Редактирование: EPOR

Erythropoietin receptor precursor (EPO-R)

==Publications==

{{medline-entry
|title=Age-associated expression of erythropoietin and its receptor in rat spiral ganglion neurons and its association with neuronal apoptosis and hearing alterations.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/27959434
|abstract=The present study aimed to determine the expression of erythropoietin ([[EPO]]) and the [[EPO]] receptor ([[EPO]]R) in spiral ganglion neurons (SGNs) in the inner ear of rats of various ages, and the associated neuronal apoptosis and hearing alterations. A total of 15 healthy rats (n=30 ears), were divided into three groups: i) A nominated infant group at post‑natal day (PND) 12‑14, ii) an adult group at PND 60 and iii) a 3‑year postnatal aged group. Auditory brainstem response ([[ABR]]) measurements were performed on all rats. [[EPO]] and [[EPO]]R expression in the inner ear was detected by immunohistochemistry. In situ terminal deoxynucleotidyl transferase dUTP nick end labeling assays were performed to detect the apoptosis of SGNs. The average hearing thresholds of the [[ABR]] (decibels above normal hearing level) were 5.625±4.955 in the infant, 15.000±8.498 in the adult and 23.500±13.134 in the aged groups. Hearing thresholds for aged and adult rats increased signiﬁcantly compared with infant rats. However, the difference in latencies of peak I was not significant (P>0.05). [[EPO]] in SGNs was detected during different developmental periods without significant alterations, but were reduced compared with Corti's organ or the stria vascularis. [[EPO]]R expression increased significantly from infant to adult stage, and this increased expression was maintained in the aged group. An age‑associated increase in the apoptosis of SGNs was detected in all three groups (P=0.0347). The potential neuroprotective effects of [[EPO]] in SGNs may not be revealed during the aging process under natural conditions, and may be associated with spontaneous neuronal apoptosis and consequently, hearing diminution. However, the age‑associated increase in [[EPO]]R in SGNs may exert a role in neuroprotection when necessary, for example in presbycusis.
|mesh-terms=* Aging
* Animals
* Apoptosis
* Ear, Inner
* Erythropoietin
* Female
* Hearing Loss
* Hearing Tests
* Immunohistochemistry
* Male
* Neurons
* Presbycusis
* Rats
* Rats, Sprague-Dawley
* Receptors, Erythropoietin
* Spiral Ganglion

|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5355685
}}
{{medline-entry
|title=Erythropoietin Does Not Enhance Skeletal Muscle Protein Synthesis Following Exercise in Young and Older Adults.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/27458387
|abstract=Erythropoietin ([[EPO]]) is a renal cytokine that is primarily involved in hematopoiesis while also playing a role in non-hematopoietic tissues expressing the [[EPO]]-receptor ([[EPO]]R). The [[EPO]]R is present in human skeletal muscle. In mouse skeletal muscle, [[EPO]] stimulation can activate the AKT serine/threonine kinase 1 (AKT) signaling pathway, the main positive regulator of muscle protein synthesis. We hypothesized that a single intravenous [[EPO]] injection combined with acute resistance exercise would have a synergistic effect on skeletal muscle protein synthesis via activation of the AKT pathway. Ten young (24.2 ± 0.9 years) and 10 older (66.6 ± 1.1 years) healthy subjects received a primed, constant infusion of [ring-13C(6)] L-phenylalanine and a single injection of 10,000 IU epoetin-beta or placebo in a double-blind randomized, cross-over design. 2 h after the injection, the subjects completed an acute bout of leg extension resistance exercise to stimulate skeletal muscle protein synthesis. Significant interaction effects in the phosphorylation levels of the members of the AKT signaling pathway indicated a differential activation of protein synthesis signaling in older subjects when compared to young subjects. However, [[EPO]] offered no synergistic effect on vastus lateralis mixed muscle protein synthesis rate in young or older subjects. Despite its ability to activate the AKT pathway in skeletal muscle, an acute [[EPO]] injection had no additive or synergistic effect on the exercise-induced activation of muscle protein synthesis or muscle protein synthesis signaling pathways.

|keywords=* aging
* anabolic signaling
* erythropoietin
* muscle protein synthesis
* resistance exercise
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4937030
}}
{{medline-entry
|title=Oxidative stress induces the decline of brain [[EPO]] expression in aging rats.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/27452792
|abstract=Brain Erythropoietin ([[EPO]]), an important neurotrophic factor and neuroprotective factor, was found to be associated with aging. Studies found [[EPO]] expression was significantly decreased in the hippocampus of aging rat compared with that of the youth. But mechanisms of the decline of the brain [[EPO]] during aging remain unclear. The present study utilized a d-galactose (d-gal)-induced aging model in which the inducement of aging was mainly oxidative injury, to explore underlying mechanisms for the decline of brain [[EPO]] in aging rats. d-gal-induced aging rats (2months) were simulated by subcutaneously injecting with d-gal at doses of 50mg·kg(-1), 150mg·kg(-1) and 250mg·kg(-1) daily for 8weeks while the control group received vehicle only. These groups were all compared with the aging rats (24months) which had received no other treatment. The cognitive impairment was assessed using Morris water maze (MWM) in the prepared models, and the amount of β-galactosidase, the lipid peroxidation product malondialdehyde (MDA) level and the superoxide dismutase (SOD) activity in the hippocampus was examined by assay kits. The levels of [[EPO]], [[EPO]]R, p-[[JAK2]] and hypoxia-inducible factor-2α (HIF-2α) in the hippocampus were detected by western blot. Additionally, the correlation coefficient between [[EPO]]/[[EPO]]R expression and MDA level was analyzed. The MWM test showed that compared to control group, the escape latency was significantly extended and the times of crossing the platform was decreased at the doses of 150mg·kg(-1) and 250mg·kg(-1) (p<0.05). Also, the amount of β-galactosidase and the MDA level in the hippocampus were significantly increased but the SOD activity was significantly decreased (p<0.05, 0.01 and 0.01, respectively). Similar to aging rats, the expressions of [[EPO]], [[EPO]]R, p-[[JAK2]], and HIF-2αin the brain of d-gal-treated rats were significantly decreased (p<0.05) at 150mg·kg(-1) and 250mg·kg(-1). Interestingly, negative correlations were found between [[EPO]]R (r=-0.699, p<0.01), [[EPO]] (r=-0.701, p<0.01) and the MDA level. These results indicated that aging could result in the decline of [[EPO]] in the hippocampus and oxidative stress might be the main reason for the decline of brain [[EPO]] in aging rats, involved with the decrease of HIF-2α stability.
|mesh-terms=* Aging
* Animals
* Cognitive Dysfunction
* Erythropoietin
* Galactose
* Hippocampus
* Linear Models
* Male
* Malondialdehyde
* Maze Learning
* Neuroprotective Agents
* Oxidative Stress
* Rats
* Rats, Sprague-Dawley
* Transcription Factors
* beta-Galactosidase
|keywords=* Aging
* Brain
* EPO
* HIF-2α
* Oxidative stress
|full-text-url=https://sci-hub.do/10.1016/j.exger.2016.07.012
}}
{{medline-entry
|title=Upregulation of erythropoietin receptor during postnatal and postpneumonectomy lung growth.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/15286000
|abstract=Circulating erythropoietin ([[EPO]]) stimulates erythrocytosis, whereas organ-specific local [[EPO]] receptor ([[EPO]]R) expression has been linked to angiogenesis, tissue growth, and development. On the basis of the observation of concurrent enhancement of lung growth and erythrocyte production during exposure to chronic hypoxia, we hypothesized that a paracrine [[EPO]] system is involved in mediating lung growth. We analyzed [[EPO]]R protein expression in normal dog lung tissue during postnatal maturation and during compensatory lung growth after right pneumonectomy (PNX). Membrane-bound [[EPO]]R was significantly more abundant in the immature lung compared with mature lung and in the remaining lung 3 wk after PNX compared with matched sham controls. COOH-terminal cytosolic [[EPO]]R peptides, which were even more abundant than membrane-bound [[EPO]]R, were also upregulated in immature lung but differentially processed after PNX. Apoptosis was enhanced during both types of lung growth in direct relationship to cellular proliferation and [[EPO]]R expression. We conclude that both developmental and compensatory lung growth involve paracrine [[EPO]] signaling with parallel upregulation but differential processing of [[EPO]]R.
|mesh-terms=* Aging
* Animals
* Animals, Newborn
* Cell Membrane
* Cytosol
* Dogs
* Immunohistochemistry
* Lung
* Pneumonectomy
* Receptors, Erythropoietin
* Up-Regulation

|full-text-url=https://sci-hub.do/10.1152/ajplung.00119.2004
}}