scholarly journals Comparative Proteomic Analysis of Polarized Human THP-1 and Mouse RAW264.7 Macrophages

2021 ◽  
Vol 12 ◽  
Author(s):  
Pengfei Li ◽  
Zhifang Hao ◽  
Jingyu Wu ◽  
Chen Ma ◽  
Yintai Xu ◽  
...  
Keyword(s):  
Protein Expression ◽  
Cell Line ◽  
Cell Lines ◽  
Expression Profiles ◽  
Mouse Cell ◽  
Activated Macrophages ◽  
M1 Macrophages ◽  
Alternatively Activated Macrophages ◽  
Raw264.7 Macrophages ◽  
Protein Expression Profiles

Macrophages can be polarized into classically activated macrophages (M1) and alternatively activated macrophages (M2) in the immune system, performing pro-inflammatory and anti-inflammatory functions, respectively. Human THP-1 and mouse RAW264.7 cell line models have been widely used in various macrophage-associated studies, while the similarities and differences in protein expression profiles between the two macrophage models are still largely unclear. In this study, the protein expression profiles of M1 and M2 phenotypes from both THP-1 and RAW264.7 macrophages were systematically investigated using mass spectrometry-based proteomics. By quantitatively analyzing more than 5,000 proteins among different types of macrophages (M0, M1 and M2) from both cell lines, we identified a list of proteins that were uniquely up-regulated in each macrophage type and further confirmed 43 proteins that were commonly up-regulated in M1 macrophages of both cell lines. These results revealed considerable divergences of each polarization type between THP-1 and RAW264.7 macrophages. Moreover, the mRNA and protein expression of CMPK2, RSAD2, DDX58, and DHX58 were strongly up-regulated in M1 macrophages for both macrophage models. These data can serve as important resources for further studies of macrophage-associated diseases in experimental pathology using human and mouse cell line models.

Methamphetamine causes neurotoxicity by promoting polarization of macrophages and inflammatory response

2017 ◽  
Vol 37 (5) ◽  
pp. 486-495 ◽  
Author(s):  
X Li ◽  
F Wu ◽  
L Xue ◽  
B Wang ◽  
J Li ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Protein Expression ◽  
Macrophage Polarization ◽  
Enzyme Linked Immunosorbent Assay ◽  
Neuronal System ◽  
Activated Macrophages ◽  
Alternatively Activated Macrophages ◽  
Raw264.7 Macrophages ◽  
Gene And Protein Expression ◽  
Anti Inflammatory

Macrophages, especially their activation state, are closely related to the progression of neurotoxicity. Classically activated macrophages (M1) are proinflammatory effectors, while alternatively activated macrophages (M2) exhibit anti-inflammatory properties. As a powerful addictive psychostimulant drug, coupled with its neurotoxicity, methamphetamine (Meth) abuse may lead to long-lasting abnormalities in the neuronal system. The present study investigated the effect of Meth at subtoxic concentration on macrophage activation state and its underlying toxicity to neuronal cells. PC12 and Murine RAW264.7 cells were coincubated with Meth to test its toxicity. 3-(4,5-Dimethylthiazol)-2,5-diphenyltetrazolium-bromide, enzyme-linked immunosorbent assay, real-time polymerase chain reaction, and Western blot assays were performed to evaluate the toxicity, cytokine secretion, gene, and protein expression. Results showed that cytotoxicity was enhanced on PC12 cells after coculturing with RAW264.7 stimulated with Meth. RAW264.7 macrophages tended to switch to the M1 phenotype, releasing more nitric oxide and proinflammatory cytokines, including tumor necrosis factor α (TNFα), interleukin (IL)-12, and IL-1β, while decreasing the release of anti-inflammatory cytokine IL-10 after treatment with Meth. Meth upregulated the gene expression of IL-6, IL-1β, and TNFα and downregulated the expression of Arg-1, IL-10, and KLF4. Meth could also upregulate the protein expression of IL-1β and TNF α and downregulate the expression of Arg-1 and KLF4. However, the abovementioned effects induced by Meth were abolished by the addition of dopamine receptor D3 antagonist. In conclusion, our study demonstrated that Meth promoted macrophage polarization from M0 to M1 and enhanced inflammatory response, which provided the scientific rationale for the neurotoxicity caused by the chronic use of Meth.

Comparative proteomic profiling of Hodgkin lymphoma cell lines

2016 ◽  
Vol 12 (1) ◽  
pp. 219-232 ◽  
Author(s):  
D. Vergara ◽  
P. Simeone ◽  
S. De Matteis ◽  
S. Carloni ◽  
P. Lanuti ◽  
...  
Keyword(s):  
Protein Expression ◽  
B Cell ◽  
Hodgkin Lymphoma ◽  
Cell Lines ◽  
Expression Profiles ◽  
Lymphoma Cell ◽  
Classical Hodgkin Lymphoma ◽  
Proteomic Profiling ◽  
Hodgkin Lymphoma Cell ◽  
Protein Expression Profiles

Classical Hodgkin lymphoma models of T- and B-cell derivation show significant differences in their protein expression profiles.

scholarly journals Correlations between RNA and protein expression profiles in 23 human cell lines

BMC Genomics ◽  
2009 ◽  
Vol 10 (1) ◽  
pp. 365 ◽  
Author(s):  
Marcus Gry ◽  
Rebecca Rimini ◽  
Sara Strömberg ◽  
Anna Asplund ◽  
Fredrik Pontén ◽  
...  
Keyword(s):  
Protein Expression ◽  
Cell Lines ◽  
Human Cell ◽  
Expression Profiles ◽  
Human Cell Lines ◽  
Protein Expression Profiles

scholarly journals Comparative Proteomic Analysis of Human Cholangiocarcinoma Cell Lines: S100A2 as a Potential Candidate Protein Inducer of Invasion

2015 ◽  
Vol 2015 ◽  
pp. 1-6 ◽  
Author(s):  
Kasima Wasuworawong ◽  
Sittiruk Roytrakul ◽  
Atchara Paemanee ◽  
Kattaleeya Jindapornprasert ◽  
Waraporn Komyod
Keyword(s):  
Protein Expression ◽  
Cell Lines ◽  
Calcium Binding ◽  
Expression Profiles ◽  
S100 Protein ◽  
Potential Candidate ◽  
Proteomic Data ◽  
Potential Biomarker ◽  
Cholangiocarcinoma Cell ◽  
Protein Expression Profiles

Cholangiocarcinoma (CCA) is a bile duct cancer, commonly found in Asia including Thailand and especially in the northeastern region of Thailand. To identify the proteins involved in carcinogenesis and metastasis of CCA, protein expression profiles of high-invasive KKU-M213 and low-invasive KKU-100 cell lines were compared using a comparative GeLC-MS/MS proteomics analysis. A total of 651 differentially expressed proteins were detected of which 27 protein candidates were identified as having functions involved in cell motility. A total of 22 proteins were significantly upregulated in KKU-M213, whereas 5 proteins were downregulated in KKU-M213. S100A2, a calcium-binding protein in S100 protein family, is upregulated in KKU-M213. S100A2 is implicated in metastasis development in several cancers. The protein expression level of S100A2 was verified by Western blot analysis. Intriguingly, high-invasive KKU-M213 cells showed higher expression of S100A2 than KKU-100 cells, consistent with proteomic data, suggesting that S100A2 may be a key protein involved in the progression of CCA. However, the biological function of S100A2 in cholangiocarcinoma remains to be elucidated. S100A2 might be a potential biomarker as well as a novel therapeutic target in CCA metastasis.

scholarly journals The PAK Inhibitor PF-3758309 Promotes the Inhibitory Effects of Multiple Chemotherapeutic Reagents on Patient-Derived Pancreatic Cancer Cell Lines

2018 ◽  
Author(s):  
Kai Wang ◽  
Nhi Huynh ◽  
Xiao Wang ◽  
Marina Pajic ◽  
Ashleigh Parkin ◽  
...  
Keyword(s):  
Protein Expression ◽  
Cell Lines ◽  
Tumour Growth ◽  
Pancreatic Cancer Cell ◽  
Expression Profiles ◽  
Ductal Adenocarcinoma ◽  
Inhibitory Effects ◽  
Protein Levels ◽  
Protein Expression Profiles

Pancreatic ductal adenocarcinoma (PDA) remains the most lethal malignancy due to lack of an effective treatment. P21-activated kinases (PAKs) play key roles in PDA growth, and the PAK inhibitor PF-3758309 synergistically reduced PDA growth with gemcitabine. The aim of this study was to determine the effect of PF-3758309 with multiple chemotherapeutic reagents on a panel of patient-derived PDA cell lines. Cells were treated with PF-3758309 plus or minus gemcitabine, 5-fluorouracil (5-FU) or abraxane, and cell proliferation was determined. Protein expression profiles were measured by Western blot. PDA cells were subcutaneously injected into the flanks of SCID mice which were then treated with PF-3758309, gemcitabine, PF-3758309 plus gemcitabine, or gemcitabine plus abraxane. Tumour growth was measured by volume and weight. PF-3758309 enhanced the inhibitory effects of 5-FU, gemcitabine and abraxane on a panel of patient-derived PDA cells, inhibited HIF-1 protein expression and reduced the protein levels of palladin and -SMA in these cells. The combination of PF-3758309 with gemcitabine maximally inhibited PDA growth in vivo, which was comparable to the combination of gemcitabine with abraxane. PF-3758309 enhanced the suppressive effects of multiple chemotherapeutic reagents on the growth of a panel of patient-derived PDA cell lines. The combination of PF-3758309 with gemcitabine provides a potential treatment option with less toxicity than gemcitabine plus abraxane.

scholarly journals Genome-Wide Role of HSF1 in Transcriptional Regulation of Desiccation Tolerance in the Anhydrobiotic Cell Line, Pv11

2021 ◽  
Vol 22 (11) ◽  
pp. 5798
Author(s):  
Shoko Tokumoto ◽  
Yugo Miyata ◽  
Ruslan Deviatiiarov ◽  
Takahiro G. Yamada ◽  
Yusuke Hiki ◽  
...  
Keyword(s):  
Cell Line ◽  
Cell Lines ◽  
Desiccation Tolerance ◽  
Expression Profiles ◽  
Insect Cell Line ◽  
Gene Expression Profiles ◽  
Late Embryogenesis Abundant ◽  
Heat Shock Factor 1 ◽  
Genome Wide ◽  
A Genome

The Pv11, an insect cell line established from the midge Polypedilum vanderplanki, is capable of extreme hypometabolic desiccation tolerance, so-called anhydrobiosis. We previously discovered that heat shock factor 1 (HSF1) contributes to the acquisition of desiccation tolerance by Pv11 cells, but the mechanistic details have yet to be elucidated. Here, by analyzing the gene expression profiles of newly established HSF1-knockout and -rescue cell lines, we show that HSF1 has a genome-wide effect on gene regulation in Pv11. The HSF1-knockout cells exhibit a reduced desiccation survival rate, but this is completely restored in HSF1-rescue cells. By comparing mRNA profiles of the two cell lines, we reveal that HSF1 induces anhydrobiosis-related genes, especially genes encoding late embryogenesis abundant proteins and thioredoxins, but represses a group of genes involved in basal cellular processes, thus promoting an extreme hypometabolism state in the cell. In addition, HSF1 binding motifs are enriched in the promoters of anhydrobiosis-related genes and we demonstrate binding of HSF1 to these promoters by ChIP-qPCR. Thus, HSF1 directly regulates the transcription of anhydrobiosis-related genes and consequently plays a pivotal role in the induction of anhydrobiotic ability in Pv11 cells.

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