Recombinant Erythropoietin Provides Protection against Renal Fibrosis in Adenine-Induced Chronic Kidney Disease

Author:

Vázquez-Méndez Estefanía12,Gutiérrez-Mercado Yanet1ORCID,Mendieta-Condado Edgar3,Gálvez-Gastélum Francisco Javier4ORCID,Esquivel-Solís Hugo1ORCID,Sánchez-Toscano Yadira5,Morales-Martínez Claudia1ORCID,Canales-Aguirre Alejandro A.1ORCID,Márquez-Aguirre Ana Laura1ORCID

Affiliation:

1. Unidad de Biotecnología Médica y Farmacéutica, Centro de Investigación y Asistencia en Tecnología y Diseño del Estado de Jalisco, A.C, Guadalajara, Jalisco, Mexico

2. Doctorado en Farmacología, Centro Universitario de Ciencias de la Salud, Universidad de Guadalajara, Jalisco, Mexico

3. Departamento de Biología Molecular y Validación de Técnicas, Instituto de Diagnóstico y Referencia Epidemiológicos-SSA, Mexico

4. Departamento de Microbiología y Patología, Centro Universitario de Ciencias de la Salud, Universidad de Guadalajara, Jalisco, Mexico

5. Escuela de Ciencias de la Salud, Universidad Guadalajara LAMAR, Campus Vallarta, Guadalajara, Mexico

Abstract

Chronic kidney disease (CKD) causes anemia by renal damage. In CKD, the kidney is submitted to hypoxia, persistent inflammation, leading to fibrosis and permanent loss of renal function. Human recombinant erythropoietin (rEPO) has been widely used to treat CKD-associated anemia and is known to possess organ-protective properties that are independent from its well-established hematopoietic effects. Nonhematopoietic effects of EPO are mediated by an alternative receptor that is proposed to consist of a heterocomplex between the erythropoietin receptor (EPOR) and the beta common receptor (βcR). The present study explored the effects of rEPO to prevent renal fibrosis in adenine-induced chronic kidney disease (Ad-CKD) and their association with the expression of the heterodimer EPOR/βcR. Male Wistar rats were randomized to control group (CTL), adenine-fed rats (Ad-CKD), and Ad-CKD with treatment of rEPO (1050 IU/kg, once weekly for 4 weeks). Ad-CKD rats exhibited anemia, uremia, decreased renal function, increased infiltration of inflammatory cells, tubular atrophy, and fibrosis. rEPO treatment not only corrected anemia but reduced uremia and partially improved renal function as well. In addition, we observed that rEPO diminishes tubular injury, prevents fibrosis deposition, and induces the EPOR/βcR heteroreceptor. The findings may explain the extrahematopoietic effects of rEPO in CKD and provide new strategies for the treatment of renal fibrosis in CKD.

Funder

Consejo Nacional de Ciencia y Tecnología

Publisher

Hindawi Limited

Subject

Cell Biology,Immunology

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