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dc.contributor.author
Costantino, Valeria Victoria
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dc.contributor.author
Bocanegra, María Victoria
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dc.contributor.author
Cacciamani, Valeria
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dc.contributor.author
Gil Lorenzo, Andrea Fernanda
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dc.contributor.author
Benardon, María Eugenia
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dc.contributor.author
Vallés, Patricia G.
dc.date.available
2020-07-22T20:15:33Z
dc.date.issued
2019-10
dc.identifier.citation
Costantino, Valeria Victoria; Bocanegra, María Victoria; Cacciamani, Valeria; Gil Lorenzo, Andrea Fernanda; Benardon, María Eugenia; et al.; Losartan through Hsp70 Avoids Angiotensin II Induced Mesenchymal Epithelial Transition Proximal Tubule Cells from Spontaneously Hypertensive Rats; Karger; Cellular Physiology and Biochemistry; 53; 4; 10-2019; 713-730
dc.identifier.issn
1015-8987
dc.identifier.uri
http://hdl.handle.net/11336/109972
dc.description.abstract
Renal injury related to hypertension is characterized by glomerular and tubulointerstitial damage. The overactivation of the renin-angiotensin system mainly by angiotensin II (AII) seems to be a main contributor to progressive renal fibrosis. Epithelial to mesenchymal transition (EMT) is a mechanism that promotes renal fibrosis. Owing to heat shock protein 70 (Hsp70) cytoprotective properties, the chaperone exhibits an important potential as a therapeutic target. We investigate the role of Hsp70 on Angiotensin II induced epithelial mesenchymal transition within the Losartan effect in proximal tubule cells (PTCs) from a genetic model of hypertension in rats (SHR). Methods: Primary cell culture of PTCs from SHR and Wistar Kyoto (WKY) rats were stimulated with AII, treated with Losartan (L), (L+AII) or untreated (Cc ). The functional Hsp70 role in Losartan effect, after silencing its expression by cell transfection, was determined by Immunofluorescence; Western blotting; Gelatin Zymography assays; Scratch wound assays; flow cytometry; and Live Cell Time-lapse microscopy. Results: (L) and (L+AII) treatments induced highly organized actin filaments and increased cortical actin in SHR PTCs. However, SHR PTCs (Cc ) and (AII) treated cells showed disorganized actin. After Hsp72 knockdown in SHR PTCs, (L) was unable to stabilize the actin cytoskeleton. We demonstrated that (L) and (L+AII) increased E-cadherin levels and decreased vinculin, α-SMA, vimentin, pERK, p38 and Smad2-3 activation compared to (AII) and (Cc ) SHR PTCs. Moreover, (L) inhibited MMP-2 and MMP-9 secretion, reduced migration and cellular displacement, stabilizing intercellular junctions. Notably, (L) treatment in shHsp72 knockdown SHR PTCs showed results similar to SHR PTCs (Cc ). Conclusion: Our results demonstrate that Losartan through Hsp70 inhibits the EMT induced by AII in proximal tubule cells derived from SHR.
dc.format
application/pdf
dc.language.iso
eng
dc.publisher
Karger
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dc.rights
info:eu-repo/semantics/openAccess
dc.rights.uri
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
dc.subject
Angiotensin II
dc.subject
Hsp70
dc.subject
Losartan
dc.subject
Mesenchymal epithelial transition
dc.subject
Proximal tubule cells
dc.subject
Hsp70
dc.subject
Losartan
dc.subject
Mesenchymal epithelial transition
dc.subject.classification
Bioquímica y Biología Molecular
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dc.subject.classification
Ciencias Biológicas
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dc.subject.classification
CIENCIAS NATURALES Y EXACTAS
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dc.title
Losartan through Hsp70 Avoids Angiotensin II Induced Mesenchymal Epithelial Transition Proximal Tubule Cells from Spontaneously Hypertensive Rats
dc.type
info:eu-repo/semantics/article
dc.type
info:ar-repo/semantics/artículo
dc.type
info:eu-repo/semantics/publishedVersion
dc.date.updated
2020-06-30T14:23:28Z
dc.journal.volume
53
dc.journal.number
4
dc.journal.pagination
713-730
dc.journal.pais
Suiza
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dc.journal.ciudad
Basel
dc.description.fil
Fil: Costantino, Valeria Victoria. Universidad Nacional de Cuyo; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mendoza. Instituto de Medicina y Biología Experimental de Cuyo; Argentina
dc.description.fil
Fil: Bocanegra, María Victoria. Universidad Nacional de Cuyo; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mendoza. Instituto de Medicina y Biología Experimental de Cuyo; Argentina
dc.description.fil
Fil: Cacciamani, Valeria. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mendoza. Instituto de Medicina y Biología Experimental de Cuyo; Argentina
dc.description.fil
Fil: Gil Lorenzo, Andrea Fernanda. Universidad Nacional de Cuyo; Argentina
dc.description.fil
Fil: Benardon, María Eugenia. Universidad Nacional de Cuyo; Argentina
dc.description.fil
Fil: Vallés, Patricia G.. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mendoza. Instituto de Medicina y Biología Experimental de Cuyo; Argentina. Universidad Nacional de Cuyo; Argentina
dc.journal.title
Cellular Physiology and Biochemistry
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dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/doi/http://dx.doi.org/10.33594/000000167
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/url/https://www.cellphysiolbiochem.com/Articles/000167/
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