scholarly journals Relaxin abrogates renal interstitial fibrosis by regulating macrophage polarization via inhibition of Toll-like receptor 4 signaling

Oncotarget ◽  
2017 ◽  
Vol 8 (13) ◽  
pp. 21044-21053 ◽  
Author(s):  
Lei Chen ◽  
Ming-Lei Sha ◽  
Deng Li ◽  
Yi-Ping Zhu ◽  
Xing-Jie Wang ◽  
...  
Keyword(s):  
Interstitial Fibrosis ◽  
Macrophage Polarization ◽  
Toll Like Receptor ◽  
Renal Interstitial Fibrosis ◽  
Toll Like Receptor 4

scholarly journals Eosinophil Activation by Toll-Like Receptor 4 Ligands Regulates Macrophage Polarization

2019 ◽  
Vol 7 ◽  
Author(s):  
Jiyoung Yoon ◽  
Han-Na Um ◽  
Jinsun Jang ◽  
Young-An Bae ◽  
Woo-Jae Park ◽  
...  
Keyword(s):  
Macrophage Polarization ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4 ◽  
Eosinophil Activation

scholarly journals Curcumin Modulates Macrophage Polarization Through the Inhibition of the Toll-Like Receptor 4 Expression and its Signaling Pathways

2015 ◽  
Vol 36 (2) ◽  
pp. 631-641 ◽  
Author(s):  
Yaoyao Zhou ◽  
Tiantian Zhang ◽  
Xiaofei Wang ◽  
Xiaowei Wei ◽  
Yizhu Chen ◽  
...  
Keyword(s):  
Molecular Mechanism ◽  
Macrophage Polarization ◽  
Mitogen Activated Protein Kinase ◽  
Enzyme Linked Immunosorbent Assay ◽  
Acute Monocytic Leukemia ◽  
Therapeutic Effects ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4 ◽  
M1 Macrophage ◽  
Wide Range

Background: Curcumin, the active ingredient in curcuma rhizomes, has a wide range of therapeutic effects. However, its atheroprotective activity in human acute monocytic leukemia THP-1 cells remains unclear. We investigated the activity and molecular mechanism of action of curcumin in polarized macrophages. Methods: Phorbol myristate acetate (PMA)-treated THP-1 cells were differentiated to macrophages, which were further polarized to M1 cells by lipopolysaccharide (LPS; 1 µg/ml) and interferon (IFN)-γ (20 ng/ml) and treated with varying curcumin concentrations. [3H]thymidine (3H-TdR) incorporation assays were utilized to measure curcumin-induced growth inhibition. The expression of tumor necrosis factor-a (TNF-a), interleukin (IL-6), and IL-12B (p40) were measured by quantitative real-time polymerase chain reaction (PCR) and enzyme-linked immunosorbent assay (ELISA). Macrophage polarization and its mechanism were evaluated by flow cytometry and western blot. Additionally, toll-like receptor 4 (TLR4) small interfering RNA and mitogen-activated protein kinase (MAPK) inhibitors were used to further confirm the molecular mechanism of curcumin on macrophage polarization. Results: Curcumin dose-dependently inhibited M1 macrophage polarization and the production of TNF-a, IL-6, and IL-12B (p40). It also decreased TLR4 expression, which regulates M1 macrophage polarization. Furthermore, curcumin significantly inhibited the phosphorylation of ERK, JNK, p38, and nuclear factor (NF)-γB. In contrast, SiTLR4 in combination with p-JNK, p-ERK, and p-p38 inhibition reduced the effect of curcumin on polarization. Conclusions: Curcumin can modulate macrophage polarization through TLR4-mediated signaling pathway inhibition, indicating that its effect on macrophage polarization is related to its anti-inflammatory and atheroprotective effects. Our data suggest that curcumin could be used as a therapeutic agent in atherosclerosis.

scholarly journals Macrophages and Uveitis in Experimental Animal Models

2015 ◽  
Vol 2015 ◽  
pp. 1-10 ◽  
Author(s):  
Salvador Mérida ◽  
Elena Palacios ◽  
Amparo Navea ◽  
Francisco Bosch-Morell
Keyword(s):  
Animal Models ◽  
Experimental Animal ◽  
Macrophage Polarization ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4 ◽  
Experimental Animal Models ◽  
Leading Role ◽  
Antigen Presenting ◽  
Experimental Autoimmune

Resident and infiltrated macrophages play relevant roles in uveitis as effectors of innate immunity and inductors of acquired immunity. They are major effectors of tissue damage in uveitis and are also considered to be potent antigen-presenting cells. In the last few years, experimental animal models of uveitis have enabled us to enhance our understanding of the leading role of macrophages in eye inflammation processes, including macrophage polarization in experimental autoimmune uveoretinitis and the major role of Toll-like receptor 4 in endotoxin-induced uveitis. This improved knowledge should guide advantageous iterative research to establish mechanisms and possible therapeutic targets for human uveitis resolution.

scholarly journals Complement C3 exacerbates renal interstitial fibrosis by facilitating the M1 macrophage phenotype in a mouse model of unilateral ureteral obstruction

2019 ◽  
Vol 317 (5) ◽  
pp. F1171-F1182 ◽  
Author(s):  
Jiong Cui ◽  
Xiaoting Wu ◽  
Yankun Song ◽  
Yi Chen ◽  
Jianxin Wan
Keyword(s):  
Ureteral Obstruction ◽  
Renal Fibrosis ◽  
Interstitial Fibrosis ◽  
Macrophage Polarization ◽  
Unilateral Ureteral Obstruction ◽  
Complement C3 ◽  
M2 Macrophage ◽  
Inflammatory Factor ◽  
Renal Interstitial Fibrosis ◽  
M1 Polarization

The impact of the renal microenvironment on macrophage phenotype determination can contribute to the progression or resolution of renal fibrosis. Although the complement proteins affect macrophage polarization, whether complement component 3 (C3) can induce macrophage polarization and regulate renal interstitial fibrosis remains undetermined. In the present study, we investigated the contribution of C3 on macrophage polarization and renal fibrosis in C3-deficient mice with unilateral ureteral obstruction and bone marrow-derived macrophages. C3-deficient mice exhibited attenuated renal fibrosis and ameliorated peritubular capillary rarefaction. Lack of C3 contributed to M2 macrophage polarization, increased IL-10 and VEGF164, and decreased TNF-α and soluble VEGF receptor 1 expression in the obstructed kidneys at the early stages of unilateral ureteral obstruction. C3a facilitated LPS-induced M1 polarization and inflammatory factor production in bone marrow-derived macrophages in vitro, accompanied by increased ERK, NF-κB, and STAT1 phosphorylation. The ERK-specific inhibitor PD98059 inhibited the phosphorylation of ERK, NF-κB, and STAT1 and attenuated M1 polarization-related inflammatory factor production. Furthermore, the culture supernatant from M1 macrophages and C3a-treated M2 macrophages were more detrimental to angiogenesis compared with M2 macrophage supernatants. Thus, complement C3 exacerbates renal interstitial fibrosis by facilitating macrophage M1 polarization, promoting proinflammatory cytokine expression, and deteriorating peritubular capillary rarefaction in the kidney.

660 Deficiency of Toll-like receptor 4 leads to cardioprotection against doxorubicin-induced cardiomyopathy

2007 ◽  
Vol 6 (1) ◽  
pp. 142-143
Author(s):  
A RIAD ◽  
S BIEN ◽  
M GRATZ ◽  
S BERESWILL ◽  
H SCHULTHEISS ◽  
...  
Keyword(s):  
Toll Like Receptor ◽  
Toll Like Receptor 4
Sign in / Sign up

Export Citation Format

Share Document