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Author Correction: EPO does not promote interaction between the erythropoietin and beta-common receptors.

ABSTRACT: A correction to this article has been published and is linked from the HTML and PDF versions of this paper. The error has not been fixed in the paper.

SUBMITTER: Cheung Tung Shing KS

PROVIDER: S-EPMC6527692 | biostudies-literature | 2019 May

REPOSITORIES: biostudies-literature

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Author Correction: EPO does not promote interaction between the erythropoietin and beta-common receptors.

Cheung Tung Shing Karen S KS Broughton Sophie E SE Nero Tracy L TL Gillinder Kevin K Ilsley Melissa D MD Ramshaw Hayley H Lopez Angel F AF Griffin Michael D W MDW Parker Michael W MW Perkins Andrew C AC Dhagat Urmi U

Scientific reports 20190521 1

A correction to this article has been published and is linked from the HTML and PDF versions of this paper. The error has not been fixed in the paper. ...[more]

PMID: 31110193

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EPO does not promote interaction between the erythropoietin and beta-common receptors.

Project description:A direct interaction between the erythropoietin (EPOR) and the beta-common (βc) receptors to form an Innate Repair Receptor (IRR) is controversial. On one hand, studies have shown a functional link between EPOR and βc receptor in tissue protection while others have shown no involvement of the βc receptor in tissue repair. To date there is no biophysical evidence to confirm a direct association of the two receptors either in vitro or in vivo. We investigated the existence of an interaction between the extracellular regions of EPOR and the βc receptor in silico and in vitro (either in the presence or absence of EPO or EPO-derived peptide ARA290). Although a possible interaction between EPOR and βc was suggested by our computational and genomic studies, our in vitro biophysical analysis demonstrates that the extracellular regions of the two receptors do not specifically associate. We also explored the involvement of the βc receptor gene (Csf2rb) under anaemic stress conditions and found no requirement for the βc receptor in mice. In light of these studies, we conclude that the extracellular regions of the EPOR and the βc receptor do not directly interact and that the IRR is not involved in anaemic stress.

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Erythropoietin (EPO) in acute kidney injury.

Project description:Erythropoietin (EPO) is a 30.4 kDa glycoprotein produced by the kidney, and is mostly well-known for its physiological function in regulating red blood cell production in the bone marrow. Accumulating evidence, however, suggests that EPO has additional organ protective effects, which may be useful in the prevention or treatment of acute kidney injury. These protective mechanisms are multifactorial in nature and include inhibition of apoptotic cell death, stimulation of cellular regeneration, inhibition of deleterious pathways, and promotion of recovery.In this article, we review the physiology of EPO, assess previous work that supports the role of EPO as a general tissue protective agent, and explain the mechanisms by which it may achieve this tissue protective effect. We then focus on experimental and clinical data that suggest that EPO has a kidney protective effect.

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Genetic variants of erythropoietin (EPO) and EPO receptor genes in familial erythrocytosis.

Project description:ObjectivesErythrocytosis is characterized by the expansion of erythrocyte compartment including elevated red blood cell number, hematocrit, and hemoglobin content. Familial erythrocytosis (FE) is a congenital disorder with different genetic background. Type 1 FE is primary FE caused by mutation in erythropoietin receptor gene (EPOR). Type 2-5 FE are secondary FEs caused by mutations of genes involved in oxygen sensing pathway important for erythropoietin (EPO) regulation. In the present study, we summarized associations between EPOR and EPO gene variations with development of FE and searched for genetic variants located within regulatory regions.MethodsPublications reporting EPOR and EPO sequence variants associated with FE or clinical features of erythrocytosis were retrieved from PubMed and WoS. In silico, sequence reanalysis was performed using Ensembl genomic browser, release 89 to screen for variants located within regulatory regions.ResultsTo date, 28 variants of the EPOR and seven variants of the EPO gene have been associated with erythrocytosis or upper hematocrit. Sequence variants were also found to be present within regulatory regions.ConclusionsRole of variants in regulatory regions of the EPO gene should be further investigated.

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Structural identification of modified amino acids on the interface between EPO and its receptor from EPO BRP, human recombinant erythropoietin by LC/MS analysis.

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Synergistic upregulation of erythropoietin receptor (EPO-R) expression by sense and antisense EPO-R transcripts in the canine lung.

Project description:We previously found increased erythropoietin receptor (EPO-R) protein levels in vigorously growing canine lungs after pneumonectomy (PNX), suggesting a role for paracrine EPO signaling in lung growth and remodeling. Now we find that sense and antisense EPO-R transcripts (sEPO-R and asEPO-R, respectively) are concordantly up-regulated in the post-PNX remaining lung, leading to the hypothesis that sEPO-R and asEPO-R interactions enhance EPO signaling during lung growth. We cloned a canine asEPO-R cDNA, which is fully complementary to the sense strand of the EPO-R gene from 2.5kb 3' to the sense stop codon, and extends into the 5' UTR of the sEPO-R transcript. Both asEPO-R and sEPO-R transcripts colocalize with EPO-R protein in the same lung cells. In cultured human embryonic kidney (HEK293) cells, transfection with sEPO-R (+FLAG tag) cDNA alone increased EPO-R protein expression (anti-EPO-R and anti-FLAG). At constant sEPO-R cDNA levels, cotransfection with escalating asEPO-R cDNA further increased recombinant EPO-R protein expression. The asEPO-R transcript harbors two putative opening reading frames (ORFs). Separate transfection of each asEPO-R ORF cDNA resulted in differential stimulatory effects on EPO-R protein expression. We conclude that both sEPO-R and asEPO-R transcripts contribute to in vivo up-regulation of EPO-R protein expression in the post-PNX remaining lung. This demonstrates synergism between sense-antisense EPO-R transcripts in response to physiological stimulation in a robust model of induced lung growth.

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