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1.
Oncol Lett ; 18(3): 3031-3038, 2019 Sep.
Artículo en Inglés | MEDLINE | ID: mdl-31452781

RESUMEN

Although erythropoietin-producing human hepatocellular receptor A2 (EphA2) signaling serves an important role in the tumor microenvironment, its contribution to vasculogenic mimicry (VM) formation in gastric cancer cells remains unclear. The aim of the present study was to investigate the role of EphA2 in VM formation induced by cancer-associated fibroblasts (CAFs). The conditioned medium of CAFs (CAF-CM) was prepared from 12 patients with gastric adenocarcinoma. VM was evaluated by the number of tubules and intersections in gastric cancer cells following CAF-CM treatment. The role of EphA2-phosphoinositide 3-kinase (PI3K) in VM was investigated using EphA2-targeted small interfering (si)RNAs (siEphA2), EphA2 inhibitors and PI3K-inhibitors. CAF-CM-induced VM formation was significantly associated with high protein expression levels of EphA2. EphA2 inhibitor and siEphA2 manipulation significantly decreased VM formation by CAF-CM. In siEphA2 cells, decreased expression levels of VM-associated proteins were observed. CAF-CM-induced VM formation was blocked by the PI3K-inhibitor. In conclusion, CAFs facilitate VM formation via EphA2-PI3K signaling in gastric cancer cells. Thus, EphA2-PI3K signaling may be required for CAF-promoted VM formation during gastric tumorigenesis.

2.
Sci Rep ; 9(1): 3414, 2019 03 04.
Artículo en Inglés | MEDLINE | ID: mdl-30833656

RESUMEN

Genetically deregulated tumor cells generate vascular channels by vasculogenic mimicry (VM) that is independent of endothelial blood vessels. The morphological characteristics of VM and the role of EphA2 in the formation of VM were evaluated in 144 clinical samples of gastric adenocarcinoma and AGS gastric cancer cell line. It has long been believed that VM consists of PAS-positive basement membrane and CD31/CD34-negative cells. Interestingly, we found that the luminal surface of gastric tumor cells that form VM channels showed PAS-positive reaction, and that the involvement of CD31/CD34-positive tumor cells in the formation of VM channels. Highly aggressive tumor cells that formed VM were found to express CD31 or CD34, implicating the angiogenic and vasculogenic potential of the genetically deregulated tumor cells. VM occurrence was positively correlated with high expression of EphA2 in our patient cohort, and the indispensable role of EphA2 in VM formation was identified by gene silencing in AGS cells. We also report that Epstein-Barr virus (EBV)-positive tumor cells were involved in the formation of VM channels in EBV-associated gastric cancer samples. Overall, our results suggest that EphA2 signaling promotes tumor metastasis by inducing VM formation during gastric tumorigenesis.


Asunto(s)
Adenocarcinoma/metabolismo , Receptor EphA2/metabolismo , Neoplasias Gástricas/metabolismo , Adenocarcinoma/genética , Adulto , Anciano , Anciano de 80 o más Años , Femenino , Humanos , Inmunohistoquímica , Hibridación in Situ , Técnicas In Vitro , Masculino , Persona de Mediana Edad , Neovascularización Patológica , Receptor EphA2/genética , Transducción de Señal/genética , Transducción de Señal/fisiología , Neoplasias Gástricas/genética
3.
J Cancer Res Clin Oncol ; 144(9): 1649-1663, 2018 Sep.
Artículo en Inglés | MEDLINE | ID: mdl-29948146

RESUMEN

PURPOSE: Under physiologic conditions, the binding of erythropoietin-producing hepatocellular (Eph) A2 receptor and its ligand ephrinA1 results in decreased EphA2 level and tumor suppression. However, EphA2 and ephrinA1 are highly expressed in human cancers including gastric adenocarcinoma. In this study, we tested our hypothesis that cancer-associated fibroblasts (CAFs) promote gastric tumorigenesis through EphA2 signaling in a ligand-independent manner. METHODS: Expression of EphA2 protein in primary tumor tissues of 91 patients who underwent curative surgery for gastric adenocarcinoma was evaluated by immunohistochemistry and western blotting. Conditioned medium of cancer-associated fibroblasts (CAF-CM) was used to evaluate the tumorigenic effect of CAFs on gastric cancer cell lines. Epithelial-mesenchymal transition (EMT), cell proliferation, migration, and invasion were assessed. EphrinA1-Fc ligand was used to determine the suppressor role of EphA2 receptor-ligand binding. RESULTS: CAF-CM-induced EMT and promoted cancer cell motility even without cell-cell interaction. Treatment with a selective EphA2 inhibitor (ALW-II-41-27) or EphA2-targeted siRNA markedly reduced CAF-CM-induced gastric tumorigenesis. EphrinA1-Fc ligand treatment showing ligand-dependent tumor suppression diminished the EphA2 expression and EMT progression. In contrast, ephrinA1-targeted siRNA did not significantly affect CAF-CM-mediated increases in EphA2 expression and EMT progression. Treatment with VEGF showed effects like CAF-CM in terms of EphA2 activation and EMT progression. CONCLUSION: CAFs may contribute to gastric tumorigenesis by activating EphA2 signaling pathway in a ligand-independent manner. Our results suggest that ligand-independent activation of EphA2 was triggered by VEGF released from CAF-CM. Our result may partially explain why ligand-dependent tumor suppressor roles of EphA2 are not evident in gastric cancer despite the prominent level of ephrinA1.


Asunto(s)
Fibroblastos Asociados al Cáncer/metabolismo , Fibroblastos Asociados al Cáncer/patología , Carcinogénesis/metabolismo , Carcinogénesis/patología , Efrina-A2/metabolismo , Neoplasias Gástricas/metabolismo , Neoplasias Gástricas/patología , Línea Celular Tumoral , Transición Epitelial-Mesenquimal/fisiología , Femenino , Mucosa Gástrica/metabolismo , Humanos , Ligandos , Masculino , Persona de Mediana Edad , ARN Interferente Pequeño/metabolismo , Receptor EphA2 , Transducción de Señal/fisiología , Estómago/patología
4.
Medicine (Baltimore) ; 97(9): e9913, 2018 Mar.
Artículo en Inglés | MEDLINE | ID: mdl-29489692

RESUMEN

BACKGROUND: The objective of this study was to investigate the underlying molecular mechanisms and the therapeutic time window for preventing astrogliosis with erythropoietin (EPO) treatment after in vitro modeled spinal cord injury (SCI). METHODS: Cultured rat spinal cord astrocytes were treated with kainate and scratching to generate an in vitro model of SCI. EPO (100U/mL or 300U/mL) was added immediately or 2, 4, or 8 hours after injury. Some cultures were also treated with AG490, an inhibitor of the EPO-EPO receptor (EpoR) pathway mediator Janus kinase 2 (JAK2). To evaluate neurite extension, rat embryonic spinal cord neurons were seeded onto astrocyte cultures and treated with EPO immediately after injury in the presence or absence of anti-EpoR antibody. RESULTS: EPO treatment at up to 8 hours after injury reduced the expression of axonal growth inhibiting molecules (glial fibrillary acidic protein, vimentin, and chondroitin sulfate proteoglycan), cytoskeletal regulatory proteins (Rho-associated protein kinase and ephephrin A4), and proinflammatory cytokines (tumor necrosis factor-alpha, transforming growth factor-beta, and phosphorylated-Smad3) in a dosedependent manner (P < .001). Most effects peaked with EPO treatment 2-4hours after injury. Additionally, EPO treatment up to 4 hours after injury promoted expression of the EpoR (>2-fold) and JAK2 (>3-fold) in a dose-dependent manner (P < .001), whereas co-treatment with AG490 precluded these effects (P < .001). EPO treatment up to 4hours after injury also enhanced axonal b-III tubulin-immunoreactivity (>12-fold), and this effect was precluded by co-treatment with an anti-EpoR antibody (P < .001). CONCLUSIONS: EPO treatment within 8 hours after injury reduced astrogliosis, and EPO treatment within 4 hours promoted neurite outgrowth. EPO therapy immediately after spinal cord injury may regulate glia to generate an environment permissive of axonal regeneration.


Asunto(s)
Eritropoyetina/administración & dosificación , Gliosis/tratamiento farmacológico , Proyección Neuronal/efectos de los fármacos , Traumatismos de la Médula Espinal/tratamiento farmacológico , Tiempo de Tratamiento , Animales , Astrocitos , Axones/efectos de los fármacos , Células Cultivadas , Esquema de Medicación , Ratas , Ratas Sprague-Dawley
5.
Anticancer Res ; 35(4): 1967-76, 2015 Apr.
Artículo en Inglés | MEDLINE | ID: mdl-25862849

RESUMEN

Sorafenib increases survival of patients with advanced hepatocellular carcinoma (HCC) by inhibiting RAF kinase and receptor tyrosine kinase activity, but involvement of sorafenib in fibrosis and epithelial-mesenchymal transition (EMT) remains unclear. To elucidate effects of sorafenib on EMT progression and matrix metalloproteinase (MMP) activity, levels of E-cadherin, N-cadherin, and MMPs were evaluated in HepG2 human HCC cells induced by hepatocyte growth factor (HGF). Scratching cell migration assay, matrigel cell invasion assay, and immuno histochemistry were performed to examine effects of sorafenib on tumor metastasis and MMP expression. Sorafenib inhibited HGF-induced EMT and suppressed cell migration and invasion. Treatment with sorafenib significantly reduced HGF-enhanced expression of MMPs, suggesting that inhibition of MMP activity contributes to suppression of cellular motility and invasiveness of HepG2 cells. Neutralization of MMP activity by antibodies to MMP2/9, broad-spectrum MMP inhibitor or selective gelatinase inhibitor resulted in significant suppression of HGF-induced EMT and cell migration/invasion. Sorafenib treatment and MMP inactivation inhibited HGF-induced c-MET and MEK/ERK pathways. Sorafenib reduced MMP activity in this HGF-induced tumorigenic model of HCC. These findings provide in vitro evidence that sorafenib suppresses HGF-induced EMT and cell migration/invasion, as well as HGF-induced c-MET and MEK/ERK pathways.


Asunto(s)
Carcinoma Hepatocelular/genética , Neoplasias Hepáticas/genética , Metaloproteinasa 2 de la Matriz/biosíntesis , Metaloproteinasa 9 de la Matriz/biosíntesis , Carcinoma Hepatocelular/tratamiento farmacológico , Carcinoma Hepatocelular/patología , Movimiento Celular/efectos de los fármacos , Transición Epitelial-Mesenquimal/efectos de los fármacos , Regulación Neoplásica de la Expresión Génica/efectos de los fármacos , Células Hep G2 , Humanos , Neoplasias Hepáticas/tratamiento farmacológico , Neoplasias Hepáticas/patología , Sistema de Señalización de MAP Quinasas/efectos de los fármacos , Invasividad Neoplásica/genética , Niacinamida/administración & dosificación , Niacinamida/análogos & derivados , Compuestos de Fenilurea/administración & dosificación , Proteínas Proto-Oncogénicas c-met/biosíntesis , Sorafenib
6.
Anticancer Res ; 35(4): 1985-95, 2015 Apr.
Artículo en Inglés | MEDLINE | ID: mdl-25862851

RESUMEN

Vitamin K plays a role in controlling cell growth. Anti-angiogenic effects of sorafenib lead to impairment of vitamin K uptake and induction of des-γ-carboxyprothrombin release by hepatocellular carcinoma (HCC) cells. We examined sorafenib and vitamin K individually and in combination regarding their ability to suppress migration and metastatic potential of HCC cells. HepG2 cells (HCC cell line) were treated with hepatocyte growth factor (HGF). E-Cadherin expression, phospho-MET (p-MET), and phospho-extracellular signal-regulated kinase (p-ERK) levels and cell migration were evaluated. HGF-stimulated HepG2 cells, which were treated with a combination of sorafenib and vitamin K, showed significantly increased expression of E-cadherin and impairment of migration ability compared to when treated with either agent alone. This combination therapy also induced marked inhibition of epithelial-mesenchymal transition phenotype; inhibition of HGF-stimulated cell proliferation, invasion and migration; and inhibition of HGF/c-MET signaling pathway. Levels of p-MET and p-ERK were also significantly reduced by this combination. Our experimental study demonstrated that sorafenib and vitamin K can function synergistically to inhibit the migration and proliferation of HCC cells. Combination therapy with sorafenib and vitamin K appears to be worthy of clinical trial with expectation of synergistic therapeutic effects.


Asunto(s)
Carcinoma Hepatocelular/tratamiento farmacológico , Neoplasias Hepáticas/tratamiento farmacológico , Niacinamida/análogos & derivados , Compuestos de Fenilurea/administración & dosificación , Vitamina K/administración & dosificación , Carcinoma Hepatocelular/patología , Movimiento Celular/efectos de los fármacos , Proliferación Celular/efectos de los fármacos , Sinergismo Farmacológico , Células Hep G2 , Factor de Crecimiento de Hepatocito/administración & dosificación , Humanos , Neoplasias Hepáticas/patología , Niacinamida/administración & dosificación , Sorafenib
7.
Korean J Hepatobiliary Pancreat Surg ; 17(1): 21-33, 2013 Feb.
Artículo en Inglés | MEDLINE | ID: mdl-26155209

RESUMEN

BACKGROUNDS/AIMS: Mesenchymal stem cells (MSCs) have the capacity to differentiate into hepatocytes, The purpose of this study is to investigate the MSCs' differentiation process and therapeutic potentials by comparing isolated MSCs with HGF-treated MSCs in rat's model with thiacetamide (TAA)-induced cirrhosis. METHODS: Male Sprague-Dawley (SD) rats, weighing 100-150 g were used in this study. To induce liver fibrosis, recipient rats were taken with 0.04% thioacetamide (TAA) in the drinking water (400 mg TAA/L) for 8 weeks. The rats underlying liver cirrhosis were divided into 3 groups according to the transplanted materials, compared to normal saline as control (I) and isolated MSCs (II) HGF-treated MSCs. RESULTS: Severe hepatic fibrosis and hepatocyte destruction were detected in the control group. Less hepatic cirrhosis and collagen formation, more hepatocyte regeneration and glycogen storage were detected in isolated MSCs compared to HGF-treated MSCs group, Distribution of red autofluorescence is mainly localized near the sinusoids in isolated MSCs, scattered away the sinusoids in HGF-treated MSCs group. MSCs transdifferentiated into CK-19 postive Oval cells and then to albulmin-producing hepatocytes, HGF treated MSCs differentiated into hepatocyte without the intermediate oval cells phase. HGF treated MSCs became the CK18-positive, MSCs became CD 90-positive. CONCLUSIONS: Significant hepatocyte differentiation occurred in not HGF-treated MSCs but isolated MSCs group unexpectedly. These results suggest that the beneficial effect of MSCs on in rat's model with TAA-induced cirrhosis may occur during early differentiation course of MSCs. Mature hepatocyte itself has a little effect on the accelerated differentiation and functional capacity of hepatic lineage cell-line.

8.
Cell Biol Int ; 36(3): 279-88, 2012 Mar 01.
Artículo en Inglés | MEDLINE | ID: mdl-21966929

RESUMEN

Implantation of bone-marrow-derived MSCs (mesenchymal stem cells) has emerged as a potential treatment modality for liver failure, but in vivo differentiation of MSCs into functioning hepatocytes and its therapeutic effects have not yet been determined. We investigated MSC differentiation process in a rat model of TAA (thioacetamide)-induced liver cirrhosis. Male Sprague-Dawley rats were administered 0.04% TAA-containing water for 8 weeks, MSCs were injected into the spleen for transsplenic migration into the liver, and liver tissues were examined over 3 weeks. Ingestion of TAA for 8 weeks induced micronodular liver cirrhosis in 93% of rats. Injected MSCs were diffusely engrafted in the liver parenchyma, differentiated into CK19 (cytokeratin 19)- and thy1-positive oval cells and later into albumin-producing hepatocyte-like cells. MSC engraftment rate per slice was measured as 1.0-1.6%. MSC injection resulted in apoptosis of hepatic stellate cells and resultant resolution of fibrosis, but did not cause apoptosis of hepatocytes. Injection of MSCs treated with HGF (hepatocyte growth factor) in vitro for 2 weeks, which became CD90-negative and CK18-positive, resulted in chronological advancement of hepatogenic cellular differentiation by 2 weeks and decrease in anti-fibrotic activity. Early differentiation of MSCs to progenitor oval cells and hepatocytes results in various therapeutic effects, including repair of damaged hepatocytes, intracellular glycogen restoration and resolution of fibrosis. Thus, these results support that the in vivo hepatogenic differentiation of MSCs is related to the beneficial effects of MSCs rather than the differentiated hepatocytes themselves.


Asunto(s)
Diferenciación Celular , Hepatocitos/citología , Cirrosis Hepática/inducido químicamente , Cirrosis Hepática/metabolismo , Células Madre Mesenquimatosas/citología , Tioacetamida/farmacología , Animales , Hepatocitos/metabolismo , Hígado/citología , Hígado/metabolismo , Masculino , Células Madre Mesenquimatosas/metabolismo , Ratas , Ratas Sprague-Dawley
9.
Biochem Biophys Res Commun ; 417(2): 753-9, 2012 Jan 13.
Artículo en Inglés | MEDLINE | ID: mdl-22197819

RESUMEN

Here, we sought to delineate the effect of EPO on the remyelination processes using an in vitro model of demyelination. We report that lysolecithin-induced demyelination elevated EPO receptor (EpoR) expression in oligodendrocyte progenitor cells (OPCs), facilitating the beneficial effect of EPO on the formation of oligodendrocytes (oligodendrogenesis). In the absence of EPO, the resultant remyelination was insufficient, possibly due to a limiting number of oligodendrocytes rather than their progenitors, which proliferate in response to lysolecithin-induced injury. By EPO treatment, lysolecithin-induced proliferation of OPCs was accelerated and the number of myelinating oligodendrocytes and myelin recovery was increased. EPO also enhanced the differentiation of neural progenitor cells expressing EpoR at high level toward the oligodendrocyte-lineage cells through activation of cyclin E and Janus kinase 2 pathways. Induction of myelin-forming oligodendrocytes by high dose of EPO implies that EPO might be the key factor influencing the final differentiation of OPCs. Taken together, our data suggest that EPO treatment could be an effective way to enhance remyelination by promoting oligodendrogenesis in association with elevated EpoR expression in spinal cord slice culture after lysolecithin-induced demyelination.


Asunto(s)
Eritropoyetina/farmacología , Vaina de Mielina/fisiología , Neurogénesis/efectos de los fármacos , Oligodendroglía/citología , Regeneración de la Medula Espinal/efectos de los fármacos , Médula Espinal/efectos de los fármacos , Animales , Enfermedades Desmielinizantes/inducido químicamente , Lisofosfatidilcolinas/farmacología , Técnicas de Cultivo de Órganos , Ratas , Ratas Sprague-Dawley , Receptores de Eritropoyetina/agonistas , Receptores de Eritropoyetina/metabolismo , Médula Espinal/fisiología
10.
Yonsei Med J ; 52(5): 856-8, 2011 Sep.
Artículo en Inglés | MEDLINE | ID: mdl-21786453

RESUMEN

Coronary artery anomalies are associated often with myocardial ischemia or sudden cardiac death. A 19-year-old woman who participated in an exertive game lost consciousness upon one such exertion. She was taken to a hospital where she died on the same day. An autopsy revealed that she had bifurcated coronary arteries, which arose from one coronary ostium in the left sinus of Valsalva. The right coronary artery arose from the left sinus and traveled between the aorta and the pulmonary trunk. The heart as well as the cardiac conduction system depended exclusively on the single coronary artery ostium for oxygenated blood supply, and the unbalanced blood distribution on her exertion probably led to sudden cardiac death. The case highlights the medicolegal importance of unexpected sudden cardiac death related to an anomalous origin of the coronary arteries.


Asunto(s)
Anomalías de los Vasos Coronarios/complicaciones , Muerte Súbita Cardíaca/etiología , Autopsia , Anomalías de los Vasos Coronarios/patología , Vasos Coronarios/patología , Muerte Súbita Cardíaca/patología , Femenino , Humanos , Esfuerzo Físico , Seno Aórtico/anomalías , Adulto Joven
11.
J Neurosci Res ; 87(1): 150-63, 2009 Jan.
Artículo en Inglés | MEDLINE | ID: mdl-18711747

RESUMEN

Although the neuroprotective effects of erythropoietin (EPO) preconditioning are well known, the potential of postapplied EPO to protect neurons against excitotoxic injury has not been clearly established. Here we show that kainate (KA)-induced excitotoxicity, which plays a key role in secondary spinal cord injury, decreased neuron survival, inhibited neurite extension, and significantly reduced the expression of erythropoietin receptors (EpoR) in cultured spinal neurons. Posttreatment with EPO for 48 hr protected neurons against KA-induced injury, opposing KA-induced apoptosis and promoting regrowth of motoneuron neurites. These neuroprotective effects were paralleled by a restoration of EpoR expression. The importance of the EpoR signaling pathway was demonstrated using an EpoR blocking antibody, which neutralized the neuroprotective action of EPO posttreatment and prevented EPO-induced increases in EpoR expression. We also found that up-regulated EpoR stimulated the Janus kinase 2 (JAK2) pathway, which is known to facilitate neuronal growth and neurite regeneration. Although EPO posttreatment modestly attenuated KA-induced reactive gliosis in mixed neuron-glial cultures, blocking EpoR activity did not alter glial fibrillary acidic protein expression or astrocyte proliferation. In conclusion, 48 hr treatment with EPO following KA exposure induced EpoR-dependent protection against excitotoxic injury, demonstrating that preconditioning is not a prerequisite for neuroprotection by EPO. The neuroprotective effects of EPO posttreatment were mediated by an EpoR-dependent signaling pathway that possibly involves JAK2. The neuroprotective effect of EPO posttreatment against KA excitotoxicity appears to reflect direct effects on neurons and not indirect effects mediated by astrocytes.


Asunto(s)
Apoptosis/efectos de los fármacos , Eritropoyetina/administración & dosificación , Fármacos Neuroprotectores/administración & dosificación , Médula Espinal/efectos de los fármacos , Análisis de Varianza , Animales , Astrocitos/fisiología , Caspasa 3/metabolismo , Recuento de Células , Células Cultivadas , Técnicas de Cocultivo/métodos , Relación Dosis-Respuesta a Droga , Esquema de Medicación , Embrión de Mamíferos , Inhibidores Enzimáticos/farmacología , Agonistas de Aminoácidos Excitadores/farmacología , Humanos , Etiquetado Corte-Fin in Situ , Janus Quinasa 2/metabolismo , Ácido Kaínico/farmacología , Neuronas Motoras/efectos de los fármacos , Proteínas del Tejido Nervioso/metabolismo , Ratas , Ratas Sprague-Dawley , Médula Espinal/citología , Técnicas de Cultivo de Tejidos
12.
Brain Res ; 1154: 31-9, 2007 Jun 18.
Artículo en Inglés | MEDLINE | ID: mdl-17493599

RESUMEN

The aim of this study was to investigate whether erythropoietin (EPO) protect the spinal GABAergic neurons against kainic acid (KA)-excitotoxic damage in rat spinal cord cell cultures. We performed immunohistochemical staining and Western blotting of glutamate decarboxylase 67 (GAD67), one isoform of GABA-producing enzyme, which was considered to have involved in nonsynaptic functions, such as energy metabolism or trophic support. T exposure to KA significantly reduced the intensity of GAD67 expression in the GABAergic neurons and whole cell lysate, indicating that the excitotoxic damage on the GABAergic neurons may lead to reduction of the GAD67 production following KA-exposure. We found that post-treatment of EPO for 48 h after KA-injury remarkably enhanced the expression level of GAD67 and erythropoietin receptors (EpoR), which were deteriorated by KA. Our confocal images clearly demonstrated a remarkably enhanced expression of EpoR on the surface of the GABAergic neurons by post-treated EPO after KA-damage. This result suggests that the neuroprotective effect of post-treated EPO on the GABAergic neurons can be related to the EPO-mediated EpoR upregulation following KA-excitotoxicity. We observed that the post-applied EPO clearly increased expression of tyrosine Janus kinase 2 (JAK2), which is known to be the first step of EpoR-stimulation. In conclusion, the post-treated EPO is a potent protector of the spinal GABAergic neurons against KA-excitotoxicity and regulates production of GAD67 for the multiple trophic roles after KA-induced disturbance. We suggested that the protective effect of post-treated EPO on the GABAergic neurons is mediated by signal transduction involving EpoR-dependent JAK2 pathway.


Asunto(s)
Eritropoyetina/farmacología , Agonistas de Aminoácidos Excitadores/farmacología , Ácido Kaínico/farmacología , Fármacos Neuroprotectores/farmacología , Médula Espinal/citología , Ácido gamma-Aminobutírico/metabolismo , Animales , Animales Recién Nacidos , Recuento de Células/métodos , Células Cultivadas , Interacciones Farmacológicas , Expresión Génica/efectos de los fármacos , Glutamato Descarboxilasa/metabolismo , Isoenzimas/metabolismo , Janus Quinasa 2/metabolismo , Neuronas/efectos de los fármacos , Fosfopiruvato Hidratasa/metabolismo , Ratas , Ratas Sprague-Dawley , Receptores de Eritropoyetina/metabolismo
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