Intrauterine Malnutrition Reduced Long Leptin Receptor Isoform Expression and Proinflammatory Cytokine Production in Male Rat Pulmonary Endothelial Cells Stimulated by Lipopolysaccharide
Background/Aims. We have previously shown that low birth weight (LBW) rats exposed to intrauterine malnutrition have an impaired lung inflammatory response and reduced levels of inflammatory mediators; however, circulating leptin levels were not increased. We evaluated long leptin receptor isoform (...
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| Format: | Article |
| Language: | English |
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Wiley
2018-01-01
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| Series: | Mediators of Inflammation |
| Online Access: | http://dx.doi.org/10.1155/2018/8597361 |
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| author | Aleksandro M. Balbino Marina M. Silva Gabriela A. Azevedo Noemi L. Gil Renaide R. Ferreira Leila A. dos Santos Rebéca M. Gasparin Liliam Fernandes Maristella A. Landgraf Richardt G. Landgraf |
| author_facet | Aleksandro M. Balbino Marina M. Silva Gabriela A. Azevedo Noemi L. Gil Renaide R. Ferreira Leila A. dos Santos Rebéca M. Gasparin Liliam Fernandes Maristella A. Landgraf Richardt G. Landgraf |
| author_sort | Aleksandro M. Balbino |
| collection | DOAJ |
| description | Background/Aims. We have previously shown that low birth weight (LBW) rats exposed to intrauterine malnutrition have an impaired lung inflammatory response and reduced levels of inflammatory mediators; however, circulating leptin levels were not increased. We evaluated long leptin receptor isoform (ObRb) expression in lung endothelial cells from low birth weight rats and examined its role in the production of lipid mediators and cytokines. Methods. Lung endothelial cells were obtained from normal birth weight (NBW) rats or LBW rats subjected to intrauterine malnutrition. These cells were stimulated with leptin (10 ng/mL), LPS (lipopolysaccharide, 1 μg/mL), or leptin plus LPS. Six hours after stimulation, the production of inflammatory mediators (PGE2, LTB4, IL-1β, and IL-6) was evaluated using commercial ELISA kits, and Western blotting was performed to investigate p38MAPK, NF-κB, and ObRb expression. Results. Leptin increased IL-1β levels in only cells from the NBW group, whereas LPS increased PGE2 and LTB4 levels in cells from both groups; leptin addition potentiated lipid mediator production induced by LPS in the NBW group. LPS enhanced the production of IL-1β and IL-6 in only endothelial cells from NBW rats. Leptin receptor expression was decreased (63%) in endothelial cells from LBW rats. None of the stimuli increased NF-κB or p38 signaling pathway expression in cells from LBW rats. Conclusion. These results suggest that intrauterine malnutrition compromises leptin receptor expression and cytokine production in pulmonary endothelial cells stimulated by LPS; these effects seem to involve the NF-κB and p38MAPK signaling pathways. |
| format | Article |
| id | doaj-art-aca81d5bc23e4f608300e62e60ca9f30 |
| institution | Kabale University |
| issn | 0962-9351 1466-1861 |
| language | English |
| publishDate | 2018-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Mediators of Inflammation |
| spelling | doaj-art-aca81d5bc23e4f608300e62e60ca9f302025-02-03T05:50:24ZengWileyMediators of Inflammation0962-93511466-18612018-01-01201810.1155/2018/85973618597361Intrauterine Malnutrition Reduced Long Leptin Receptor Isoform Expression and Proinflammatory Cytokine Production in Male Rat Pulmonary Endothelial Cells Stimulated by LipopolysaccharideAleksandro M. Balbino0Marina M. Silva1Gabriela A. Azevedo2Noemi L. Gil3Renaide R. Ferreira4Leila A. dos Santos5Rebéca M. Gasparin6Liliam Fernandes7Maristella A. Landgraf8Richardt G. Landgraf9Department of Pharmaceuticals Sciences, Universidade Federal de São Paulo-Campus Diadema, Diadema, SP, BrazilDepartment of Pharmaceuticals Sciences, Universidade Federal de São Paulo-Campus Diadema, Diadema, SP, BrazilDepartment of Pharmaceuticals Sciences, Universidade Federal de São Paulo-Campus Diadema, Diadema, SP, BrazilDepartment of Pharmaceuticals Sciences, Universidade Federal de São Paulo-Campus Diadema, Diadema, SP, BrazilBiotério Central, Universidade de São Paulo, São Paulo, SP, BrazilDepartment of Pharmaceuticals Sciences, Universidade Federal de São Paulo-Campus Diadema, Diadema, SP, BrazilDepartment of Pharmaceuticals Sciences, Universidade Federal de São Paulo-Campus Diadema, Diadema, SP, BrazilDepartment of Pharmaceuticals Sciences, Universidade Federal de São Paulo-Campus Diadema, Diadema, SP, BrazilDepartment of Pharmaceuticals Sciences, Universidade Federal de São Paulo-Campus Diadema, Diadema, SP, BrazilDepartment of Pharmaceuticals Sciences, Universidade Federal de São Paulo-Campus Diadema, Diadema, SP, BrazilBackground/Aims. We have previously shown that low birth weight (LBW) rats exposed to intrauterine malnutrition have an impaired lung inflammatory response and reduced levels of inflammatory mediators; however, circulating leptin levels were not increased. We evaluated long leptin receptor isoform (ObRb) expression in lung endothelial cells from low birth weight rats and examined its role in the production of lipid mediators and cytokines. Methods. Lung endothelial cells were obtained from normal birth weight (NBW) rats or LBW rats subjected to intrauterine malnutrition. These cells were stimulated with leptin (10 ng/mL), LPS (lipopolysaccharide, 1 μg/mL), or leptin plus LPS. Six hours after stimulation, the production of inflammatory mediators (PGE2, LTB4, IL-1β, and IL-6) was evaluated using commercial ELISA kits, and Western blotting was performed to investigate p38MAPK, NF-κB, and ObRb expression. Results. Leptin increased IL-1β levels in only cells from the NBW group, whereas LPS increased PGE2 and LTB4 levels in cells from both groups; leptin addition potentiated lipid mediator production induced by LPS in the NBW group. LPS enhanced the production of IL-1β and IL-6 in only endothelial cells from NBW rats. Leptin receptor expression was decreased (63%) in endothelial cells from LBW rats. None of the stimuli increased NF-κB or p38 signaling pathway expression in cells from LBW rats. Conclusion. These results suggest that intrauterine malnutrition compromises leptin receptor expression and cytokine production in pulmonary endothelial cells stimulated by LPS; these effects seem to involve the NF-κB and p38MAPK signaling pathways.http://dx.doi.org/10.1155/2018/8597361 |
| spellingShingle | Aleksandro M. Balbino Marina M. Silva Gabriela A. Azevedo Noemi L. Gil Renaide R. Ferreira Leila A. dos Santos Rebéca M. Gasparin Liliam Fernandes Maristella A. Landgraf Richardt G. Landgraf Intrauterine Malnutrition Reduced Long Leptin Receptor Isoform Expression and Proinflammatory Cytokine Production in Male Rat Pulmonary Endothelial Cells Stimulated by Lipopolysaccharide Mediators of Inflammation |
| title | Intrauterine Malnutrition Reduced Long Leptin Receptor Isoform Expression and Proinflammatory Cytokine Production in Male Rat Pulmonary Endothelial Cells Stimulated by Lipopolysaccharide |
| title_full | Intrauterine Malnutrition Reduced Long Leptin Receptor Isoform Expression and Proinflammatory Cytokine Production in Male Rat Pulmonary Endothelial Cells Stimulated by Lipopolysaccharide |
| title_fullStr | Intrauterine Malnutrition Reduced Long Leptin Receptor Isoform Expression and Proinflammatory Cytokine Production in Male Rat Pulmonary Endothelial Cells Stimulated by Lipopolysaccharide |
| title_full_unstemmed | Intrauterine Malnutrition Reduced Long Leptin Receptor Isoform Expression and Proinflammatory Cytokine Production in Male Rat Pulmonary Endothelial Cells Stimulated by Lipopolysaccharide |
| title_short | Intrauterine Malnutrition Reduced Long Leptin Receptor Isoform Expression and Proinflammatory Cytokine Production in Male Rat Pulmonary Endothelial Cells Stimulated by Lipopolysaccharide |
| title_sort | intrauterine malnutrition reduced long leptin receptor isoform expression and proinflammatory cytokine production in male rat pulmonary endothelial cells stimulated by lipopolysaccharide |
| url | http://dx.doi.org/10.1155/2018/8597361 |
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