Postprandial dietary fatty acids exert divergent inflammatory responses in retinal-pigmented epithelium cells

2016 ◽  
Vol 7 (3) ◽  
pp. 1345-1353 ◽  
Author(s):  
Sergio Montserrat-de la Paz ◽  
M. Carmen Naranjo ◽  
Beatriz Bermudez ◽  
Sergio Lopez ◽  
Wenceslao Moreda ◽  
...  

Postprandial triglyceride-rich lipoproteins (TRLs) lead to a complex series of events that are potentially oxidative and inflammatory.

2015 ◽  
Vol 56 (2) ◽  
pp. 449-460 ◽  
Author(s):  
Xin-Ling Wang ◽  
Tao Yu ◽  
Qi-Chang Yan ◽  
Wei Wang ◽  
Nan Meng ◽  
...  

Stroke ◽  
2019 ◽  
Vol 50 (8) ◽  
pp. 2197-2206 ◽  
Author(s):  
Hung Nguyen ◽  
Jea Young Lee ◽  
Paul R. Sanberg ◽  
Eleonora Napoli ◽  
Cesar V. Borlongan

Background and Purpose— Retinal ischemia is a major cause of visual impairment in stroke patients, but our incomplete understanding of its pathology may contribute to a lack of effective treatment. Here, we investigated the role of mitochondrial dysfunction in retinal ischemia and probed the potential of mesenchymal stem cells (MSCs) in mitochondrial repair under such pathological condition. Methods— In vivo, rats were subjected to middle cerebral artery occlusion then randomly treated with intravenous MSCs or vehicle. Laser Doppler was used to evaluate the blood flow in the brain and the eye, while immunohistochemical staining assessed cellular degeneration at days 3 and 14 poststroke. In vitro, retinal pigmented epithelium cells were exposed to either oxygen-glucose deprivation or oxygen-glucose deprivation and coculture with MSCs, and subsequently, cell death and mitochondrial function were examined immunocytochemically and with Seahorse analyzer, respectively. Results— Middle cerebral artery occlusion significantly reduced blood flow in the brain and the eye accompanied by mitochondrial dysfunction and ganglion cell death at days 3 and 14 poststroke. Intravenous MSCs elicited mitochondrial repair and improved ganglion cell survival at day 14 poststroke. Oxygen-glucose deprivation similarly induced mitochondrial dysfunction and cell death in retinal pigmented epithelium cells; coculture with MSCs restored mitochondrial respiration, mitochondrial network morphology, and mitochondrial dynamics, which likely attenuated oxygen-glucose deprivation-mediated retinal pigmented epithelium cell death. Conclusions— Retinal ischemia is closely associated with mitochondrial dysfunction, which can be remedied by stem cell-mediated mitochondrial repair.


2019 ◽  
Vol 60 (5) ◽  
pp. 554-568 ◽  
Author(s):  
Sandra Rutting ◽  
Razia Zakarya ◽  
Jack Bozier ◽  
Dia Xenaki ◽  
Jay C. Horvat ◽  
...  

2002 ◽  
Vol 34 (6) ◽  
pp. 338-342 ◽  
Author(s):  
M. Castillo ◽  
J.L. Bellot ◽  
C. García-Cabanes ◽  
J. Miquel ◽  
A. Orts ◽  
...  

Proceedings ◽  
2017 ◽  
Vol 1 (4) ◽  
pp. 530
Author(s):  
Jocelyn Boutzen ◽  
Manon Valet ◽  
Valérie Fradot ◽  
Lionel Rousseau ◽  
Olivier Français ◽  
...  

2015 ◽  
Vol 12 (2) ◽  
pp. 2231-2238 ◽  
Author(s):  
LANGEN LI ◽  
WEI WEI ◽  
YUFENG ZHANG ◽  
GERILE TU ◽  
YANMEI ZHANG ◽  
...  

Nutrients ◽  
2020 ◽  
Vol 12 (10) ◽  
pp. 3139
Author(s):  
Carlos Vazquez-Madrigal ◽  
Soledad Lopez ◽  
Elena Grao-Cruces ◽  
Maria C. Millan-Linares ◽  
Noelia M. Rodriguez-Martin ◽  
...  

Dietary fatty acids have been demonstrated to modulate systemic inflammation and induce the postprandial inflammatory response of circulating immune cells. We hypothesized that postprandial triglyceride-rich lipoproteins (TRLs) may have acute effects on immunometabolic homeostasis by modulating dendritic cells (DCs), sentinels of the immunity that link innate and adaptive immune systems. In healthy volunteers, saturated fatty acid (SFA)-enriched meal raised serum levels of granulocyte/macrophage colony-stimulating factor GM-CSF (SFAs > monounsaturated fatty acids (MUFAs) = polyunsaturated fatty acids (PUFAs)) in the postprandial period. Autologous TRL-SFAs upregulated the gene expression of DC maturation (CD123 and CCR7) and DC pro-inflammatory activation (CD80 and CD86) genes while downregulating tolerogenic genes (PD-L1 and PD-L2) in human monocyte-derived DCs (moDCs). These effects were reversed with oleic acid-enriched TRLs. Moreover, postprandial SFAs raised IL-12p70 levels, while TRL-MUFAs and TRL-PUFAs increased IL-10 levels in serum of healthy volunteers and in the medium of TRL-treated moDCs. In conclusion, postprandial TRLs are metabolic entities with DC-related tolerogenic activity, and this function is linked to the type of dietary fat in the meal. This study shows that the intake of meals enriched in MUFAs from olive oil, when compared with meals enriched in SFAs, prevents the postprandial production and priming of circulating pro-inflammatory DCs, and promotes tolerogenic response in healthy subjects. However, functional assays with moDCs generated in the presence of different fatty acids and T cells could increase the knowledge of postprandial TRLs’ effects on DC differentiation and function.


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