RT info:eu-repo/semantics/article
T1 FKBP51, AmotL2 and IQGAP1 Involvement in Cilastatin Prevention of Cisplatin-Induced Tubular Nephrotoxicity in Rats.
A1 Morales González, Manuel José
A1 González-Fernández, Rebeca
A1 González-Nicolás, María Ángeles
A1 Ávila, Julio
A1 Lázaro, Alberto
A1 Martín-Vasallo, Pablo
A2 Medicina InternaDermatología y Psiquiatría
K1 FKBP51
K1 IQGAP1
K1 AmotL2
K1 cisplatin toxicity
AB The immunophilin FKBP51, the angiomotin AmotL2, and the scaffoldin IQGAP1 are overexpressed in many types of cancer, with the highest increase in leucocytes from patients undergoingoxaliplatin chemotherapy. Inflammation is involved in the pathogenesis of nephrotoxicity induced byplatinum analogs. Cilastatin prevents renal damage caused by cisplatin. This functional and confocalmicroscopy study shows the renal focal-segmental expression of TNFα after cisplatin administrationin rats, predominantly of tubular localization and mostly prevented by co-administration of cilastatin.FKBP51, AmotL2 and IQGAP1 protein expression increases slightly with cilastatin administration andto a much higher extent with cisplatin, in a cellular- and subcellular-specific manner. Kidney tubulecells expressing FKBP51 show either very low or no expression of TNFα, while cells expressing TNFαhave low levels of FKBP51. AmotL2 and TNFα seem to colocalize and their expression is increased intubular cells. IQGAP1 fluorescence increases with cilastatin, cisplatin and joint cilastatin-cisplatintreatment, and does not correlate with TNFα expression or localization. These data suggest a role forFKBP51, AmotL2 and IQGAP1 in cisplatin toxicity in kidney tubules and in the protective effect ofcilastatin through inhibition of dehydropeptidase-I.
YR 2022
FD 2022
LK http://riull.ull.es/xmlui/handle/915/40031
UL http://riull.ull.es/xmlui/handle/915/40031
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DS Repositorio institucional de la Universidad de La Laguna
RD 29-nov-2024