Anti-ICAM1 polyclonal antibody

Background MiR-27 has been found to present an overt myocardial expression during cardiogenesis. However, whether miR-27 involves in myocarditis development and the possible molecular mechanism remain unknown. The purpose of this study was to investigate the biological characteristic of miR-27 in LPS-damaged H9c2 cells. Methods H9c2 cells were treated with lipopolysaccharide (LPS, 10 mu g/ml) for 12 h to form cell injury. MiR-27 mimic and inhibitor were used to up-regulate or down-regulate miR-27 expression. MTT assay and flow cytometry analysis were conducted to test cell viability and apoptosis. The relative RNA expression level of miR-27 and intercellular adhesion molecule 1 (ICAM1) was determined by qRT-PCR. Luciferase reporter gene assay was utilized to confirm the interaction between miR-27 and ICAM1. Western blot was used to determine the protein expression levels. Results We observed that LPS treatment significantly decreased the level of miR-27 in H9c2 cells. Moreover, LPS exposure suppressed cell viability, promoted cell apoptosis and increased the relative expression of p-NF-kappa B p65/NF-kappa B p65 and p-I kappa B alpha/I kappa B alpha. Up-regulation of miR-27 increased cell proliferation and reduced cell apoptosis, while down-regulation of miR-27 suppressed cell growth and promoted cell apoptosis. ICAM1 was predicted and verified as a target of miR-27, and the expression of ICAM1 is negatively regulated by miR-27. The relative expression of p-NF-kappa B p65/NF-kappa B p65 and p-I kappa B alpha/I kappa B alpha was dramatically decreased by miR-27 mimic and increased by miR-27 inhibitor. Conclusion Our study illustrated that up-regulation of miR-27 exhibits a protective effect on LPS-damaged H9c2 cells, which may be achieved by regulating ICAM1 and NF-kappa B signaling.

Background: Cardiovascular events are the primary cause of death for chronic kidney disease patients, which occurred via vascular calcification evolving pathogenically. Although a high level of phosphorus contributes to the induction of osteogenic differentiation of vascular smooth muscle cells (VSMCs), the role of lncRNA in this process awaits further study. Methods: In this study, we systematically investigated the variation of gene expression in human VSMCs induced by high phosphorus. LncRNAs and mRNAs expression were revealed by microarray analyses of the control group and high-phosphorus (HP) group. LncRNA-mRNA co-expression network was established based on the specific lncRNA-mRNA relationships. Hierarchical clustering was used to identify a common set of regulated genes. In addition, Gene Ontology enrichment, Kyoto Gene-Encyclopedia and genomic analyses were conducted for the mRNAs differentially expressed under high phosphorus. Result: RT-qPCR results confirmed that the expression of RUNX2, BMP2 and osteocalcin in HP group exhibited significant increases than in control group (p < .05). VSMC in HP group also showed higher intracellular calcium content. Volcano plots results show that 379 mRNAs and 728 lncRNAs different expressed in HP group. LncRNA-mRNA co-expression networks analysis revealed that 8 lncRNAs were the most highly connected lncRNAs. Quantitative analysis indicated that two lncRNAs were confirmed to increase significantly in the HP group. The mRNA expression of NT5E and ICAM1 were higher in group HP, while MAP3K7CL was lower than CON group (p < .05). Conclusion: This study provided a working list of lncRNAs that may be relevant to osteogenic differentiation, which presents a new insights into the mechanism of vascular calcification induced by high phosphorus in VSMCs.