| Texto completo | |
| Autor(es): |
de Ponte, Mariana Charleaux
[1]
;
Cardoso, Vanessa Gerolde
[1]
;
Goncalves, Guilherme Lopes
[1]
;
Costa-Pessoa, Juliana Martins
[1]
;
Oliveira-Souza, Maria
[1]
Número total de Autores: 5
|
| Afiliação do(s) autor(es): | [1] Univ Sao Paulo, Inst Biomed Sci, Dept Physiol & Biophys, Lab Renal Physiol, BR-05508900 Sao Paulo, SP - Brazil
Número total de Afiliações: 1
|
| Tipo de documento: | Artigo Científico |
| Fonte: | SCIENTIFIC REPORTS; v. 11, n. 1 SEP 24 2021. |
| Citações Web of Science: | 0 |
| Resumo | |
The present study aimed to investigate the interaction between early diabetes and renal IR-induced AKI and to clarify the mechanisms involved. C57BL/6J mice were assigned to the following groups: (1) sham-operated; (2) renal IR; (3) streptozotocin (STZ-55 mg/kg/day) and sham operation; and (4) STZ and renal IR. On the 12th day after treatments, the animals were subjected to bilateral IR for 30 min followed by reperfusion for 48 h, at which time the animals were euthanized. Renal function was assessed by plasma creatinine and urea levels, as well urinary protein contents. Kidney morphology and gene and protein expression were also evaluated. Compared to the sham group, renal IR increased plasma creatinine, urea and albuminuria levels and decreased Nphs1 mRNA expression and nephrin and WT1 protein staining. Tubular injury was observed with increased Havcr1 and Mki67 mRNA expression accompanied by reduced megalin staining. Renal IR also resulted in increased SQSTM1 protein expression and increased proinflammatory and profibrotic factors mRNA expression. Although STZ treatment resulted in hyperglycemia, it did not induce significant changes in renal function. On the other hand, STZ treatment aggravated renal IR-induced AKI by exacerbating renal dysfunction, glomerular and tubular injury, inflammation, and profibrotic responses. Thus, early diabetes constitutes a relevant risk factor for renal IR-induced AKI. (AU) | |
| Processo FAPESP: | 17/02020-0 - Mecanismos envolvidos na transição da injúria renal aguda pós-isquêmica para a doença renal crônica: contribuição da angiotensina II e da albumina |
| Beneficiário: | Maria Oliveira de Souza |
| Modalidade de apoio: | Auxílio à Pesquisa - Regular |
| Processo FAPESP: | 16/12354-0 - Análise da transição da lesão renal aguda pós-isquêmica para a doença renal crônica e a contribuição da diabetes mellitus neste processo |
| Beneficiário: | Mariana Charleaux de Ponte |
| Modalidade de apoio: | Bolsas no Brasil - Doutorado |
| Processo FAPESP: | 18/26528-5 - Mecanismos adaptativos da função renal em um modelo de nefrotoxicidade induzido por adriamicina: participação da sirtuína 1 e claudina-1 |
| Beneficiário: | Guilherme Lopes Gonçalves |
| Modalidade de apoio: | Bolsas no Brasil - Doutorado |
| Processo FAPESP: | 19/13584-7 - Mecanismos envolvidos na progressão de doenças renais em modelos experimentais de nefrotoxicidade induzida por adriamicina ou de isquemia/reperfusão e Diabetes |
| Beneficiário: | Maria Oliveira de Souza |
| Modalidade de apoio: | Auxílio à Pesquisa - Regular |