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Myeloid CD11c+ antigen-presenting cells ablation prevents hypertension in response to angiotensin II plus high-salt diet

dc.contributor.authorHevia D.
dc.contributor.authorAraos P.
dc.contributor.authorPrado C.
dc.contributor.authorLuppichini E.F.
dc.contributor.authorRojas M.
dc.contributor.authorAlzamora R.
dc.contributor.authorCifuentes-Araneda F.
dc.contributor.authorGonzalez A.A.
dc.contributor.authorAmador C.A.
dc.contributor.authorPacheco R.
dc.contributor.authorMichea L.
dc.date.accessioned2020-09-02T22:20:29Z
dc.date.available2020-09-02T22:20:29Z
dc.date.issued2018
dc.identifier10.1161/HYPERTENSIONAHA.117.10145
dc.identifier.citation71, 4, 709-718
dc.identifier.issn0194911X
dc.identifier.urihttps://hdl.handle.net/20.500.12728/4894
dc.descriptionIncreasing evidence shows that antigen-presenting cells (APCs) are involved in the development of inflammation associated to hypertension. However, the potential role of APCs in the modulation of renal sodium transport has not been addressed. We hypothesized that APCs participate in renal sodium transport and, thus, development of high blood pressure in response to angiotensin II plus a high-salt diet. Using transgenic mice that allow the ablation of CD11chigh APCs, we studied renal sodium transport, the intrarenal renin-angiotensin system components, blood pressure, and cardiac/renal tissue damage in response to angiotensin II plus a high-salt diet. Strikingly, we found that APCs are required for the development of hypertension and that the ablation/restitution of APCs produces rapid changes in the blood pressure in mice with angiotensin II plus a high-salt diet. Moreover, APCs were necessary for the induction of intrarenal renin-angiotensin system components and affected the modulation of natriuresis and tubular sodium transporters. Consistent with the prevention of hypertension, the ablation of APCs also prevented cardiac hypertrophy and the induction of several indicators of renal and cardiac damage. Thus, our fndings indicate a prominent role of APCs as modulators of blood pressure by mechanisms including renal sodium handling, with kinetics that suggest the involvement of tubular cell functions in addition to the modulation of inflammation and adaptive immune response. © 2017 The Authors.
dc.language.isoen
dc.publisherLippincott Williams and Wilkins
dc.subjectAngiotensin II
dc.subjectAntigen-presenting cells
dc.subjectEpithelial sodium channel
dc.subjectHypertension
dc.subjectInflammation
dc.subjectangiotensin II
dc.subjectCD4 antigen
dc.subjectCD86 antigen
dc.subjectdipeptidyl carboxypeptidase
dc.subjectepithelial sodium channel
dc.subjectglycoprotein p 15095
dc.subjectinterleukin 10
dc.subjectinterleukin 1beta
dc.subjectinterleukin 6
dc.subjectmajor histocompatibility antigen class 1
dc.subjectmajor histocompatibility antigen class 2
dc.subjectmessenger RNA
dc.subjectprorenin receptor
dc.subjectreduced nicotinamide adenine dinucleotide phosphate oxidase 2
dc.subjectreduced nicotinamide adenine dinucleotide phosphate oxidase 4
dc.subjectsodium chloride cotransporter
dc.subjectsodium proton exchange protein 3
dc.subjecttranscription factor FOXP3
dc.subjecttumor necrosis factor
dc.subjectangiotensin II
dc.subjectepithelial sodium channel
dc.subjectglycoprotein p 15095
dc.subjectadaptive immunity
dc.subjectanimal experiment
dc.subjectanimal model
dc.subjectanimal tissue
dc.subjectantigen presenting cell
dc.subjectArticle
dc.subjectblood pressure
dc.subjectbone marrow cell
dc.subjectcontrolled study
dc.subjectheart injury
dc.subjectheart ventricle hypertrophy
dc.subjecthypertension
dc.subjectimmunomodulation
dc.subjectinflammation
dc.subjectkidney injury
dc.subjectmale
dc.subjectmouse
dc.subjectnatriuresis
dc.subjectnonhuman
dc.subjectoxidative stress
dc.subjectpriority journal
dc.subjectprotein expression
dc.subjectregulatory T lymphocyte
dc.subjectrenin angiotensin aldosterone system
dc.subjectsalt intake
dc.subjectsodium transport
dc.subjectanimal
dc.subjectantigen presenting cell
dc.subjectbone marrow cell
dc.subjectdisease model
dc.subjectimmunology
dc.subjection transport
dc.subjectmetabolism
dc.subjectpathophysiology
dc.subjecttransgenic mouse
dc.subjectAngiotensin II
dc.subjectAnimals
dc.subjectAntigen-Presenting Cells
dc.subjectBlood Pressure
dc.subjectCD11c Antigen
dc.subjectDisease Models, Animal
dc.subjectEpithelial Sodium Channels
dc.subjectHypertension
dc.subjectInflammation
dc.subjectIon Transport
dc.subjectMice
dc.subjectMice, Transgenic
dc.subjectMyeloid Cells
dc.subjectSodium Chloride, Dietary
dc.titleMyeloid CD11c+ antigen-presenting cells ablation prevents hypertension in response to angiotensin II plus high-salt diet
dc.typeArticle


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