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Tytuł pozycji:

Rosiglitazone-induced CD36 up-regulation resolves inflammation by PPARγ and 5-LO-dependent pathways.

Tytuł :
Rosiglitazone-induced CD36 up-regulation resolves inflammation by PPARγ and 5-LO-dependent pathways.
Autorzy :
Ballesteros I; 2.Depto. de Farmacología, Facultad de Medicina, Universidad Complutense, Avda. Complutense s/n, 28040 Madrid, Spain. .
Cuartero MI
Pradillo JM
de la Parra J
Pérez-Ruiz A
Corbí A
Ricote M
Hamilton JA
Sobrado M
Vivancos J
Nombela F
Lizasoain I
Moro MA
Pokaż więcej
Źródło :
Journal of leukocyte biology [J Leukoc Biol] 2014 Apr; Vol. 95 (4), pp. 587-98. Date of Electronic Publication: 2013 Dec 12.
Typ publikacji :
Journal Article; Research Support, Non-U.S. Gov't
Język :
English
Imprint Name(s) :
Publication: Hoboken, NJ : Wiley on behalf of the Society for Leukocyte Biology
Original Publication: New York : Alan R. Liss, c1984-
MeSH Terms :
Arachidonate 5-Lipoxygenase/*physiology
CD36 Antigens/*physiology
Hypoglycemic Agents/*pharmacology
Inflammation/*immunology
Neutrophils/*immunology
PPAR gamma/*physiology
Thiazolidinediones/*pharmacology
Animals ; Brain Ischemia/immunology ; CD36 Antigens/analysis ; Cells, Cultured ; Lipoxins/biosynthesis ; Mice ; Mice, Inbred C57BL ; PPAR gamma/agonists ; Phagocytosis ; Rats ; Rosiglitazone ; Up-Regulation
Contributed Indexing :
Keywords: lipoxin; microglia; phagocytosis; resolution; stroke
Substance Nomenclature :
0 (CD36 Antigens)
0 (Hypoglycemic Agents)
0 (Lipoxins)
0 (PPAR gamma)
0 (Thiazolidinediones)
0 (lipoxin A4)
05V02F2KDG (Rosiglitazone)
EC 1.13.11.34 (Arachidonate 5-Lipoxygenase)
Entry Date(s) :
Date Created: 20131217 Date Completed: 20140520 Latest Revision: 20181202
Update Code :
20210210
DOI :
10.1189/jlb.0613326
PMID :
24338629
Czasopismo naukowe
PPARγ-achieved neuroprotection in experimental stroke has been explained by the inhibition of inflammatory genes, an action in which 5-LO, Alox5, is involved. In addition, PPARγ is known to promote the expression of CD36, a scavenger receptor that binds lipoproteins and mediates bacterial recognition and also phagocytosis. As phagocytic clearance of neutrophils is a requisite for resolution of the inflammatory response, PPARγ-induced CD36 expression might help to limit inflammatory tissue injury in stroke, an effect in which 5-LO might also be involved. Homogenates, sections, and cellular suspensions were prepared from brains of WT and Alox5(-/-) mice exposed to distal pMCAO. BMMs were obtained from Lys-M Cre(+) PPARγ(f/f) and Lys-M Cre(-) PPARγ(f/f) mice. Stereological counting of double-immunofluorescence-labeled brain sections and FACS analysis of cell suspensions was performed. In vivo and in vitro phagocytosis of neutrophils by microglia/macrophages was analyzed. PPARγ activation with RSG induced CD36 expression in resident microglia. This process was mediated by the 5-LO gene, which is induced in neurons by PPARγ activation and at least by one of its products--LXA4--which induced CD36 independently of PPARγ. Moreover, CD36 expression helped resolution of inflammation through phagocytosis, concomitantly to neuroprotection. Based on these findings, in addition to a direct modulation by PPARγ, we propose in brain a paracrine model by which products generated by neuronal 5-LO, such as LXA4, increase the microglial expression of CD36 and promote tissue repair in pathologies with an inflammatory component, such as stroke.

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