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The present study aimed to assess the expression and functional role of aquaporin-1 (AQP1) in glioblastoma multiforme (GBM) migration, invasion and vasculogenic mimicry (VM). In the primary human gliomas and human glioma-derived cell lines tested, it was observed that the expression of AQP1 was upregulated. In addition, it was demonstrated that silencing of AQP1 expression resulted in decreased migration and invasion, in addition to vasculogenic mimicry in vitro. It was additionally observed that silencing of AQP1 expression resulted in in vivo inhibition of tumor growth, a decrease in the expression of invasion-associated protein, and suppression of VM formation. Based on these data, it was concluded that AQP1 may serve a role in GBM migration, invasion and VM formation, and that it may serve as a novel diagnostic/prognostic biomarker and a potential therapeutic target. [ABSTRACT FROM AUTHOR]

Long-term peritoneal dialysis (PD) leads to ultrafiltration failure (UFF). Peritoneal mesothelial cells, which form the innermost monolayer of the peritoneal cavity, have been shown to regulate various responses, including inflammation, in UFF. The present study was designed to investigate the effect of the peroxisome proliferator-activated receptor-γ (PPAR-γ) agonist, rosiglitazone, on peritoneal dialysis solution (PDS)-induced injuries in rat peritoneal mesothelial cells (RPMCs). RPMCs were cultured for different durations and with different concentrations of PDS. The gene expression levels of aquaporin-1 (AQP-1) and zonula occluden-1 (ZO-1) were determined using reverse transcription-quantitative polymerase chain reaction analysis. The protein levels of AQP-1, ZO-1 and PPAR-γ were measured using western blot analysis. Interleukin (IL)-6 and IL-8 were detected using ELISA. The RPMCs were damaged by stimulation with 4.25% PDS for 72 h. The expression levels of AQP-1 and ZO-1 were increased, and the secretion of IL-6 and IL-8 were decreased by rosiglitazone. The use of the PPAR-γ inhibitor, GW-9662, completely prevented the effects of rosiglitazone. These results indicated that PDS exposure stimulated an inflammatory response in the RPMCs. The PPAR-γ activator, rosiglitazone, appeared to relieve the injury by inhibiting inflammation, and regulating the expression of AQP-1 and ZO-1, however further investigations are required to elucidate the potential underlying mechanism. [ABSTRACT FROM AUTHOR]

Aquaporins (AQPs), water channel proteins in the cell membranes of mammals, have been reported to be important in maintaining the water balance of the respiratory system. However, little is known regarding the role of AQP in occupational pulmonary diseases such as silicosis. The present study investigated the expression of AQP1 and AQP4 in the human A549 alveolar epithelial cell line stimulated by silica (SiO2). A549 cells were cultured and divided into four groups: Control, SiO2-stimulated, AQP1 inhibitor and AQP4 inhibitor. The cells of the SiO2-stimulated group were stimulated with SiO2 dispersed suspension (50 mg/ml). The cells of the inhibitor group were pretreated with mercury (II) chloride (HgCl2; a specific channel inhibitor of AQP1) and 2-(nicotinamide)-1,3,4-thiadiazole (TGN-020; a specific channel inhibitor of AQP4) and stimulated with SiO2. The mRNA expression levels of AQP1 and AQP4 were detected by reverse transcription-quantitative polymerase chain reaction, and the protein expression levels of AQP1 and AQP4 were detected by western blotting and immunocytochemistry. Compared with the control group, the expression levels of AQP1 and AQP4 mRNA and protein in SiO2-stimulated groups increased and subsequently decreased (AQP1 peaked at 2 h and AQP4 at 1h; both P<0.001 compared with control group). In the inhibitor group, expression levels were increased compared with controls; however, they were significantly decreased compared with the SiO2-stimulated group at 2 h (AQP1; P<0.001) and 1 h (AQP4; P<0.001). The expression of AQP1 and AQP4 increased when exposed to SiO2, and this was inhibited by HgCl2 and TGN-020, suggesting that AQP1 and AQP4 may contribute to A549 cell damage induced by SiO2. AQP1 and AQP4 may thus be involved in the initiation and development of silicosis. [ABSTRACT FROM AUTHOR]

The brain maintains its mass and physiological functional capacity compared with other organs under harsh conditions such as starvation, a mechanism termed the 'selfish brain' theory. To further investigate this phenomenon, mice were examined following water and/or food deprivation. Although the body weights of the mice, the weight of the organs except the brain and blood glucose levels were significantly reduced in the absence of water and/or food, the brain weight maintained its original state. Furthermore, no significant differences in the water content of the brain or its energy balance were observed when the mice were subjected to water and/or food deprivation. To further investigate the mechanism underlying the brain maintenance of water and substance homeostasis, the expression levels of aquaporins (AQPs) and autophagy-specific protein long-chain protein 3 (LC3) were examined. During the process of water and food deprivation, no significant differences in the transcriptional levels of AQPs were observed. However, autophagy activity levels were initially stimulated, then suppressed in a time-dependent manner. LC3 and AQPs have important roles for the survival of the brain under conditions of food and water deprivation, which provided further understanding of the mechanism underlying the 'selfish brain' phenomenon. Although not involved in the energy regulation of the 'selfish brain', AQPs were observed to have important roles in water and food deprivation, specifically with regards to the control of water content. Additionally, the brain exhibits an 'unselfish strategy' using autophagy during water and/or food deprivation. The present study furthered current understanding of the 'selfish brain' theory, and identified additional regulating target genes of AQPs and autophagy, with the aim of providing a basis for the prevention of nutrient shortage in humans and animals. [ABSTRACT FROM AUTHOR]

In the present study, the effect of aquaporin-1 (AQP1) on fluid transportation in pulmonary epithelial cells, and the role of AQP1 in alveolar fluid clearance were investigated to provide an experimental foundation to elucidate the pathogenesis of hyperoxic lung edema. An siRNA transfection technique was used to silence AQP1 in the A549 cell line. The transfected cells were randomized into a hyperoxia exposure and an air control group, with a negative control group set for each group. Cell volume was determined using flow cytometry, and Pf values were used to determine osmotic water permeability. Cell volume was found to be reduced in the AQP1-silenced A549 cells, compared with t he n egative c ontrol g roup 72 h following air exposure. In addition, cell volume was reduced in the AQP1-silenced A549 cells, compared with the negative control group 48 and 72 h following hyperoxia exposure. The osmotic water permeability of the AQP1-silenced cells was reduced in the air control and hyperoxia exposure groups, compared with the negative control group 48 and 72 h following exposure. The volume and cell membrane osmotic water permeability of the A549 cells were reduced, compared with those in the control group following AQP1-silencing, which indicated that the downregulation of AQP1 impedes extracellular to intracellular fluid transportation. Therefore, the disturbance in alveolar fluid clearance resulting from the downregulation of AQP1 following hyperoxia exposure may be one of the key mechanisms responsible for hyperoxic lung edema. [ABSTRACT FROM AUTHOR]

The aim of this study was to investigate the curative effect of Zeng Ye decoction on primary Sjögren's syndrome (pSS) and further explore its underlying mechanism involving aquaporin (AQP)-1 and AQP-5. The pSS model was established based on the immune induction method, and the saliva flow, submandibular gland index, morphological structures of salivary glands, and AQP-1 and AQP-5 protein expression levels in the salivary glands were determined. The saliva flow and the submandibular gland index were significantly reduced in the model group (P<0.01, compared with those in the control group), and significantly increased following interferon (IFN), Zeng Ye decoction extraction (ZYE) and Zeng Ye decoction (ZY) treatment (P<0.01, compared with those of the model group). Submandibular gland atrophy, fibrous tissue hyperplasia and multiple focal lymphocytic infiltration were observed in the model group and were attenuated when subjected to IFN, ZYE and ZY treatment. The AQP-1 and AQP-5 expression levels increased following IFN, ZYE and ZY treatment (P<0.01, compared with those of the model group), particularly in the ZYE-35 group. This result indicated that ZYE had a significant protective effect on pSS via upregulation of the expression levels of AQP-1 and/or AQP-5. However, the AQP-1 expression levels increased and the AQP-5 expression levels decreased in the model groups compared with those in the control group, which indicated different regulatory pathways of the salivary gland damage on the basis of AQP-1 and AQP-5. This study provided a significant reference for the prevention and treatment of pSS. [ABSTRACT FROM AUTHOR]