RESUMEN
Memory drove a critical process of feeding habit transformation in Chinese perch when they re-trained to eat dead prey fish. To investigate the regulatory mechanism of cAMP-response element-binding protein (CREB) signaling pathway on the memory of Chinese perch during feeding habit transformation, the phosphorylation levels of upstream signal proteins of CREB between the control group (trained once) and the experimental group (trained twice) were measured. The results illustrated that the re-training was correlated to phosphorylation of extracellular regulated protein kinase (ERK1/2) and calcium/calmodulin-dependent protein kinase II (CaMKII), and dephosphorylation of protein kinase A (PKA) of Chinese perch. Inhibition of ERK1/2-CREB pathway decreased the mRNA levels of memory-related genes ((fos-related antigen 2 (fra2), CCAAT enhancer-binding protein delta (c/ebpb), immediate-early gene zif268 (zif268), proto-oncogenes c-fos (c-fox) and synaptotagmin-IV (sytIV)) and mRNA levels of appetite-related genes (agouti-related peptide (agrp) and ghrelin), and activation of PP1-CREB pathway increased the phosphorylated levels of CREB, the mRNA levels of memory-related genes (fra2, c/ebpb, zif268, and c-fox), and the mRNA levels of appetite-related genes (pro-opiomelanocortin (pomc) and leptin) in primary brain cells of Chinese perch. The memory in Chinese perch feeding habit transformation was associated with the ERK1/2-CREB and PP1-CREB pathways, which could regulate the transcription of memory-related genes and appetite-related genes.
Asunto(s)
Proteína de Unión a Elemento de Respuesta al AMP Cíclico , Conducta Alimentaria , Memoria , Percas , Animales , Proteína de Unión a Elemento de Respuesta al AMP Cíclico/metabolismo , ARN MensajeroRESUMEN
An emerging concept is that the hypothalamic nutrient sensor can regulate peripheral energy metabolism via a brain-liver circuit. Valine is an essential branched-chain amino acid (BCAA) that drives intracellular signaling cascades by the activation of target of rapamycin complex 1 (TORC1) which is critical to protein metabolism in mammals. However, in teleost fish, it remains scarce in this area especially about how the intraventricular (ICV) injection of valine can mediate the protein metabolism in peripheral organs. This study would tentatively explore the effects of ICV injection of valine on protein metabolism in peripheral organs through evaluating the postprandial ammonia-N excretion rate in Chinese perch. The control group was injected with 5-µL PBS, and the Val group was injected with 20-µg L valine dissolved into 5-µL PBS. The ammonia-N excretion rate of Val group was lower than control group at 4-, 12-, and 24-h postinjection, while the concertation of plasma glucose was increased sharply at 0.5-, 4-, 12-, and 24-h postinjection. We further checked both mRNA level and the enzyme activity of glutamate dehydrogenase (GDH) in the liver and adenosine monophosphate deaminase (AMPD) in muscle, and we found that they were obviously decreased in Val group at 4-, 12-, and 24-h postinjection. The phosphorylation level of ribosomal protein S6, a downstream target protein of TORC1, was markedly enhanced in the liver of Val group at 4-, 12-, and 24-h postinjection. Collectively, these results illustrated that ICV injection of valine can attenuate protein degradation in peripheral organs by depressing the GDH and AMPD enzyme activity; on the other hand, the injected valine can trigger the activation of TORC1 in the liver via a brain-liver circuit and then interdict proteolysis.
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AMP Desaminasa/metabolismo , Amoníaco/metabolismo , Encéfalo/efectos de los fármacos , Proteínas de Peces/metabolismo , Glutamato Deshidrogenasa/metabolismo , Diana Mecanicista del Complejo 1 de la Rapamicina/metabolismo , Percas/metabolismo , Valina/farmacología , AMP Desaminasa/genética , Animales , Encéfalo/metabolismo , Proteínas de Peces/genética , Glutamato Deshidrogenasa/genética , Inyecciones Intraventriculares , Hígado/efectos de los fármacos , Hígado/metabolismo , Músculos/efectos de los fármacos , Músculos/metabolismo , Percas/genética , Periodo Posprandial , Proteína S6 Ribosómica/metabolismo , Transducción de Señal/efectos de los fármacosRESUMEN
Social learning plays important roles in gaining new foraging skills and food preferences. However, the potential role and molecular mechanism of social learning in acquiring new feeding habits is less clear in fish. In the present study, we examined the success rate of feeding habit domestication from live prey fish to dead prey fish, as well as the food intake of dead prey fish in mandarin fish with or without feeders of dead prey fish as demonstrators. Here, we found that mandarin fish can learn from each other how to solve novel foraging tasks, feeding on dead prey fish. In addition, the analysis of gene expressions and signaling pathways of learning through Western blotting and transcriptome sequencing shows that the expression of the c-fos, fra2, zif268, c/ebpd and sytIV genes were significantly increased, and the anorexigenic pomc and leptin a expressions were decreased in fish of the learning group. The phosphorylation levels of protein kinase A (PKA) and Ca2+/calmodulin-dependent protein kinase II (CaMKII) in the learning group were significantly higher than those of the control group, while the phosphorylation level of S6 ribosomal protein (S6) was lower. With the inhibitors of PKA and CaMKII signaling and the chromatin immunoprecipitation (ChIP) assay, we further found that the social learning of new feeding habits in mandarin fish could be attributed to the activation of the CaMKII signaling pathway and then the stimulation of the expression of the c-fos gene, which might be an important transcriptional factor to inhibit the expression of the anorexigenic gene pomc, resulting in the food intake of dead prey fish in mandarin fish. Altogether, our results support the hypothesis that social learning could facilitate the acquisition of novel feeding habits in fish, and it considerably increases the rate of subsequent individual food intake and domestication through the interaction between the learning gene c-fos and the appetite control gene pomc.
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Proteínas de Peces/genética , Peces/fisiología , Preferencias Alimentarias/fisiología , Aprendizaje Social/fisiología , Animales , Conducta Animal , Domesticación , Ingestión de Alimentos , Proteínas de Peces/metabolismo , Perfilación de la Expresión Génica/veterinaria , Regulación de la Expresión Génica , Fosforilación , Conducta Predatoria , Análisis de Secuencia de ARN/veterinariaRESUMEN
Mandarin fish refuse dead prey fish or artificial diets and can be trained to transform their inborn feeding habit. To investigate the effect of memory on feeding habit transformation, we compared the reaction time to dead prey fish and the success rate of feeding habit transformation to dead prey fish with training of mandarin fish in the 1st experimental group (trained once) and the 2nd experimental group (trained twice). The mandarin fish in the 2nd group had higher success rate of feeding habit transformation (100%) than those in the 1st group (67%), and shorter reaction time to dead prey fish (<1 s) than those in the 1st group (>1 s). Gene expression of cAMP responsive element binding protein I (Creb I), brain-derived neurotrophic factor (Bdnf), CCAAT enhancer binding protein delta (C/EBPD), fos-related antigen 2 (Fra2), and proto-oncogenes c-fos (c-fos) involved in long-term memory formation were significantly increased in the 2nd group after repeated training, and taste 1 receptor member 1 (T1R1), involved in feeding habit formation, was significantly increased in brains of the 2nd group after repeated training. DNA methylation levels at five candidate CpG (cytosineâ»guanine) sites contained in the predicted CpG island in the 5′-flanking region of T1R1 were significantly decreased in brains of the 2nd group compared with that of the 1st group. These results indicated that the repeated training can improve the feeding habit transformation through the memory formation of accepting dead prey fish. DNA methylation of the T1R1 might be a regulatory factor for feeding habit transformation from live prey fish to dead prey fish in mandarin fish.
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Hábitos , Memoria/fisiología , Animales , Islas de CpG/genética , Metilación de ADN/fisiología , Peces , Receptores Acoplados a Proteínas G/genética , Receptores Acoplados a Proteínas G/metabolismoRESUMEN
OBJECTIVE: To quantify the roles and relationships between age at implantation, duration of deafness (DoD), and daily processor use via data logging on speech recognition outcomes for postlingually deafened adults with cochlear implants. STUDY DESIGN: Retrospective case review. SETTING: Cochlear implant (CI) program at a tertiary medical center. PATIENTS: Six-hundred fourteen postlingually deafened adult ears with CIs (mean age, 63 yr; 44% female) were included. MAIN OUTCOME MEASURES: A stepwise multiple regression analysis was completed to investigate the combined effects of age, DoD, and daily processor use on CI-aided speech recognition (Consonant-Nucleus-Consonant monosyllables and AzBio sentences). RESULTS: Results indicated that only daily processor use was significantly related to Consonant-Nucleus-Consonant word scores ( R2 = 0.194, p < 0.001) and AzBio in quiet scores ( R2 = 0.198, p < 0.001), whereas neither age nor DoD was significantly related. In addition, there was no significant relationship between daily processor use, age at implantation, or DoD and AzBio sentences in noise ( R2 = 0.026, p = 0.005). CONCLUSIONS: Considering the clinical factors of age at implantation, DoD, and daily processor use, only daily processor use significantly predicted the ~20% of variance in postoperative outcomes (CI-aided speech recognition) accounted for by these clinical factors.
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Implantación Coclear , Implantes Cocleares , Sordera , Percepción del Habla , Adulto , Humanos , Femenino , Persona de Mediana Edad , Masculino , Estudios Retrospectivos , Implantación Coclear/métodos , Sordera/cirugía , Sordera/rehabilitación , Resultado del TratamientoRESUMEN
Long non-coding (lnc)RNA HAND2 antisense RNA 1 (HAND2-AS1) exhibited tumor suppression activity in different types of cancer. However, its role in cervical squamous cell carcinoma (CSCC), which is frequently diagnosed among females, has not been elucidated. The current study revealed that lncRNA HAND2-AS1 was downregulated, while Rho-associated protein kinase 1 (ROCK1) was upregulated in serum of human papillomavirus (HPV)-positive and -negative patients with CSCC compared with healthy controls. Correlation analysis revealed that the expression levels of lncRNA HAND2-AS1 were negatively correlated with the expression levels of ROCK1 in HPV-positive and -negative patients with CSCC but not in healthy controls. Downregulation of lncRNA HAND2-AS1 distinguished patients with CSCC from healthy controls. Additionally, lncRNA HAND2-AS1 overexpression led to reduced expression levels of ROCK1 in HPV-positive and -negative human CSCC cell lines but not in normal cervical cell lines. ROCK1 overexpression did not significantly affect the expression of lncRNA HAND2-AS1 in all the cell lines investigated. lncRNA HAND2-AS1 overexpression inhibited, while ROCK1 overexpression promoted the proliferation, migration and invasion of HPV-positive and -negative human CSCC cell lines but not normal cervical cell lines. ROCK1 overexpression attenuated the effects of lncRNA HAND2-AS1 overexpression on cancer cell proliferation, migration and invasion. lncRNA HAND2-AS1 may inhibit cancer cell proliferation, migration and invasion by downregulating ROCK1 in HPV-positive and -negative CSCC.
RESUMEN
OBJECTIVE: To study lung squamamouscarcinoma and lung adenocarcinoma gene expression profiles by cDNA microarrays, compare them with those of pulmonary inflammatory pseudoneoplasma, and screen the differential expression gene and the common expression gene in these types of lung cancer in order to further study early diagnosis and treatment of lung cancer. METHODS: cDNA microarray chips containing 4096 human target genes were used to identify gene expression profiles in lung squamous cell carcinoma, adenocarcinoma, and pulmonary inflammatory pseudoneoplasma. RESULTS: Among the target genes, 591 differentially expressed genes were identified in lung squamous cell carcinoma; among them, there were 476 genes unexpressed in pulmonary inflammatory pseudoneoplasma; 293 of 476 differentially expressed genes were up-regulated and the other 183 were down-regulated. There were 524 differentially expressed genes in adenocarcinoma; among them, 460 genes were not expressed in pulmonary inflammatory pseudoneoplasma; 214 of the 460 differentially expressed genes were up-regulated and 246 were down-regulated. However, there were a total of 113 genes differentially expressed the both lung squamous cell carcinoma and adenocarcinoma. CONCLUSION: There were distinct gene expression profiles among lung squamous cell carcinoma and adenocarcinoma. All those gene expression profiles and genes screened out provide important clues for further investigation of carcinogenesis, invasion and metastasis of non small cell lung cancer and its molecular characteristics.
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Carcinoma de Pulmón de Células no Pequeñas/genética , Perfilación de la Expresión Génica , Neoplasias Pulmonares/genética , Análisis de Secuencia por Matrices de Oligonucleótidos , Adenocarcinoma/genética , Carcinoma de Células Escamosas/genética , Expresión Génica , HumanosRESUMEN
AIM:To investigate the pathophysiologic basis of syndrome of Liver-Qi stagnation and parameters for clinical differentiation.METHODS:Plasma L-ENK, AVP, ANP and serum gastrin were determined by RIA in 84 patients with neurasthenia, mastodynia,chronic gastritis, and chronic cholecystitis presenting the same syndrome of Liver-Qi stagnation in traditional Chinese medicine (TCM). Healthy subjects served as controls in comparison with patients having the same syndrome but with different diseases.RESULTS:Among the patients with Liver-Qi stagnation, the plasma L-ENK, ANP and gastrin levels were 38.83ng/L ± 6.32ng/L, 104.11ng/L ± 29.01ng/L and 32.20ng/L ± 6.68ng/L, being significantly lower than those in the healthy controls (P < 0.01, t = 3.34, 6.17, 4.48). The plasma AVP of the patient group (52.82ng/L ± 19.09ng/L) was significantly higher than that of the healthy controls (P <0.01, t = 5.79 =. The above changes in patients having the same symptom complex but different diseases entities showed no significant differences, P >0.05.CONCLUSION:The syndrome of Liver-Qi stagnation is closely related to the emotional modulatory abnormality of the brain, with decrease of plasma L-ENK, ANP and gastrin, and increase of plasma AVP as the important pathophysiologic basis.