Abstract

Erythropoietin (EPO), known for its role in erythroid differentiation, has been shown to be an important growth factor for brain and heart. EPO is synthesized by fibroblast-like cells in the renal cortex. Prompted by this anatomical relationship and its significant impact on the maturation process of brain and heart, we asked whether EPO could play a role during the development of renal cortex. The relationship between the development of renal cortex and the change of EPO receptor (EPOR), through which EPO could act as a renotropic cytokine, became interesting to us. In this study, the day of birth was recorded as postnatal day 0(P0). P7, P14, P21, P28, P35, P42 and mature mice (postnatal days>56) were used as the animal model of different developmental stages. Immunohistochemistry and Western blotting were used to detect the expression of EPOR in mouse renal cortex. Results showed that expression of EPOR decreased with the development of renal cortex and became stable when kidney became mature. The expression of EPOR was detected at the renal tubule of all developmental stages and a relatively higher expression was observed at P14. However, at the renal corpuscle the expression was only observed at P7 and quickly became undetectable after that. All these suggested that a translocation of EPOR from renal corpuscle to renal tubule may take place during the developmental process of renal cortex. Also, EPO may be an essential element for the maturation of renal cortex, and the requirement for EPO was changed during postnatal development process.

Highlights

  • Erythropoietin (EPO), a hormone-like substance that can promote the generation of red blood cells, is mainly secreted by the fibroblast-like cells in the renal cortex

  • Immunohistochemistry and Western blotting were used to detect the expression of erythropoietin receptor (EPOR) in the renal cortex of P7, P14, P21, P28, P35, P42 and mature mice

  • There was a relatively higher expression of EPOR in the renal tubule than that of glomerulus at P14, and it dropped dramatically after P14. All these results indicated that there was a translocation of EPOR during the postnatal development and the expression was decreased, and became relatively stable after P28

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Summary

Introduction

Erythropoietin (EPO), a hormone-like substance that can promote the generation of red blood cells, is mainly secreted by the fibroblast-like cells in the renal cortex. Targeted disruption of EPO-EPOR system caused utero death in mice between embryonic days E11 and E13, because of lacking definitive erythropoiesis in the fetal liver [1,2]. These suggested that the vital role of EPO–EPOR signaling was in the proliferation, survival and terminal differentiation of erythroid progenitors, and it might play as an important developmental factor. The increased apoptosis was observed in the myocardium of EPOR-null mouse during the embryonic development [13] All these suggested that EPO could be regarded as a hematopoiesis-related cytokines, and might play a significant role during the development process of nonhaematopoietic tissues

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