scholarly journals Reciprocal interference between the NRF2 and LPS signaling pathways on the immune‐metabolic phenotype of peritoneal macrophages

2020 ◽  
Vol 8 (4) ◽  
Author(s):  
Federica Mornata ◽  
Giovanna Pepe ◽  
Chiara Sfogliarini ◽  
Electra Brunialti ◽  
Gianenrico Rovati ◽  
...  
Keyword(s):  
Signaling Pathways ◽  
Peritoneal Macrophages ◽  
Metabolic Phenotype ◽  
Lps Signaling

scholarly journals Association of mitogen-activated protein kinases with microtubules in mouse macrophages.

1996 ◽  
Vol 183 (4) ◽  
pp. 1899-1904 ◽  
Author(s):  
A Ding ◽  
B Chen ◽  
M Fuortes ◽  
E Blum
Keyword(s):  
Genetic Control ◽  
Protein Kinases ◽  
Peritoneal Macrophages ◽  
Mitogen Activated Protein Kinases ◽  
Microtubule Associated Proteins ◽  
Primary Mouse ◽  
Mouse Macrophages ◽  
Mitogen Activated Protein ◽  
Associated Proteins ◽  
Lps Signaling

Taxol, a microtubule-binding diterpene, mimics many effects of lipopolysaccharide (LPS) on mouse macrophages. The LPS-mimetic effects of taxol appear to be under the same genetic control as responses to LPS itself. Thus we have postulated a role for microtubule-associated proteins (MAP) in the response of macrophages to LPS. Stimulation of macrophages by LPS quickly induces the activation of mitogen-activated protein kinases (MAPK). MAPK are generally considered cytosolic enzymes. Herein we report that much of the LPS-activatable pool of MAPK in primary mouse peritoneal macrophages is microtubule associated. By immunofluorescence, MAPK were localized to colchicine- and nocodazole-disruptible filaments. From both mouse brain and RAW 264.7 macrophages, MAPK could be coisolated with polymerized tubulin. Fractionation of primary macrophages into cytosol-, microfilament-, microtubule-, and intermediated filament-rich extracts revealed that approximately 10% of MAPK but none of MAPK kinase (MEK1A and MEK2) was microtubule bound. Exposure of macrophages to LPS did not change the proportion of MAPK bound to microtubules, but preferentially activated the microtubule-associated pool. These findings confirm the prediction that LPS activates a kinase bound to microtubules. Together with LPS-mimetic actions of taxol and the shared genetic control of responses to LPS and taxol, these results support the hypothesis that a major LPS-signaling pathway in mouse macrophages may involve activation of one or more microtubule-associated kinases.

scholarly journals Lysophosphatidylcholine Triggers TLR2- and TLR4-Mediated Signaling Pathways but Counteracts LPS-Induced NO Synthesis in Peritoneal Macrophages by Inhibiting NF-κB Translocation and MAPK/ERK Phosphorylation

PLoS ONE ◽  
2013 ◽  
Vol 8 (9) ◽  
pp. e76233 ◽  
Author(s):  
Alan Brito Carneiro ◽  
Bruna Maria Ferreira Iaciura ◽  
Lilian Lie Nohara ◽  
Carla Duque Lopes ◽  
Esteban Mauricio Cordero Veas ◽  
...  
Keyword(s):  
Signaling Pathways ◽  
Peritoneal Macrophages ◽  
Erk Phosphorylation

scholarly journals LPS-TLR4 Signaling to IRF-3/7 and NF-κB Involves the Toll Adapters TRAM and TRIF

2003 ◽  
Vol 198 (7) ◽  
pp. 1043-1055 ◽  
Author(s):  
Katherine A. Fitzgerald ◽  
Daniel C. Rowe ◽  
Betsy J. Barnes ◽  
Daniel R. Caffrey ◽  
Alberto Visintin ◽  
...  
Keyword(s):  
Signaling Pathways ◽  
Adaptor Protein ◽  
Dominant Negative ◽  
Tlr4 Signaling ◽  
Tir Domain ◽  
Toll Receptor ◽  
Inducible Protein ◽  
Myeloid Differentiation Factor ◽  
Lps Signaling ◽  
Interferon Inducible Protein

Toll–IL-1–resistance (TIR) domain–containing adaptor-inducing IFN-β (TRIF)–related adaptor molecule (TRAM) is the fourth TIR domain–containing adaptor protein to be described that participates in Toll receptor signaling. Like TRIF, TRAM activates interferon regulatory factor (IRF)-3, IRF-7, and NF-κB-dependent signaling pathways. Toll-like receptor (TLR)3 and 4 activate these pathways to induce IFN-α/β, regulated on activation, normal T cell expressed and secreted (RANTES), and γ interferon–inducible protein 10 (IP-10) expression independently of the adaptor protein myeloid differentiation factor 88 (MyD88). Dominant negative and siRNA studies performed here demonstrate that TRIF functions downstream of both the TLR3 (dsRNA) and TLR4 (LPS) signaling pathways, whereas the function of TRAM is restricted to the TLR4 pathway. TRAM interacts with TRIF, MyD88 adaptor–like protein (Mal)/TIRAP, and TLR4 but not with TLR3. These studies suggest that TRIF and TRAM both function in LPS-TLR4 signaling to regulate the MyD88-independent pathway during the innate immune response to LPS.

Oleocanthal Modulates LPS-Induced Murine Peritoneal Macrophages Activation via Regulation of Inflammasome, Nrf-2/HO-1, and MAPKs Signaling Pathways

2019 ◽  
Vol 67 (19) ◽  
pp. 5552-5559 ◽  
Author(s):  
Tatiana Montoya ◽  
Maria L. Castejón ◽  
Marina Sánchez-Hidalgo ◽  
Alejandro González-Benjumea ◽  
José G. Fernández-Bolaños ◽  
...  
Keyword(s):  
Signaling Pathways ◽  
Peritoneal Macrophages ◽  
Murine Peritoneal Macrophages
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