Please use this identifier to cite or link to this item: https://scholarhub.balamand.edu.lb/handle/uob/5650
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dc.contributor.authorBeaini, Shadiaen_US
dc.contributor.authorSaliba, Youakimen_US
dc.contributor.authorHajal, Joelleen_US
dc.contributor.authorSmayra, Vivianeen_US
dc.contributor.authorBakhos, Jules-Joelen_US
dc.contributor.authorJoubran, Najaten_US
dc.contributor.authorChelala, Daniaen_US
dc.contributor.authorFares, Nassimen_US
dc.date.accessioned2022-05-24T08:15:46Z-
dc.date.available2022-05-24T08:15:46Z-
dc.date.issued2019-
dc.identifier.issn00219541-
dc.identifier.urihttps://scholarhub.balamand.edu.lb/handle/uob/5650-
dc.description.abstractSalt-sensitive hypertension is a major risk factor for renal impairment leading to chronic kidney disease. High-salt diet leads to hypertonic skin interstitial volume retention enhancing the activation of the tonicity-responsive enhancer-binding protein (TonEBP) within macrophages leading to vascular endothelial growth factor C (VEGF-C) secretion and NOS3 modulation. This promotes skin lymphangiogenesis and blood pressure regulation. Whether VEGF-C administration enhances renal and skin lymphangiogenesis and attenuates renal damage in salt-sensitive hypertension remains to be elucidated. Hypertension was induced in BALB/c mice by a high-salt diet. VEGF-C was administered subcutaneously to high-salt-treated mice as well as control animals. Analyses of kidney injury, inflammation, fibrosis, and biochemical markers were performed in vivo. VEGF-C reduced plasma inflammatory markers in salt-treated mice. In addition, VEGF-C exhibited a renal anti-inflammatory effect with the induction of macrophage M2 phenotype, followed by reductions in interstitial fibrosis. Antioxidant enzymes within the kidney as well as urinary RNA/DNA damage markers were all revelatory of abolished oxidative stress under VEGF-C. Furthermore, VEGF-C decreased the urinary albumin/creatinine ratio and blood pressure as well as glomerular and tubular damages. These improvements were associated with enhanced TonEBP, NOS3, and lymphangiogenesis within the kidney and skin. Our data show that VEGF-C administration plays a major role in preserving renal histology and reducing blood pressure. VEGF-C might constitute an interesting potential therapeutic target for improving renal remodeling in salt-sensitive hypertension.en_US
dc.language.isoengen_US
dc.publisherNational Library of Medicineen_US
dc.subjectNOS3en_US
dc.subjectKidneyen_US
dc.subjectRenal lymphangiogenesisen_US
dc.subjectSalt-sensitive hypertensionen_US
dc.subjectSkin lymphangiogenesisen_US
dc.subjectVascular endothelial growth factor C (VEGF-C)en_US
dc.titleVEGF-C attenuates renal damage in salt-sensitive hypertensionen_US
dc.typeJournal Articleen_US
dc.identifier.doi10.1002/jcp.27648-
dc.identifier.pmid30378108-
dc.identifier.scopus2-s2.0-85055732024-
dc.identifier.urlhttps://api.elsevier.com/content/abstract/scopus_id/85055732024-
dc.contributor.affiliationFaculty of Medicineen_US
dc.description.volume234en_US
dc.description.issue6en_US
dc.description.startpage9616en_US
dc.description.endpage9630en_US
dc.date.catalogued2022-05-24-
dc.description.statusPublisheden_US
dc.identifier.ezproxyURLhttp://ezsecureaccess.balamand.edu.lb/login?url=https://onlinelibrary.wiley.com/doi/10.1002/jcp.27648en_US
dc.relation.ispartoftextJournal of Cellular Physiologyen_US
dc.description.campusSGH campusen_US
Appears in Collections:Faculty of Medicine
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