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Palmitoleic acid has stronger anti-inflammatory potential in human endothelial cells compared to oleic and palmitic acids

Palmitoleic acid has stronger anti-inflammatory potential in human endothelial cells compared to oleic and palmitic acids
Palmitoleic acid has stronger anti-inflammatory potential in human endothelial cells compared to oleic and palmitic acids
1 Scope
Fatty acids (FAs) may affect endothelial cell (EC) function, influencing atherogenesis and inflammatory processes. Palmitoleic acid (POA) has been described as an anti‐inflammatory FA. However, its effects on ECs are underexplored. This study compares the effects of POA with those of palmitic acid (PA) and oleic acid (OA) on EC inflammatory responses.

2 Methods and Results
EAHy926 cells (EC lineage) are exposed to PA, OA, or POA, and stimulated with tumor necrosis factor (TNF)‐α. Associated with the FA's own incorporation, PA induces a twofold increase in arachidonic acid, while POA increases the amount of cis‐vaccenic acid. PA, but not OA, enhances the production of IL‐6 and IL‐8 in response to TNF‐α. In contrast, POA decreases production of monocyte chemotactic protein (MCP)‐1, IL‐6, and IL‐8 compared to PA. TNF‐α increases surface intercellular adhesion molecule‐1 expression previously decreased by POA. TNF‐α stimulation increases the expression of NFκB, cyclooxygenase (COX)‐2, MCP‐1, and IL‐6 genes and reduces the expression of peroxisome proliferator‐activated receptor (PPAR)‐α gene. PA enhances the expression of MCP‐1, IL‐6, and COX‐2 genes, while POA downregulates these genes, decreases expression of NFκB, and upregulates PPAR‐α gene expression.

3 Conclusion
POA has anti‐inflammatory effects on ECs stimulated with TNF‐α and may counter endothelial dysfunction.
de Souza, Camila
df8676e9-b890-492f-8725-bcfe652277c3
Valenzuela, Carina A.
1a12a9b9-6504-4392-90c5-246644b0ad5c
Baker, Ella
7cd5b762-d7d7-4584-b9a7-dba555085440
Miles, Elizabeth A.
20332899-ecdb-4214-95bc-922dde36d416
Rosa Neto, José C.
98dea0e7-fd39-4c44-b5f0-2a72161565c1
Calder, Philip C.
1797e54f-378e-4dcb-80a4-3e30018f07a6
de Souza, Camila
df8676e9-b890-492f-8725-bcfe652277c3
Valenzuela, Carina A.
1a12a9b9-6504-4392-90c5-246644b0ad5c
Baker, Ella
7cd5b762-d7d7-4584-b9a7-dba555085440
Miles, Elizabeth A.
20332899-ecdb-4214-95bc-922dde36d416
Rosa Neto, José C.
98dea0e7-fd39-4c44-b5f0-2a72161565c1
Calder, Philip C.
1797e54f-378e-4dcb-80a4-3e30018f07a6

de Souza, Camila, Valenzuela, Carina A., Baker, Ella, Miles, Elizabeth A., Rosa Neto, José C. and Calder, Philip C. (2018) Palmitoleic acid has stronger anti-inflammatory potential in human endothelial cells compared to oleic and palmitic acids. Molecular Nutrition & Food Research, 62 (20), [e1800322]. (doi:10.1002/mnfr.201800322).

Record type: Article

Abstract

1 Scope
Fatty acids (FAs) may affect endothelial cell (EC) function, influencing atherogenesis and inflammatory processes. Palmitoleic acid (POA) has been described as an anti‐inflammatory FA. However, its effects on ECs are underexplored. This study compares the effects of POA with those of palmitic acid (PA) and oleic acid (OA) on EC inflammatory responses.

2 Methods and Results
EAHy926 cells (EC lineage) are exposed to PA, OA, or POA, and stimulated with tumor necrosis factor (TNF)‐α. Associated with the FA's own incorporation, PA induces a twofold increase in arachidonic acid, while POA increases the amount of cis‐vaccenic acid. PA, but not OA, enhances the production of IL‐6 and IL‐8 in response to TNF‐α. In contrast, POA decreases production of monocyte chemotactic protein (MCP)‐1, IL‐6, and IL‐8 compared to PA. TNF‐α increases surface intercellular adhesion molecule‐1 expression previously decreased by POA. TNF‐α stimulation increases the expression of NFκB, cyclooxygenase (COX)‐2, MCP‐1, and IL‐6 genes and reduces the expression of peroxisome proliferator‐activated receptor (PPAR)‐α gene. PA enhances the expression of MCP‐1, IL‐6, and COX‐2 genes, while POA downregulates these genes, decreases expression of NFκB, and upregulates PPAR‐α gene expression.

3 Conclusion
POA has anti‐inflammatory effects on ECs stimulated with TNF‐α and may counter endothelial dysfunction.

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Accepted/In Press date: 20 July 2018
e-pub ahead of print date: 13 August 2018

Identifiers

Local EPrints ID: 422764
URI: http://eprints.soton.ac.uk/id/eprint/422764
PURE UUID: f050b319-fd1f-4fc3-8824-e239592e541c
ORCID for Ella Baker: ORCID iD orcid.org/0000-0003-1008-5506
ORCID for Elizabeth A. Miles: ORCID iD orcid.org/0000-0002-8643-0655
ORCID for Philip C. Calder: ORCID iD orcid.org/0000-0002-6038-710X

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Date deposited: 03 Aug 2018 16:30
Last modified: 29 Oct 2023 05:56

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Contributors

Author: Camila de Souza
Author: Carina A. Valenzuela
Author: Ella Baker ORCID iD
Author: José C. Rosa Neto

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