The Mechanism of Anti-inflammation Effects of Propolis Components in Raw264.7 Macrophage Cell

2021 ◽  
Vol 36 (4) ◽  
pp. 243-250
Author(s):  
Sung-Kuk Kim ◽  
Sang Mi Han ◽  
Se Gun Kim ◽  
Hyo Young Kim ◽  
Sik Ryu ◽  
...  
Keyword(s):  
Macrophage Cell ◽  
Anti Inflammation ◽  
Raw264.7 Macrophage

WNT/β-catenin pathway is modulated in asthma patients and LPS-stimulated RAW264.7 macrophage cell line

2011 ◽  
Vol 34 (1) ◽  
pp. 56-65 ◽  
Author(s):  
Haeyong Lee ◽  
Sungmin Bae ◽  
Byoung Whui Choi ◽  
Yoosik Yoon
Keyword(s):  
Cell Line ◽  
Macrophage Cell Line ◽  
Macrophage Cell ◽  
Asthma Patients ◽  
Raw264.7 Macrophage

scholarly journals Suppression of methylmercury-induced MIP-2 expression by N-acetyl-l-cysteine in murine RAW264.7 macrophage cell line

2017 ◽  
Vol 22 (1) ◽  
Author(s):  
Juliet David ◽  
Athira Nandakumar ◽  
Muflihatul Muniroh ◽  
Suminori Akiba ◽  
Megumi Yamamoto ◽  
...  
Keyword(s):  
Cell Line ◽  
Macrophage Cell Line ◽  
Macrophage Cell ◽  
Raw264.7 Macrophage

scholarly journals CRISPR/CAS9-Mediated Genome Editing of miRNA-155 Inhibits Proinflammatory Cytokine Production by RAW264.7 Cells

2015 ◽  
Vol 2015 ◽  
pp. 1-7 ◽  
Author(s):  
Weixia Jing ◽  
Xuewu Zhang ◽  
Wenyan Sun ◽  
Xiujuan Hou ◽  
Zhongqiang Yao ◽  
...  
Keyword(s):  
Genome Editing ◽  
Therapeutic Strategy ◽  
Cytokine Production ◽  
Macrophage Cell ◽  
Src Homology 2 ◽  
Receptor Activator ◽  
Short Palindromic Repeat ◽  
Src Homology ◽  
Src Homology 2 Domain ◽  
Raw264.7 Macrophage

MicroRNA 155 (miR-155) is a key proinflammatory regulator in clinical and experimental rheumatoid arthritis (RA). Here we generated a miR-155 genome knockout (GKO) RAW264.7 macrophage cell line using the clustered regulatory interspaced short palindromic repeat (CRISPR)/CRISPR-associated protein 9 (CAS9) technology. While upregulating the Src homology-2 domain-containing inositol 5-phosphatase 1 (SHIP1), the miR-155 GKO line is severely impaired in producing proinflammatory cytokines but slightly increased in osteoclastogenesis upon treatment with receptor activator of nuclear factor-κB ligand (RANKL). Taken together, our results suggest that genome editing of miR-155 holds the potential as a therapeutic strategy in RA.

scholarly journals Lipopolysaccharide induces calcitonin gene-related peptide in the RAW264.7 macrophage cell line

Immunology ◽  
2010 ◽  
Vol 130 (3) ◽  
pp. 399-409 ◽  
Author(s):  
Weiya Ma ◽  
Yvan Dumont ◽  
Freya Vercauteren ◽  
Remi Quirion
Keyword(s):  
Cell Line ◽  
Calcitonin Gene Related Peptide ◽  
Macrophage Cell Line ◽  
Macrophage Cell ◽  
Related Peptide ◽  
Calcitonin Gene ◽  
Raw264.7 Macrophage

Induction of nitric oxide production in RAW264.7 macrophage cell une by mineral fibers

1994 ◽  
Vol 74 ◽  
pp. 69-70
Author(s):  
M. Ruotsalainen ◽  
M.-R. Hirvonen ◽  
K.M. Savolainen
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Production ◽  
Macrophage Cell ◽  
Mineral Fibers ◽  
Oxide Production ◽  
Raw264.7 Macrophage

Chemotaxis of Lipopolysaccharide-Stimulated RAW264.7 Macrophage Cell Line in Microfluidic Channels

2017 ◽  
Vol 17 (11) ◽  
pp. 7996-8000
Author(s):  
Junhyun Park ◽  
Jayoung Koo ◽  
Ji-Youn Kim ◽  
Kyung-Jin Chung ◽  
Eun-Surk Yi ◽  
...  
Keyword(s):  
Cell Line ◽  
Microfluidic Channels ◽  
Macrophage Cell Line ◽  
Macrophage Cell ◽  
Raw264.7 Macrophage

scholarly journals Alkyl Glycerols Activate RAW264.7 Macrophage Cell Line

2019 ◽  
Vol 14 (6) ◽  
pp. 1934578X1985851 ◽  
Author(s):  
Igor V. Manzhulo ◽  
Anna A. Tyrtyshnaia ◽  
Polina V. Mischenko ◽  
Anastasia A. Egoraeva ◽  
Alisa S. Belova ◽  
...  
Keyword(s):  
Cell Line ◽  
Macrophage Cell Line ◽  
Macrophage Cell ◽  
Raw264.7 Macrophage

Differential iron transport into phagosomes isolated from the RAW264.7 macrophage cell lines transfected with Nramp1Gly169 or Nramp1Asp169

1999 ◽  
Vol 66 (1) ◽  
pp. 113-119 ◽  
Author(s):  
Donald E. Kuhn ◽  
Beth D. Baker ◽  
William P. Lafuse ◽  
Bruce S. Zwilling
Keyword(s):  
Cell Lines ◽  
Iron Transport ◽  
Macrophage Cell ◽  
Raw264.7 Macrophage

scholarly journals Papillomavirus-Like Particles Stimulate Murine Bone Marrow-Derived Dendritic Cells To Produce Alpha Interferon and Th1 Immune Responses via MyD88

2004 ◽  
Vol 78 (20) ◽  
pp. 11152-11160 ◽  
Author(s):  
Rongcun Yang ◽  
Francisco Martinez Murillo ◽  
Hengmi Cui ◽  
Richard Blosser ◽  
Satoshi Uematsu ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Dendritic Cells ◽  
Immune Responses ◽  
Cell Line ◽  
Adaptor Protein ◽  
Enzyme Linked Immunosorbent Assay ◽  
Macrophage Cell Line ◽  
Macrophage Cell ◽  
Murine Bone Marrow ◽  
Raw264.7 Macrophage

ABSTRACT Dendritic cells (DCs) link innate and adaptive immunity by sensing pathogens or vaccinogens and signaling a variety of defense responses. Since human papillomavirus type 16 L1 virus-like particles (HPV16 VLPs) induce a potent, protective immune response after vaccination, we examined their recognition by DCs. HPV16 VLPs cause phenotypic maturation of murine bone marrow-derived DCs (BMDCs), and immunization of mice with HPV16 VLP-loaded BMDCs or HPV16 VLPs alone induced T helper 1 (Th1)-biased immune responses. Analysis of transcriptional responses of murine BMDCs by microarray suggested that alpha/beta interferon (IFN-α/β) transcripts and numerous proinflammatory cytokines and chemokines are up regulated in response to HPV16 VLPs. Indeed, the induction of IFN-α, IFN-γ, and interleukin-12 (IL-12) production by BMDCs after stimulation with HPV16 VLPs was demonstrated by quantitative enzyme-linked immunosorbent assay. Many microbial products that induce proinflammatory responses are recognized via Toll-like receptor (TLR) signaling through the key adaptor protein MyD88 and activation of NF-κB, nuclear factor of activated T cells (NF-AT), and activating protein 1 (AP-1). Reporter assays indicated that HPV16 VLPs activated NF-κB-, NF-AT-, and AP-1-dependent transcription in the RAW264.7 macrophage cell line. Knockdown of MyD88 transcripts by small interfering RNA in the RAW264.7 macrophage cell line inhibited the activation of NF-κB-, NF-AT- and AP-1-dependent transcription by HPV16 VLP. Furthermore, MyD88−/− BMDCs failed to up regulate IL-12 and IFN-α and -γ in response to HPV16 VLPs. Finally, Th1-biased immune responses to HPV16 VLPs are dramatically impaired in MyD88 and IFN-α/β receptor-deficient mice. This implicates TLR recognition as central to immune recognition of HPV16 L1 VLPs.

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