Β-catenin-dependent signaling pathway contributes to renal fibrosis in hypertensive rats

Catherina A. Cuevas, Cheril Tapia-Rojas, Carlos Cespedes, Nibaldo C. Inestrosa, Carlos P. Vio*

*Autor correspondiente de este trabajo

Producción científica: Contribución a una revistaArtículorevisión exhaustiva

19 Citas (Scopus)

Resumen

The mechanism of hypertension-induced renal fibrosis is not well understood, although it is established that high levels of angiotensin II contribute to the effect. Since β-catenin signal transduction participates in fibrotic processes, we evaluated the contribution of β-catenin-dependent signaling pathway in hypertension-induced renal fibrosis. Two-kidney one-clip (2K1C) hypertensive rats were treated with lisinopril (10 mg/kg/day for four weeks) or with pyrvinium pamoate (Wnt signaling inhibitor, single dose of 60 ug/kg, every 3 days for 2 weeks). The treatment with lisinopril reduced the systolic blood pressure from 220 ± 4 in 2K1C rats to 112 ± 5 mmHg (P < 0.05), whereas the reduction in blood pressure with pyrvinium pamoate was not significant (212 ± 6 in 2K1C rats to 170 ± 3 mmHg, P > 0.05). The levels of collagen types I and III, osteopontin, and fibronectin decreased in the unclipped kidney in both treatments compared with 2K1C rats. The expressions of β-catenin, p-Ser9-GSK-3beta, and the β-catenin target genes cyclin D1, c-myc, and bcl-2 significantly decreased in unclipped kidney in both treatments (P < 0.05). In this study we provided evidence that β-catenin-dependent signaling pathway participates in the renal fibrosis induced in 2K1C rats.

Idioma originalInglés
Número de artículo726012
PublicaciónBioMed Research International
Volumen2015
DOI
EstadoPublicada - 2015
Publicado de forma externa

Nota bibliográfica

Publisher Copyright:
© 2015 Catherina A. Cuevas et al.

Áreas temáticas de ASJC Scopus

  • Bioquímica, Genética y Biología Molecular General
  • Inmunología y Microbiología General

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