RESUMO
SUMMARY: Respiration and water-liquid transportation are controlled by many factors in the lung. The aim of this study was to explore the structure and proteins expression in lungs of Phrynocephalus vlangalii by means of gross anatomy, light microscope observation, scanning electron microscope and immunohistochemistry. Results show that there were many alveoli in the lung and the walls of alveoli and capillaries were very thin. The inner surface of the lung was divided into many cystic chambers by reticular diaphragm, and the network of pulmonary capillaries was dense. Immunohistochemistry showed that AQP1 was mainly expressed in the epithelium of interstitial bronchi, parabronchiole endothelium, capillary endothelium and alveolar epithelial cells. VIP positive nerve fibers are mainly distributed in trachea, bronchial smooth muscle layer, the walls of pulmonary vessels and bronchial vessels and around submucosal glands. CECR2 is distributed in peripheral capillaries and small. Investigations of structure and proteins biology could be relevant with the adaptive strategy to drought and hypoxia environment in Phrynocephalus vlangalii.
La respiración y el transporte de agua y líquido están controlados en el pulmón por muchos factores. El objetivo de este estudio fue explorar la estructura y la expresión de proteínas en los pulmones de Phrynocephalus vlangalii por medio de la anatomía macroscópica, observación con microscopio óptico, microscopio electrónico de barrido e inmunohistoquímica. Los resultados muestran que había muchos alvéolos en el pulmón y que las paredes de los alvéolos y de los capilares eran muy delgadas. La superficie interna del pulmón estaba dividida en cámaras quísticas por el diafragma reticular y se observó una densa red de capilares pulmonares. La inmunohistoquímica mostró que AQP1 se expresaba principalmente en el epitelio de los bronquios intersticiales, el endotelio parabronquial, el endotelio capilar y las células epiteliales alveolares. Las fibras nerviosas VIP positivas se distribuyen principalmente en la tráquea, la capa de músculo liso bronquial, las paredes de los vasos pulmonares y los vasos bronquiales y alrededor de las glándulas submucosas. CECR2 se distribuye en pequeño capilares periféricos. Las investigaciones de la biología de la estructura y las proteínas podrían ser relevantes con la estrategia de adaptación al entorno de sequía e hipoxia en Phrynocephalus vlangalii.
Assuntos
Animais , Adaptação Fisiológica , Lagartos/anatomia & histologia , Pulmão/anatomia & histologia , Imuno-Histoquímica , Microscopia Eletrônica de Varredura , Pulmão/ultraestruturaRESUMO
PURPOSE: Glutamine plays an important role in tumor metabolism and progression. This research aimed to find out how Gln exert their effects on laryngeal squamous cell carcinoma (LSCC). METHODS: Cell proliferation was measured by CCK8 and EdU assay, mitochondrial bioenergetic activity was measured by mitochondrial stress tests. Gene expression profiling was revealed by RNA sequencing and validated by RT-qPCR. In LSCC patients, protein expression in tumor and adjacent tissues was examined and scored by IHC staining. RNAi was performed by stably expressed shRNA in TU177 cells. In vivo tumor growth analysis was performed using a nude mouse tumorigenicity model. RESULTS: Gln deprivation suppressed TU177 cell proliferation, which was restored by αKG supplementation. By transcriptomic analysis, we identified CECR2, which encodes a histone acetyl-lysine reader, as the downstream target gene for Gln and αKG. In LSCC patients, the expression of CECR2 in tumors was lower than adjacent tissues. Furthermore, deficiency of CECR2 promoted tumor cell growth both in vitro and in vivo, suggesting it has tumor suppressor effects. Besides, cell proliferation inhibited by Gln withdrawal could be restored by CECR2 depletion, and the proliferation boosted by αKG supplementation could be magnified either, suggested that CECR2 feedback suppressed Gln and αKG's effect on tumor growth. Transcriptomic profiling revealed CECR2 regulated the expression of a series of genes involved in tumor progression. CONCLUSION: We confirmed the Gln-αKG-CECR2 axis contributes to tumor growth in LSCC. This finding provided a potential therapeutic opportunity for the use of associated metabolites as a potential treatment for LSCC.