrecht, Hurrle Thomas, Volz Nicole, Mohr Florian, van der Stelt Mario, Bräse Stefan, Fiebich Bernd L,



(3) Alteration of Myeloid-Derived Suppressor Cells, Chronic Inflammatory Cytokines, and Exosomal miRNA Contribute to the Peritoneal Immune Disorder of Patients With Endometriosis.[TOP]

Pubmed ID :30453861
Publication Date : //
Immunologic disorder has been reported to promote the progression of endometriosis (EMT). It has been known that myeloid-derived suppressor cells (MDSCs) drive the progression of many types of diseases. Few studies have shown the relation between MDSCs and EMT. To test whether MDSCs play a role in the progression of EMT, we defined MDSCs, cytokines, and the exosomal microRNA (miRNA) profile in peritoneal fluid (PF) from EMT patients. Characteristics of MDSCs, regulatory T cells (Tregs) and effector T cells were quantified by flow cytometry. Peritoneal fluid monocyte chemoattractant protein (MCP) 1/3, hepatocyte growth factor (HGF), chemokine (C-X-C motif) ligand (CXCL) 1/2, and 13 other cytokines were performed by enzyme-linked immunosorbent assay kit. Exosomal miRNA sequencing was prepared from PF of 3 women with early-stage EMT, 3 women with advanced stage EMT, and 3 women from control group. Our results showed that accumulations of monocytic MDSCs (Mo-MDSCs) and Tregs were detected in advanced patients with EMT. Patients with EMT displayed a significantly higher production of PF CXCL1, CXCL2, MCP-1, MCP-3, and HGF as compared to those from controls. MicroRNA sequencing showed 13 exosomal miRNAs (miRNA-1908, -130b, -451a, -486-5p, -4488, -432, -342, -425, -505, -6508, -145, -365a, and -365b) which are involved in immune alteration and cell proliferation and were differentially expressed in patients with EMT (fold-change ± 2.0). In conclusion, our study revealed that Mo-MDSCs, inflammatory cytokines, and exosomal miRNA seem to be involved in the progression of EMT; however, the relation between Mo-MDSCs, cytokines, and miRNA needs further research.

Authors : Chen Ya, Wang Kangxia, Xu Yuping, Guo Peipei, Hong Baoli, Cao Yunxia, Wei Zhaolian, Xue Rufeng, Wang Chao, Jiang Huanhuan,



(4) The Release of Monocyte-Derived Tissue Factor-Positive Microparticles Contributes to a Hypercoagulable State in Idiopathic Membranous Nephropathy.[TOP]

Pubmed ID :30429407
Publication Date : //
Idiopathic membranous nephropathy (IMN) is an immune-mediated inflammatory disease characterized by a high risk of thromboembolic complications. Microparticles (MPs), a type of extracellular vesicles, have procoagulant properties, especially when they display tissue factor (TF). This study aimed to investigate whether circulating TF-positive MPs contributed to the hypercoagulable state in patients with IMN.

Authors : Wang Gui Hua, Lu Jian, Ma Kun Ling, Zhang Yang, Hu Ze Bo, Chen Pei Pei, Lu Chen Chen, Zhang Xiao Liang, Liu Bi Cheng,



(5) The role of NOX2-derived reactive oxygen species in collagenase-induced osteoarthritis.[TOP]

Pubmed ID :30195046
Publication Date : //
Synovitis in collagenase-induced osteoarthritis (CiOA) is driven by locally released S100A8/A9 proteins and enhances joint destruction. S100A8/A9 can induce reactive oxygen species (ROS) release by phagocytes in OA synovium via neutrophil cytosolic factor-1 (Ncf1)-regulated NOX2 activation. In the present study we investigated whether NOX2-derived ROS affect joint pathology during CiOA.

Authors : van Dalen S C M, Kruisbergen N N L, Walgreen B, Helsen M M A, Slöetjes A W, Cremers N A J, Koenders M I, van de Loo F A J, Roth J, Vogl T, Blom A B, van der Kraan P M, van Lent P L E M, van den Bosch M H J,



(6) Inhibition of C-X-C Motif Chemokine 10 (CXCL10) Protects Mice from Cigarette Smoke-Induced Chronic Obstructive Pulmonary Disease.[TOP]

Pubmed ID :30118441
Publication Date : //
BACKGROUND Chronic obstructive pulmonary disease (COPD) is a type of obstructive lung disease characterized by long-term breathing problems and poor airflow. COPD can progress to persistent decline of pulmonary function. This study explored the effect of CXCL10 on COPD induced by cigarette smoke (CS) and its underlying mechanism. MATERIAL AND METHODS Wild-type (WT) mice were randomly assigned into 3 groups: the control group, the CS group, and the intervention group. Mice in the CS group were exposed to CS and mice in the CXCL10 group were exposed to CS and CXCL10 neutralizing antibody. At 24 h after the last CS exposure, body weight and lung functions of each mouse were recorded. Mice were then anesthetized for collecting bronchoalveolar lavage fluid (BALF) and lung tissues. Levels of interleukin-6 (IL-6), keratinocyte chemotactic factor (KC), and monocyte chemoattractant protein-1 (MCP-1) in supernatant and lung homogenate were detected by ELISA and real-time PCR (RT-PCR), respectively. For in vitro experiments, human bronchial epithelial cells 16HBE were stimulated with different concentrations of cigarette smoke extract (CSE) and CXCL10. Cell viability and levels of inflammatory cytokines in the cell supernatant were detected by Cell Counting Kit-8 (CCK-8) and ELISA assay, respectively. RESULTS Our data showed significant weight loss and reduction of lung functions in mice in the CS group compared with those in the control group and intervention group. Increased levels of IL-6, KC, and MCP-1 in BALF and lung homogenate were observed in mice in the model group compared to those in the control group and intervention group. In vitro experiments also confirmed that CXCL10-neutralizing antibody can inhibit CSE-induced cell necrosis and activation of inflammatory cytokines. CONCLUSIONS Inhibited CXCL10 protects against COPD progression by decreasing secretion of inflammatory factors, which provides a new direction for the clinical prevention and treatment of COPD.

Authors : Jing Hongyu, Liu Lingyun, Zhou Junfeng, Yao Hanxin,



(7) Zedoarondiol Attenuates Endothelial Cells Injury Induced by Oxidized Low-Density Lipoprotein via Nrf2 Activation.[TOP]

Pubmed ID :30064139
Publication Date : //
Zedoarondiol, a sesquiterpene lactone compound, showed an anti-proliferative activity on vascular smooth muscle cells in our previous study. However, whether it has a beneficial effect on endothelial cells injury induced by oxidized low-density lipoprotein (ox-LDL) remains unclear. This study was designed to investigate the protective effect of zedoarondiol on ox-LDL-induced injury of endothelial cells and explored its underlying mechanism.

Authors : Mao Huimin, Tao Tianqi, Wang Xiaoren, Liu Mi, Song Dandan, Liu Xiuhua, Shi Dazhuo,



(8) Tumour necrosis factor-related apoptosis-inducing ligand expression in patients with diabetic nephropathy.[TOP]

Pubmed ID :29999450
Publication Date : //
The objective of this study was to evaluate the expression profile of tumour necrosis factor-related apoptosis-inducing ligand (TRAIL) in patients with diabetic nephropathy (DN).

Authors : Chang Wei-Wei, Liang Wei, Yao Xin-Ming, Zhang Liu, Zhu Li-Jun, Yan Chen, Jin Yue-Long, Yao Ying-Shui,



(9) [Methyltransferase-like 3 Promotes the Proliferation of Acute Myeloid Leukemia Cells by Regulating N6-methyladenosine Levels of MYC].[TOP]

Pubmed ID :29978784
Publication Date : //
Objective To investigate the role of methyltransferase-like 3(METTL3) in the proliferation of acute myeloid leukemia (AML) cells and its mechanism. Methods METTL3 expression in AML patients was analyzed in Gene Expression Omnibus data files. METTL3 expression was inhibited by lentivirus-mediated gene transduction in MOLM13 cells,after which cell proliferation was analyzed by cell counting kit-8,N6-methyladenosine (m6A) levels of total mRNA was analyzed by ELISA,specific m6A on MYC was analyzed by gene-specific m6A RNA immunoprecipitation,and MYC expression was analyzed by RT-qPCR and Western blot analysis. Results METTL3 level was slightly increased in AML-M5 patients,and its expression was significantly higher in immature cells than in mature monocytes (t=4.504,P=0.0098). METTL3 knock-down significantly suppressed cell proliferation (P<0.001),reduced m6A level of total mRNA (t=3.606,P=0.042) and specific m6A level on MYC mRNA (P<0.01),and suppressed MYC expression (P<0.01). Conclusion METTL3 acts as an oncogene in MOLM13 cells by upregulating MYC expression.

Authors : Wang Xiao-Shuang, He Jin-Rong, Yu Shan, Yu Jia,



(10) Macrophage M1/M2 polarization in patients with pregnancy-induced hypertension.[TOP]

Pubmed ID :29972321
Publication Date : //
This study aimed to validate whether macrophage polarization imbalance and abnormal cytokines production occurred in pregnancy-induced hypertension (PIH) patients. PIH women (n = 26) were enrolled and the level of biochemical parameters were determined. The percentage of CD86- and CD163-positive cells, representing M1 and M2 macrophages, were determined by flow cytometry. The concentrations of cytokines (TNF-α, IL-1β, IL-4, IL-13, and IL-10) were determined using enzyme-linked immunosorbent assay kit. THP-1 cells were incubated with 10% serum from PIH and control groups, and then macrophage polarization and cytokines production were analyzed. The levels of high-density lipoprotein cholesterol and apolipoprotein A1 were significantly lower, and the levels of fasting blood glucose, total cholesterol, triacylglycerol, low-density lipoprotein cholesterol, apolipoprotein B, and lipoprotein a were significantly higher in the PIH group than that in the control group. The PIH group contained a significant higher percentage of CD86-positive cells (M1) and a significant lower percentage of CD163-positive cells (M2), representing higher M1/M2 ratio, than the control group. The PIH group expressed higher concentrations of TNF-α and IL-1β, and expressed lower concentrations of IL-4, IL-10, and IL-13 than the control group. The in vitro experiment also showed macrophage polarization imbalance and abnormal cytokines production in THP-1 cells treated with PIH serum as compared with that treated with control serum. Macrophage polarization imbalance and abnormal cytokines production occurred in PIH patients and in THP-1 cells treated with PIH serum.

Authors : Li Yan, Xie Zhen, Wang Yaning, Hu Hongyi,