Dataset Information

Inflammatory Proteomic Network Analysis of Statin-treated and Lipopolysaccharide-activated Macrophages.

ABSTRACT: A significant component of immune biology research is the investigation of protein encoding genes that play central roles in contributing inflammatory response. A gel-free quantitative bottom-up proteomics study was performed on immune cell macrophages after the combined treatment of lipopolysaccharide (LPS) and statin drugs using mass spectrometry and a detailed bioinformatics analyses were conducted. Systematic bioinformatics analysis was applied for discovering novel relationships among proteins and effects of statin and lipopolysaccharide in macrophage cells. Based on gene ontology, majority of protein encoding genes was involved in metabolic and cellular processes and are actively associated with binding, structural molecular, and catalytic activity. Notably, proteomic data analyzed by Ingenuity Pathway Analysis (IPA), discovered the plectin and prohibitin 2 protein interactions network and inflammatory-disease based protein networks. Two up-regulated proteins, plectin and prohibitin 2, were further validated by immunoblotting. Plectin was also cross-validated by immunocytochemistry, since its expression was highly modulated by statin but inhibited during LPS-stimulation. Collectively, the significant up-regulation of plectin due to the treatment of statin, suggests that statin has a significant impact on the cytoskeletal networks of cells. Plectin might have a significant role in the intermediate filament assembly and dynamics, and possibly stabilizing and crosslinking intermediate filament networks.

SUBMITTER: Kamal AHM

PROVIDER: S-EPMC5760528 | biostudies-literature | 2018 Jan

REPOSITORIES: biostudies-literature

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Inflammatory Proteomic Network Analysis of Statin-treated and Lipopolysaccharide-activated Macrophages.

Kamal Abu Hena M AHM Chakrabarty Jayanta K JK Udden S M Nashir SMN Zaki Md Hasan MH Chowdhury Saiful M SM

Scientific reports 20180109 1

A significant component of immune biology research is the investigation of protein encoding genes that play central roles in contributing inflammatory response. A gel-free quantitative bottom-up proteomics study was performed on immune cell macrophages after the combined treatment of lipopolysaccharide (LPS) and statin drugs using mass spectrometry and a detailed bioinformatics analyses were conducted. Systematic bioinformatics analysis was applied for discovering novel relationships among prote ...[more]

PMID: 29317699

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Project description:Context Torin2 has various pharmacological properties. However, its anti-inflammatory activity has not been reported. Objective This study focused on the potential anti-inflammatory properties of Torin2 in lipopolysaccharide (LPS)-evoked RAW264.7 murine macrophages. The study aimed to shed light on the molecular mechanisms that ameliorate these effects. Methods Torin2 was applied to 100 ng/mL lipopolysaccharide-induced RAW 264.7 macrophages in vitro. Nitric oxide (NO) levels were detected using the Griess reagent kit. Prostaglandin E2 (PGE2), pro-inflammatory cytokines interleukin (IL)-1β, interleukin (IL)-6, and tumor necrosis factor in the supernatant fraction were determined using enzyme-linked immunosorbent assay (ELISA). Gene expression of pro-inflammatory cytokines, cyclooxygenase-2 (COX-2), and inducible nitric oxide synthase (iNOS) were tested using real-time quantitative polymerase chain reaction (qPCR). Cyclooxygenase-2 and inducible nitric oxide synthase proteins, phosphorylation of mitogen-activated protein kinase (MAPK) subgroups, extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK), p38, I-kappa-B-alpha (IκBα), and nuclear factor-kappa-B (NF-κB), and activation in extracts were detected via western blotting. Nuclear factor-kappa-B/p65 nuclear translocation was tested using an immunofluorescence assay. Results The results demonstrated that pre-treatment with Torin2 profoundly attenuated the lipopolysaccharide-stimulated levels of nitric oxide and prostaglandin E2, pro-inflammatory cytokines, messenger ribonucleic acid (mRNA), and protein expression of cyclooxygenase-2 and inducible nitric oxide synthase. Collectively, Torin2 pre-treatment notably weakened lipopolysaccharide-induced damage by reducing the phosphorylation of nuclear factor-kappa-B, p38, c-Jun N-terminal kinase, extracellular signal-regulated kinase proteins, and nuclear factor-kappa-B/p65 nuclear translocation. Conclusion Numerous pieces of evidence indicated that Torin2 reversed inflammatory activation by regulating nuclear factor-kappa-B and mitogen-activated protein kinase signaling pathways and provided a tentative potential candidate for preventing and treating inflammatory diseases. Torin2; RAW264.7 murine macrophages; Lipopolysaccharide; Anti-inflammation; Mechanisms.

Dataset Information

Inflammatory Proteomic Network Analysis of Statin-treated and Lipopolysaccharide-activated Macrophages.

Publications

Inflammatory Proteomic Network Analysis of Statin-treated and Lipopolysaccharide-activated Macrophages.

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