Structure and function adaption of lung in Phrynocephalus vlangalii by multiple mechanisms / Estructura y adaptación funcional del pulmón en Phrynocephalus vlangalii por múltiples mecanismos

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.

Discovery of novel diarylamides as orally active diuretics targeting urea transporters

Urea transporters (UT) play a vital role in the mechanism of urine concentration and are recognized as novel targets for the development of salt-sparing diuretics. Thus, UT inhibitors are promising for development as novel diuretics. In the present study, a novel UT inhibitor with a diarylamide scaffold was discovered by high-throughput screening. Optimization of the inhibitor led to the identification of a promising preclinical candidate,

Effect of yaobishu on protein expression of aquaporin 1 and aquaporin 3 in nucleus pulposus of the degenerated lumbar intervertebral disc in a rabbit / 中国组织工程研究

BACKGROUND: The aging and lesions of the intervertebral disc are closely related to the lack of nutritional blood supply to the disc. Aquaporin plays an important role in the nutritional supply to the intervertebral discs, but the specific mechanism has not been fully defined. OBJECTIVE: To study the mechanism of Yaobishu on degenerated intervertebral disc in rabbits based on the changes of aquaporin (AQP) 1 and AQP3 protein expression. METHODS: Thirty-six New Zealand white rabbits were randomly divided into model group, low-dose Yaobishu group and high-dose Yaobishu group. Animal models of lumbar intervertebral disc prolapse were prepared through an injection of normal saline into L4/5 and L5/6 segments. The model group was intragastrically given normal saline 5 mL/kg per day, the low-dose group was intragastrically given Yaobishu 5 mL/kg per day, and the high-dose group was intragastrically given Yaobishu 10 mL/kg per day, twice a day, for 21 days. After 6 weeks of treatment, the intervertebral discs were taken for anatomical and histological observation using hematoxylin-eosin staining. Expression of AQP1 and AQP3 in the nucleus pulposus at protein and mRNA levels was quantified by RT-PCR and western blot assay. RESULTS AND CONCLUSION: In all the three groups, the annulus fibrosus was destroyed, abnormal cartilage tissue appeared, and the nucleus pulposus was reduced in number. Severest degeneration of the intervertebral disc was found in the model group, followed by the low-dose Yaobishu and high-dose Yaobishu groups in turn. The expression of AQP1 and AQP3 mRNA and protein in the high-dose Yaobishu group and low-dose Yaobishu group increased significantly after 6 weeks of treatment (P 0.05). There were significant differences in the expression of AQP1 and AQP3 mRNA and protein among the three groups (P < 0.05). Therefore, Yaobishu may alleviate the degeneration of the rabbit intervertebral disc by increasing the expression of AQP1 and AQP3.

Immunohistochemical identification of AQP1 in livers of the high-fat diet rats / Identificación inmunohistoquímica de AQP1 en hígados de ratas con dieta de alto contenido de grasa

One of the key functions of the hepatobiliary system is bile formation. Aquaporins (AQPs) are likely to play a role in water transport that is essential for appropriate hepatobiliary tract function. The increasing prevalence of fatty liver parallels the rise of obesity and its complications over the past several decades. In this paper, general morphology observation, histopathology and AQP1 immunohistochemical expression were observed in livers of the high-fat diet (HFD) rats. For the liver of HFD rats, immunolight microscopy revealed weak labeling of AQP1 on the surface of central veins and liver sinusoid compared with the normal diet (ND) rats. It was suggested that bile secreted by the liver of HFD rats was maybe abnormal, thereby causing abnormalities in the composition and secretion of bile. However, the deeper understanding of mechanisms involved to the fatty liver is still unclear, in particular AQPs in the liver of obesity, additional studies would be required to study the signalling cascades involved in these processes.

Una de las funciones clave del sistema hepatobiliar es la formación de bilis. Es probable que las acuaporinas (AQP) desempeñen un papel en el transporte de agua que es esencial para la función apropiada del tracto hepatobiliar. En las últimas décadas, la creciente prevalencia de hígado graso es paralela al aumento de la obesidad y sus complicaciones. En este trabajo, se identificaron características morfológicas generales, histopatología y expresión inmunohistoquímica de AQP1 en hígados de ratas con dieta rica en grasas (DRG). En el hígado de ratas con DRG, la expresión inmunohistoquímica determinó un marcaje débil de AQP1 en la superficie de las venas centrales y del sinusoide hepático en comparación con las ratas de dieta normal (DN). Se sugirió que la bilis secretada por el hígado de ratas con DRG era tal vez anormal, lo que causaba anomalías en la composición y secreción de la bilis. Sin embargo, se necesita un conocimiento mayor de los mecanismos involucrados en el hígado graso, en particular de las AQP y se requieren estudios adicionales para determinar las cascadas de señalización involucradas en estos procesos.

Renal expression of AQP1 in the high-fat nutritional obesity of rat / Expresión renal de AQP1 en la obesidad nutricional alta en grasas en ratas

AQP1 plays an essential role in maintaining body water balance. In the kidney, AQP1 is localized to the apical and basolateral membrane of epithelial cells in the proximal tubule and descending thin limb of Ansa nephroni (Henle's loop) where it reabsorbs the vast majority of filtered water. The growing epidemic of obesity and metabolic diseases particularly obesity-related kidney disease is getting more and more attention in this century. However, a full understanding of mechanisms involved to the progressive renal disease is still unclear, in particular AQPs in the kidney of obesity. In this paper, we examined the localization of AQP1 in renal cortex and medulla of ND (normal diet) and HFD (high-fat diet) at rats. In the renal cortex and medulla, immunolight microscopy revealed weak expression of AQP1 in the apical and basolateral membrane of epithelial cells at the proximal straight/convoluted tubule of HFD compared with ND, respectively. The same result was confirmed in the thick descending limb and descending thin limb of Henle's loop. In the high-fat nutritional obesity of rats, decreased AQP1 levels may not directly cause serious obesity-related kidney disease, e.g. chronic kidney disease, even end-stage renal disease. But at least, AQPs (AQP1 in this study) was one of initially conditions to the incentive of obesity-related kidney disease.

Las acuoporinas tipo 1 (AQP1) constituyen una parte esencial en el mantenimiento del equilibrio del agua en el cuerpo. En el riñón, la AQP1 se localiza en la membrana apical y basolateral de las células epiteliales, en el túbulo proximal y en el segmento descendente del Ansa nephroni o asa nefrónica (asa de Henle), donde reabsorbe la gran mayoría de agua filtrada. La creciente epidemia de obesidad y enfermedades metabólicas en el siglo actual, hacen que la enfermedad renal relacionada con la obesidad esté recibiendo cada vez más atención. Sin embargo, aún no existe un conocimiento definitivo de los mecanismos implicados en la enfermedad renal progresiva, en particular los relacionados a las acuoporinas renales en la obesidad. En este trabajo, examinamos la localización de AQP1 en la corteza y la médula renales de la dieta normal (DN) y dieta alta en grasa (DAG) en ratas. En la corteza y médula renales, la microscopía de luz reveló una expresión débil de AQP1 en la membrana apical y basolateral de las células epiteliales en el túbulo contorneado proximal del grupo DAG en comparación con el grupo DN, respectivamente. El mismo resultado se confirmó en la porción descendente gruesa y en la porción descendente delgada del asa nefrónica. En ratas del grupo DAG, la disminución de los niveles de AQP1 pudo no ser la causa directa de una enfermedad renal grave relacionada con obesidad, como por ejemplo, enfermedad renal crónica, o una enfermedad renal terminal. No obstante, en este estudio, la expresión renal de AQP1 constituyó una de las condiciones iniciales para inducir la enfermedad renal relacionada con obesidad.

Inhibitory effect of ZX-1201 on pancreatic cancer and the relevant molecular mechanism / 中国药理学与毒理学杂志

Pancreatic ductal adenocarcinoma (PDAC) is one of the five most malignant cancer. ZX-1201 is one of the active constituents in Alismatis Rhizoma,a well-known traditional Chinese medi-cine with a wide variety of pharmacological properties including diuretic,anti-hyperlipidemic,anti-atheroscle-rotic,anti-cancer,anti-inflammatory and anti-oxidative activities.We investigated the inhibitory effect of ZX-1201 on pancreatic cancer and the relevant molecular mechanism in vitro and in vivo. ZX-1201 inhibited the growth and metastasis of PANC-1 cells in BALB/c nude mice significantly.ZX-1201 inhibited the function of AQP1 via directly interaction and involved in the reversion process of ZX-1201 on TGF-β1. CTGF was an important protein in the reversion process of ZX-1201 on TGF-β1.ZX-1201 inhibited the migration of PANC-1 and CPFAC-1 cells induced by TGF-β1in vitro.ZX-1201 reversed the down-regu-lated of epithelial markers and up-regulated of mesenchymal markers, as well as the up-regulated of Snail and p-Smad2/3 induced by TGF-β1.And ZX-1201 reversed Epithelial-Mesenchymal Transition by down-regulating AQP1 and inhibiting translocation of β-catenin, the promotor of CTGF. According to these,ZX-1201 inhibited the migration of pancreatic cancer cells.We concluded that ZX-1201 inhibited the growth and metastasis of PANC-1 cells in vivo significantly.And AQP1,β-catenin and CTGF were the pivotal proteins in the process of ZX-1201 inhibiting PANC-1 cells migration induced by TGF-β1.

Effects of electroacupuncture preconditioning on expression of aquaporin-1 and activity of protein kinase C in myocardium of rats with acute myocardial ischemia-reperfusion injury / 中国针灸

<p><b>OBJECTIVE</b>To explore the partial action mechanism and the myocardial protective effect differences between electroacupuncture (EA) preconditioning at "Neiguan"(PC 6) and "Taiyuan"(LU 9) in rats with acute myocardial ischemia-reperfusion injury.</p><p><b>METHODS</b>Ninety-six Wistar rats were randomly assigned into a sham-operation group, a model group, a Neiguan group and a Taiyuan group, 24 rats in each one. The rats in the Neiguan group and Taiyuan group were treated with EA (2 Hz in frequency, 1 mA in intensity) at "Neiguan" (PC 6) and "Taiyuan" (LU 9) respectively, 20 min per treatment, once a day for consecutive 7 days. The rats in the sham-operation group and model group were treated with immobilization for the same time, and no EA was given. The model of myocardial ischemia-reperfusion injury was established in the model group, Neiguan group and Taiyuan group 24 h after the end of EA, while the rats in the sham-operation group were treated with sham operation (no ligation was made during surgery). The myocardial ischemic size, infarction size, activity of protein kinase C (PKC) and expression of aquaporin1 (AQP1) in each group were detected.</p><p><b>RESULTS</b>Compared with sham-operation group, the myocardial ischemic size, infarction size, AQP1 expression and PKC activity in the model group were significantly increased (all<0.01); compared with the model group and Taiyuan group, the myocardial ischemic size, infarction size, PKC activity and AQP1 expression were significantly decreased in the Neiguan group (<0.01,<0.05). By Pearson correlation analysis, the changes of AQP1 expression were positively correlated with those of PKC activity after EA preconditioning.</p><p><b>CONCLUSIONS</b>EA preconditioning at "Neiguan" (PC 6) could significantly decrease myocardial AQP1 expression and PKC activity in rats with acute myocardial ischemia-reperfusion injuing, but the effect of EA preconditioning at "Taiyuan"(LU 9) is not obvious; its protective effect is likely to be achieved by inhibiting PKC activity and AQP1 expression.</p>

Research progress of aquaporin 1 and 4 in diabetic retinopathy / 国际眼科杂志(Guoji Yanke Zazhi)

Diabetic retinopathy(DR), one of the most common retinal vascular disease, is one of the causes of blindness for people over the age of 50.In the early stage of DR, microvascular cells are damaged, expand, start to leak, form micro hemangioma, then show occlusion, and non-perfusion area come into being, eventually form new blood vessels because of ischemia and hypoxia of retina.Illness develop into proliferative diabetic retinopathy(PDR).With the aggravation of the disease, PDR can cause the formation of fibrovascular membrane, the more serious fibrillation of epiretinal membrane, resulting in traction retinal detachment(tRD).Present studies suggest that aquaporins, the essential component of new blood vessels, including aquaporin 1 and aquaporin 4, play a significant pole in the development of diabetic retinopathy, causing the destruction of blood retinal barrier, inducing retinal edema, even macular edema, and participating in the formation of retinal angiogenesis.

A Mechanism Study of NMDAR1 in A Rat Alzheimer Disease (AD) Model

ABSTRACT This study aimed to investigate the expression and mechanism of N- methyl -D- aspartate receptor 1 (NMDAR1) in the pathogenesis of Alzheimer disease (AD). Eighty adult Wistar rats were randomly divided into 4 groups (n=20 each) to receive an injection of 0, 5, 7 and 10 μl of 1 μg/μl amyloid-β 42 (Aβ1-42) in the hippocampus. Twenty rats in normal control group were injected with equal volume of saline. After 10 days, the hippocampus was isolated from 5 randomly selected rats in each group. The NMDAR1 protein and mRNA expression was determined by immunohistochemical staining and qRT-PCR. The aquaporin-1 (AQP-1) mRNA expression was also measured by qRT-PCR. We found that both NMDAR1 and AQP-1 expression in Aβ1-42 groups was increased in a dose-dependent manner. NMDAR1 and AQP-1 expression in 7 and 10 μl Aβ1-42 groups was significantly higher compared with 0 μl Aβ1-42 group (P <0.01). Further, the 10 μl Aβ1-42 group was randomly divided into 3 subgroups: AD-NMDA, AD-MK-801, and AD-Ctrl subgroup, which was given an intraperitoneal injection of NMDAR agonist NMDA, NMDAR antagonist MK-801 and saline, respectively. The relative APQ-1 expression in each subgroup was determined by qRT-PCR and Western blot analysis after 24 h. The AQP-1 expression was significantly decreased in AD-MK-801 group (P < 0.05), but was markedly increased in AD-NMDA group when compared with AD-Ctrl group (P <0.01). Our study suggested that expression abnormity of NMDAR1 is involved in the pathogenesis of AD. NMDAR1 might regulate the pathogenic process through stimulating the expression of AQP-1.

Expression of AQP1 and AQP5 is decreased in the alveolar-capillary membrane in rats with acute lung injury / 中国比较医学杂志

Objective To determine if aquaporin1 ( AQP1) and aquaporin5 ( AQP5) are expressed in the alveolar-capillary membrane in rats, and to investigate the changes of AQP1 and AQP5 expression in the rat with acute lung injury.Methods The distribution of AQP1 and AQP5 in alveolar capillary membrane was investigated by immunohistochemistry and immunoelectron microscopy with affinity-purified antibodies to human AQP1 and AQP5.The possibility that alveolar capillary membrane AQP1 and AQP5 undergo altered regulation was studied by a rat model established using intra-tracheal instillation of lipopolysaccharide (LPS).Results Immunolabelling showed that AQP1 was stained primarily in the microvascular endothelium of normal lungs, while AQP5 was expressed in type I pneumocytes. Immunohistochemical analysis showed a significant decrease in the expression of AQP1 and AQP5 in injured lungs at 4 -48 h after LPS instillation.AQP1 protein was resumed partly at 24 h after LPS instillation and steroid administration, whereas AQP5 was unchanged.Conclusions The decreased expressions of AQP1 and AQP5 in injured lungs suggest that both of them may play a role in abnormal fluid transportation.

The expressions of AQP1 and VEGF in hepatitis B associated HCC and the significance / 实用医学杂志

Objective To examine the expressions of AQP1 and VEGF in human hepatitis B associated hepatocellular c arcinoma and to investigate its relationship with the occurrence and development of hepatocellularcarcinoma. Methods AQP1 and VEGF expressionsin the cancer tissues and AQP1 and VEGF levels in the serum were detected in 62 cases of hepatocellula carcinomaby immunohistochemistry and ELISA , respectively. Results The expressions of AQP1 and VEGF in the liver cancers were significantly higher than in the normal tissues (P<0.01). The higher expression was related to pathologic type,degrees of differentiation and lymph node metastasis, but not related to sex, age and TNM stages. In the serum of liver cancer, the concentrations of AQP1 and VEGF were significantly higher than those in the control group. Conclusion High expressions of AQP1 and VEGF in the patients with liver cancer may be correlated to the occurrence and development of liver cancer. Plasma levels ofAQP1 and VEGF may be more meaningful for the evaluation of clinical prognosis.

Effect of rosiglitazone on the expression of AQP-1, VEGF-A and COX-2 in uremic rat of peritoneal dialysis / 中华肾脏病杂志

Objective To investigate the effect of rosiglitazone(RGZ) on peritoneal morphology,function and the expressions of Aquaporin 1 (AQP-1),vascular endothelial growth factor A (VEGF-A) and cyclooxygenase 2(COX-2) in uremic rat of peritoneal dialysis.Methods Thirty Sprague-Dawley rats were randomly divided into five groups.Group S (n=6) was subjected to sham operation.Group N (n=6) was subjected to nephrectomy with silicon catheter inserted,but no peritoneal exposure.Group P (n=6) was subjected to nephrectomy with silicon catheter inserted and receiving daily peritoneal injection through the catheter,using 4.25％ peritoneal dialysis fluid 10 ml twice a day for 2 weeks.Group R (n=6) was subjected to nephrectomy with silicon catheter inserted and receiving daily peritoneal injection through the catheter,using 4.25％ peritoneal dialysis fluid containing rosiglitazone (0.2 mg/kg) 10 ml twice a day for 2 weeks.Group GW (n=6) was subjected to nephrectomy with silicon catheter inserted and receiving daily peritoneal injection through the catheter,using 4.25％ peritoneal dialysis fluid containing rosiglitazone (0.2 mg/kg) and GW9662 (0.2 mg/kg) 10 ml twice a day for 2 weeks.After two weeks of dialysis,a 90 min peritoneal equilibration test was performed and the amount of ultrafiltration was accurately measured.The partial peritoneum tissues of rats were harvested and stained by hematoxylin-eosin (HE),then morphology changes of partial peritoneum were examined by light microscopy.The expression of AQP-1,VEGF-A and COX-2 in omentum were detected with immunohistochemistry assay.AQP-1,VEGF-A and COX-2 mRNA were detected by qRT-PCR.Results Morphology changes of partial peritoneum showed that compared with Group S,a dramatic increase in thickness of the mesothelium-to-muscle layer of peritoneum in Group N,P,R and GW(P ＜0.05).Compared with group P,the thickness significantly decreased in Group R(P ＜ 0.05).PET results showed that compared with Group S,ultrafiltration (UF) significantly reduced in Group P,R,and GW (P ＜ 0.05).Compared with Group P,ultrafiltration significantly increased in Group P,R,and GW (P ＜0.05).Compared with group S,the expressions of AQP1,VEGF-A and COX-2 mRNA and protein were significantly increased in group P,R and GW(P ＜ 0.05).Compared with group P,the expressions of AQP1,VEGF-A mRNA and protein were significantly decreased in Group R and GW(P ＜ 0.05).Compared with group P,the expressions of COX-2 mRNA and protein were significantly decreased in group R (P ＜ 0.05),while no differences in the expression of COX-2 mRNA and protein in group GW (P ＜ 0.05).Conclusions Rosiglitazone can inhibit peritoneal interstitial and vascular proliferation,protect peritoneal function and increase ultrafiltration.Rosiglitazone can protect peritoneal function probably by inhibiting expression of VEGF-A and COX-2.

Research progress on AQP1 in gliomas / 中国肿瘤临床

Aquaporin 1 (AQP1) is a specific protein that transports water molecules through the cell membrane. AQP1 mainly ex-presses in the choroid plexus epithelial cells of the central nervous system and participates in the formation of cerebrospinal fluid. In gli-omas, AQP1 expresses in neoplastic astrocytes and vascular endothelial cells. AQP1 expression is increased in parallel with histological grade in gliomas. AQP1 expression in gliosarcoma cell line is induced by dexamethasone, platelet-derived growth factor, sodium chlo-ride, hypoxia, D-glucose, and fructose. AQP1 mRNA expression is upregulated with increasing dosage. Through the expression of AQP1 in gliomas and the existing research on its function, we suggest that AQP1 may participate in tumor angiogenesis and tumor-relat-ed edema. AQP1 is closely associated with glioma cell migration. The function of AQP1 and its mechanism has been elucidated. Thus, this protein can be used as a new therapeutic target to inhibit the metastasis and recurrence of gliomas.

Effect of Niaochangshu Capsule on eNOS, AQP1 in Bladder and Serum of Ovariectomized ;Female Rats / 中国中医药信息杂志

Objective To explore the mechanism of Niaochangshu capsule in the treatment of postmenopausal overactive bladder, through observing its influence on bladder weight and the expression of eNOS and AQP1 of ovariectomized female rats. Methods Female SD rats were divided into blank group, model group, Nilestriol group and Niaochangshu group. Rats were removed ovaries except the blank group. The treatment groups were given corresponding drugs, blank group and model group were given normal saline by gavage. After 4 weeks, the bladders' weight and thickness were detected, the expressions of eNOS and AQP1 in serum and bladder tissue were determined by ELISA, and NO by spectrophotometry. Results Ovariectomy resulted in decreased bladder weight, bladder mucosal and muscular atrophy, and opposite changes showed after given Niaochangshu. The expressions of eNOS and NO in bladder and serum were decreased significantly after ovariectomy, while increased by given Niaochangshu capsule or nylestriol (P<0.05), and there was significant difference between Niaochangshu group and Nilestriol group (P<0.05). The expression of AQP1 was decreased in the model group, and increased after given nylestriol or Niaochangshu capsule. While the expression of AQP1 in bladder had no significant difference among the four groups. Conclusion Niaochangshu capsule can reverse bladder mucosal and muscular atrophy caused by estrogen deficiency, and increase the content of eNOS in serum and bladder, thus play the role in the treatment of postmenopausal overactive bladder.

Time-Dependent Expression Patterns of Cardiac Aquaporins Following Myocardial Infarction

Aquaporins (AQPs) are expressed in myocardium and the implication of AQPs in myocardial water balance has been suggested. We investigated the expression patterns of AQP subtypes in normal myocardium and their changes in the process of edema formation and cardiac dysfunction following myocardial infarction (MI). Immunostaining demonstrated abundant expression of AQP1, AQP4, and AQP6 in normal mouse heart; AQP1 in blood vessels and cardiac myocytes, AQP4 exclusively on the intercalated discs between cardiac myocytes and AQP6 inside the myocytes. However, neither AQP7 nor AQP9 proteins were expressed in CD1 mouse myocardium. Echocardiography revealed that cardiac function was reduced at 1 week and recovered at 4 weeks after MI, whereas myocardial water content determined by wet-to-dry weight ratio increased at 1 week and rather reduced below the normal at 4 weeks. The expression of cardiac AQPs was up-regulated in MI-induced groups compared with sham-operated control group, but their time-dependent patterns were different. The time course of AQP4 expression coincided with that of myocardial edema and cardiac dysfunction following MI. However, expression of both AQP1 and AQP6 increased persistently up to 4 weeks. Our findings suggest a different role for cardiac AQPs in the formation and reabsorption of myocardial edema after MI.

Expression of Aquaporin-1, Vascular Endothelial Growth Factor and Vascular Endothelial Growth Factor Receptor-1 in the Peritoneal Tissues of Peritoneal Dialysis Patients / 대한신장학회지

PURPOSE: AQP-1 (Aquaporin-1) and VEGF (vascular endothelial growth factor) are known to play an important role in ultrafiltration in peritoneal dialysis. The aim of this study was to evaluate the expression of AQP-1 and VEGF and VEGFR-1 (VEGF type 1 receptor) in peritoneums obtained from uremic non-dialyzed patients and peritoneal dialysis patients and to see if expression of these molecules are correlated with each other and with pathological findings in peritoneum. METHODS: Peritoneal expressions of AQP-1, VEGF and VEGFR-1 were examined by immunohistochemistry using specific antibody to each molecule. The degree of vascular proliferation and inflammation in peritoneal tissues were assessed semi-quantitatively by a single pathologist. RESULTS: AQP-1, VEGF and VEGFR-1 were mainly expressed in the vascular endothelial cells in the peritoneum. No significant difference in peritoneal expression of these molecules was found according to the clinical situations in which peritoneal tissues were obtained. The degree of expression of AQP-1 and VEGF were related to each other but not related to expression of VEGFR-1. The expressions of AQP-1 and VEGF were related to the vascular proliferation. The expression of AQP-1 was also related to inflammation. CONCLUSION: In end-stage renal disease patients before and after initiation of peritoneal dialysis, the peritoneal expressions of AQP-1 and VEGF were related to vascular proliferation. Inflammation might have some influence in expression of AQP-1.

The Expression of AQP1 and eNOS in Menopausal Rat Urinary Bladder / 대한배뇨장애요실금학회지

PURPOSE: Aquaporins (AQPs) have been reported to be expressed in rat and human urothelium. Nitric oxide (NO) is thought to play an important role in the bladder overactivity related to menopause. The purpose of this study was to investigate the effect of hormonal alteration on the expression of AQP1 and eNOS in menopausal rat urinary bladder. MATERIALS AND METHODS: Female Sprague-Dawley rats (230-240 g, N=30) were divided into three groups: control (N=10), bilateral ovariectomy (Ovx, N=10), and bilateral ovariectomy followed by subcutaneous injections of 17beta-estradiol (50 mg/kg/day, Ovx+Est, N=10). After 4 weeks, urodynamic studies measuring the contraction interval and contraction pressure were done. The expression and cellular localization of AQP1 and eNOS were determined by performing Western blotting and immunohistochemistry on the rat urinary bladder. RESULTS: The approximate contraction interval (min) was significantly decreased in the Ovx group (3.9+/-0.25) compared to the control group (6.7+/-0.15), and was increased after estrogen treatment (9.7+/-0.22) (p<0.05). The AQP1 and eNOS immunoreactivities were localized in the same areas: capillaries, arterioles, and venules of the lamina propria. The protein expression of AQP1 was not changed significantly, whereas eNOS expression was significantly decreased in the Ovx group and restored to the control value in the Ovx+Est group. CONCLUSIONS: This study showed that ovariectomy causes a significant change in e-NOS expression without a change in AQP1 in menopausal rat urinary bladder. This may imply that e-NOS has a functional role in the bladder overactivity that occurs in association with menopause.

Expression of Aquaporin-3 and Aquaporin-4 in Aquaporin-1 Knockout Mice / 대한해부학회지

Recent studies demonstrated impaired urinary concentrating ability in AQP1 knockout mice. To establish of the lack of AQP1 was associated with compensatory changes in other aquaporins, we examined the expression of AQP3 and AQP4 in AQP1 knockout mice. In AQP1 (+/+) mice, there was strong basolateral AQP3 immunostaining in principal cells throughout the collecting duct and strong basolateral AQP4 immunostaining in IMCD cells and principal cells in the medulla. In AQP1 (-/-) mice, there was an increase in AQP3 immunostaining in principal cells in cortex and outer medulla, but no changes in cellular distribution of labeling. In contrast, AQP4 immunostaining was slightly decreased and there was a surprising decrease in cell height and disappearance of immunolabeling of the lateral cell membrane in IMCD cells with only basal labeling remaining. Immunnoblot analysis confirmed the increase in AQP3 expression in cortex (259+/-50%, P<.0.01), outer medulla (607+/-115%, P<0.01) and inner medulla (1,289+/-174%, P<0.0001), and the decrease in AQP4 expression in the inner medulla (31+/-2%, P<0.02) of AQP1 (-/-) compared with AQP1 (+/+) mice (values in AQP1 (-/-) expressed as percentage of AQP1 (+/+)). In summary, AQP1 gene deletion is associated with an upregulation of AQP3 and a downregulation of AQP4. Taken together, these observations suggest that AQP3 and AQP4 are differently regulated and the basolateral water channel expression is upregulated in the cortical and outer medullary collecting duct in AQP1 knockout mice. The significance of the disappererance of AQP4 immunoreactivity in the lateral plasma membrane of IMCD cells in AQP1 knockout mice remains to be established.

The influence of polyI:C on blood capillary in mouse prostate carcinoma / 中国药理学通报

Aim To investigate the effects of polyI:C on angiogenesis in mouse prostate carcinoma and its mechanisms.Methods Prostate carcinoma bearing mice were randomly divided into two groups according to tumor volume:contrl group and polyI:C group.After seven times′treatment,the mice were sacrificed.The content of NO in tumor was measured by nitric oxide assay kit.Tumor tissues were partly performed hematoxylin-eosin staining to observe morphological changes and distribution of vasa.Immunohisto chemical staining was used to observe the expression of VEGF,eNOS and AQP1.Results The content of NO in polyI:C group and the control was(1.22?0.77)?mol and(8.73?5.34)?mol respectively,and there was significant difference between two groups(P

Expression of alphasmooth Muscle Actin, Aquaporin 1 and Renin after Blocking AT1 Receptor in Developing Renal Arterial System of Rat / 대한신장학회잡지

BACKGROUND: Recent studies have demonstrated that renin, alphasmooth muscle actin(ASMA) and aquaporin-1(AQP1) participate in the development of renal arterial system. The components of the renin- angiotensin system have been shown to function as growth factors, apart from their classical roles in controlling blood volume and homeostasis. Interestingly, the vasoconstrictor angiotensin II(ANG II) appears to participate in the regulation of angiogenesis in various tissues. The present study examined the effect of ANG II type-1(AT1) receptor blocker losartan given during pregnancy or newborn rats on the expression of renin, ASMA and AQP1 in the developing renal arterial system. METHODS: Pregnant and newborn rats received losartan(10 mg/kg/day) or saline for 4 and 8 days from E14 to parturition, and for 4 and 9 days starting at day 1 after birth, respectively. Kidneys of 17-day-old fetuses and 1-, 4-, and 9-day- old pups were processed for immunohistochemistry using antibodies to renin(1 : 10,000), ASMA(1 : 1,000), and AQP1(1 : 1,000). RESULTS: In all pregnant groups, there were no differences in immunostaining for renin, ASMA, and AQP1 between losartan treated groups and saline treated groups. In all newborn groups, however, blockade of AT1 receptor with losartan found to increase expression of renin and ASMA but to have no effect on expression of AQP1 in the developing renal arterial system. CONCLUSION: These results suggest that AQP1 expression is not associated with renin or ASMA expression during development of renal arterial system.