P-AKT2/SPK1 (P-SPK1) and P-MEK/P-ERK cell signaling pathways are involved in LPS-induced macrophage migration.
Macrophage migration
P-MEK/P-ERK
P-SPK1
macrophage recruitment
Journal
American journal of translational research
ISSN: 1943-8141
Titre abrégé: Am J Transl Res
Pays: United States
ID NLM: 101493030
Informations de publication
Date de publication:
2019
2019
Historique:
received:
05
11
2018
accepted:
23
03
2019
entrez:
21
6
2019
pubmed:
21
6
2019
medline:
21
6
2019
Statut:
epublish
Résumé
Macrophage recruitment to the inflammation site is essential for LPS-induced myocarditis, although the underlying mechanism remains elusive. This study was designed to examine the role of the P-AKT2/SPK1 (P-SPK1) and P-MEK/P-ERK signaling cascades in the regulation of macrophage migration and LPS-induced myocarditis. Our data revealed that (1) the P-AKT2/SPK1 (P-SPK1) and P-MEK/P-ERK signaling cascades acted separately in the regulation of macrophage migration; (2) P-AKT2/SPK1 (P-SPK1) played a relatively important role compared to P-MEK/P-ERK cell signaling in LPS-induced macrophage migration; (3) atorvastatin (ATV) inhibited macrophage migration by inhibiting P-AKT2/SPK1 (P-SPK1) cell signaling, but ATV could increase P-MEK and P-ERK protein expression; (4) ATV has a beneficial effect on LPS-induced myocarditis via inhibition of P-AKT2/SPK1-mediated macrophage recruitment, apoptosis, TNFα, IL-1β, and IL-6; (5) ATV-offered protection against LPS-induced myocarditis was eliminated from SPK1-KO mice; (6) SPK1 may play a harmful role in LPS-induced myocarditis. Taken together, our data revealed that SPK1 represents a novel regulating factor for macrophage migration and cardiac protection under LPS-induced myocarditis.
Types de publication
Journal Article
Langues
eng
Pagination
2725-2741Déclaration de conflit d'intérêts
None.
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