scholarly journals CCR2 Antagonist PF-04136309

2020 ◽  
Author(s):  
Keyword(s):  
Ccr2 Antagonist

Analgesic effects evoked by a CCR2 antagonist or an anti-CCL2 antibody in inflamed mice

2016 ◽  
Vol 30 (3) ◽  
pp. 235-247 ◽  
Author(s):  
María Llorián-Salvador ◽  
Marta Pevida ◽  
Sara González-Rodríguez ◽  
Ana Lastra ◽  
María-Teresa Fernández-García ◽  
...  
Keyword(s):  
Analgesic Effects ◽  
Ccr2 Antagonist

scholarly journals Reversal of Vascular Macrophage Accumulation and Hypertension by a CCR2 Antagonist in Deoxycorticosterone/Salt-Treated Mice

Hypertension ◽  
2012 ◽  
Vol 60 (5) ◽  
pp. 1207-1212 ◽  
Author(s):  
Christopher T. Chan ◽  
Jeffrey P. Moore ◽  
Klaudia Budzyn ◽  
Elizabeth Guida ◽  
Henry Diep ◽  
...  
Keyword(s):  
Ccr2 Antagonist ◽  
Macrophage Accumulation

scholarly journals Discovery of a 4-Azetidinyl-1-thiazoyl-cyclohexane CCR2 Antagonist as a Development Candidate

2012 ◽  
Vol 3 (12) ◽  
pp. 1039-1044 ◽  
Author(s):  
Xuqing Zhang ◽  
Cuifen Hou ◽  
Heather Hufnagel ◽  
Monica Singer ◽  
Evan Opas ◽  
...  
Keyword(s):  
Ccr2 Antagonist

Treatment with CCR2 antagonist is neuroprotective but does not alter epileptogenesis in the pilocarpine rat model of epilepsy

2020 ◽  
Vol 102 ◽  
pp. 106695
Author(s):  
Maira Licia Foresti ◽  
Gabriel Maisonnave Arisi ◽  
James J. Campbell ◽  
Luiz E. Mello
Keyword(s):  
Rat Model ◽  
Ccr2 Antagonist

scholarly journals SYNTHESIS, CHARACTERIZATION, AND IN VIVO IMMUNOMODULATION OF CCR2 AND VASCULAR ENDOTHELIAL GROWTH FACTOR ANTAGONISTS-LOADED PEGYLATED NANOPARTICLES

2019 ◽  
Vol 12 (1) ◽  
pp. 275
Author(s):  
Ahmed A Abd-rabou ◽  
Hanaa H Ahmed ◽  
Mohamed S Kishta
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Concentration Ratio ◽  
Immune Cell ◽  
Drug Clearance ◽  
Vascular Endothelial ◽  
Pegylated Nanoparticles ◽  
Endothelial Growth Factor ◽  
Ccr2 Antagonist

Objective: Chemokine (C-C motif) ligand 2 (CCL2), a candidate of cytokines, orchestrates immune cell recruitment to inflamed organs. CCL2 has been shown to have direct angiogenic effects, so providing an anti-angiogenic agent, Avastin (AV), to be combined with the CCR2 antagonist (concentration ratio [CR]) plays an essential role in the hemostatic strategy for immunomodulation. Lack of targetability and the adverse effects of chemical treatments are the main obstacles led scientists to develop novel strategies using nano-delivery approaches such as pegylated nanoparticles (NPs) which exhibits reduced drug clearance rates. The rationale of the current study is to test the in vivo immunomodulatory effects of AV and/or CR in their NPs or free counterparts.Methods: These NPs were synthesized and characterized using different physicochemical techniques. Males Wistar rats (n=114) were used and divided into 7 groups treated with vehicle, AV, AVNP, CCR2 antagonist (CR), CCR2 antagonist NPs (CRNP), AV-CCR2 antagonist (AVCR), and AV-CCR2 antagonist NPs (AVCRNP). Groups were subdivided into three subgroups according to the administrated dose. Blood was taken from rats for differential leukocyte and platelet profile measurements. Sera were collected to test vascular endothelial growth factor (VEGF) levels. Autopsy samples from liver were taken for histopathological investigation.Results: The morphology of the NPs was spherical and had sizes ranging from 89.89 nm to 146 nm. Monocytes and lymphocytes accumulated in the blood circulation and VEGF levels were inhibited after AV and CR administrations. In addition, large platelets concentration ratio was elevated in the blood circulation.Conclusion: We concluded that AV ad CR therapeutic regimens have an immunomodulatory role through induction of monocyte-platelet aggregation and inhibition of VEGF.

APOBEC3B interaction with PRC2 modulates microenvironment to promote HCC progression

Gut ◽  
2019 ◽  
Vol 68 (10) ◽  
pp. 1846-1857 ◽  
Author(s):  
Duowei Wang ◽  
Xianjing Li ◽  
Jiani Li ◽  
Yuan Lu ◽  
Sen Zhao ◽  
...  
Keyword(s):  
Cytidine Deaminase ◽  
Suppressor Cells ◽  
Nuclear Factor Κb ◽  
Luciferase Reporter ◽  
Cell Models ◽  
Repressor Complex ◽  
Mutation Pattern ◽  
Immunocompetent Mice ◽  
Ccr2 Antagonist

ObjectiveAPOBEC3B (A3B), a cytidine deaminase acting as a contributor to the APOBEC mutation pattern in many kinds of tumours, is upregulated in patients with hepatocellular carcinoma (HCC). However, APOBEC mutation patterns are absent in HCC. The mechanism of how A3B affects HCC progression remains elusive.DesignA3B ­promoter luciferase reporter and other techniques were applied to elucidate mechanisms of A3B upregulation in HCC. A3B overexpression and knockdown cell models, immunocompetent and immune-deficient mouse HCC model were conducted to investigate the influence of A3B on HCC progression. RNA­seq, flow cytometry and other techniques were conducted to analyse how A3B modulated the cytokine to enhance the recruitment of myeloid­-derived suppressor cells (MDSCs) and tumour­-associated macrophages (TAMs).ResultsA3B upregulation through non-classical nuclear factor-κB (NF-κB)signalling promotes HCC growth in immunocompetent mice, associated with an increase of MDSCs, TAMs and programmed cell death1 (PD1) exprssed CD8+ T cells. A CCR2 antagonist suppressed TAMs and MDSCs infiltration and delayed tumour growth in A3B and A3BE68Q/E255Q­ expressing mouse tumours. Mechanistically, A3B upregulation in HCC depresses global H3K27me3 abundance via interaction with polycomb repressor complex 2 (PRC2) and reduces an occupancy of H3K27me3 on promoters of the chemokine CCL2 to recruit massive TAMs and MDSCs.ConclusionOur observations uncover a deaminase-independent role of the A3B in modulating the HCC microenvironment and demonstrate a proof for the concept of targeting A3B in HCC immunotherapy.

Sign in / Sign up

Export Citation Format

Share Document