The role of aquaporin-1 in idiopathic and drug-induced intracranial hypertension

Idiopathic intracranial hypertension is a common disorder affecting mainly healthy, young, overweight women. The pathogenesis of this condition is unknown, but it has been shown to follow treatment with several compounds including corticosteroids and vitamin A derivatives. This paper will offer a novel hypothesis and insight on the pathogenesis of drug induced intracranial hypertension following a review and analysis of the literature. Both corticosteroids and vitamin A derivatives have been shown to upregulate the expression of aquaporin 1, a water channel protein. Aquaporin 1 is widely distributed in the human brain and is associated with water secretion into the subarachnoid space. Aquaporin 1 was also shown to participate in the regulation of weight. Agents used for treating idiopathic intracranial hypertension reduce aquaporin 1 expression. Based on these observations, we propose that aquaporin 1 has a pathogenetic role in drug induced idiopathic intracranial hypertension. Over expression of this gene causes increased intracranial pressure, and downregulation reduces pressure and alleviates the symptomatology and complications of idiopathic intracranial hypertension.     

The peritoneal microcirculation in peritoneal dialysis.

This paper deals with the peritoneal microcirculation and with peritoneal exchange occurring in peritoneal dialysis (PD). The capillary wall is a major barrier to solute and water exchange across the peritoneal membrane. There is a bimodal size-selectivity of solute transport between blood and the peritoneal cavity, through pores of radius approximately 40-50 A as well as through a very low number of large pores of radius approximately 250 A. Furthermore, during glucose-induced osmosis during PD, nearly 40% of the total osmotic water flow occurs through molecular water channels, termed "aquaporin-1." This causes an inequality between 1 - sigma and the sieving coefficient for small solutes, which is a key feature of the "three-pore model" of peritoneal transport. The peritoneal interstitium, coupled in series with the capillary walls, markedly modifies small-solute transport and makes large-solute transport asymmetric. Thus, although severely restricted in the blood-to-peritoneal direction, the absorption of large solutes from the peritoneal cavity occurs at a high clearance rate ( approximately 1 mL/min), largely independent of molecular radius. True absorption of macromolecules to the blood via lymphatics, however, seems to be occurring at a rate of approximately 0.2 mL/min. Several controversial issues regarding transcapillary and transperitoneal exchange mechanisms are discussed in this paper.     

The role of aquaporin-1 in idiopathic and drug-induced intracranial hypertension

Idiopathic intracranial hypertension is a common disorder affecting mainly healthy, young, overweight women. The pathogenesis of this condition is unknown, but it has been shown to follow treatment with several compounds including corticosteroids and vitamin A derivatives. This paper will offer a novel hypothesis and insight on the pathogenesis of drug induced intracranial hypertension following a review and analysis of the literature. Both corticosteroids and vitamin A derivatives have been shown to upregulate the expression of aquaporin 1, a water channel protein. Aquaporin 1 is widely distributed in the human brain and is associated with water secretion into the subarachnoid space. Aquaporin 1 was also shown to participate in the regulation of weight. Agents used for treating idiopathic intracranial hypertension reduce aquaporin 1 expression. Based on these observations, we propose that aquaporin 1 has a pathogenetic role in drug induced idiopathic intracranial hypertension. Over expression of this gene causes increased intracranial pressure, and downregulation reduces pressure and alleviates the symptomatology and complications of idiopathic intracranial hypertension.     

三七总皂甙对脑出血后大鼠脑水肿及水通道蛋白-4表达的影响

目的观察三七总皂甙对脑出血大鼠脑水肿形成及水通道蛋白-4(AQP4)表达的影响。方法Wistar大鼠198只随机分为A、B、C 3个部分,分别检测脑含水量、AQP4蛋白和AQP4 mRNA,每部分又随机分为假手术组,模型组,治疗组,采用干湿重法、免疫组织化学染色、逆转录聚合酶链反应技术分别测定脑含水量、AQP4蛋白和AQP4 mRNA的表达。结果治疗组和模型组12 h之后脑含水量增加(P<0.05),1天时脑含水量明显增加(P<0.01),3天时脑含水量达到高峰并持续到5天,在相同的时间点,治疗组脑含水量比模型组明显少(P<0.05);模型组和治疗组12 h之后AQP4蛋白和AQP4 mRNA表达水平增加(P<0.05),1天时明显升高(P<0.01),3天达到高峰持续至5天,以后逐渐下降,与模型组比较,治疗组大鼠在各时间点AQP4蛋白、AQP4 mRNA均在低水平表达(P<0.05),1-5天表达水平明显下降(P<0.01)。结论三七总皂甙可能通过抑制AQP4的表达减轻脑出血后脑水肿的形成。     

The role of aquaporins in dendritic cell macropinocytosis

Immature dendritic cells (DCs) constitutively take up large volumes of fluid by macropinocytosis and concentrate the macrosolutes in the endocytic compartment. This concentration mechanism that is the basis of their high capacity to present soluble antigens requires that DCs be capable of rapidly exchanging water across their membranes. We report that two members of the aquaporin family, AQP3 and AQP7, are expressed in immature DCs and are downregulated after maturation. Treatment of DCs with p-chloromercuribenzenesulphonate (pCMBS), a mercuric drug that blocks aquaporins, inhibited uptake and concentration of macrosolutes taken up by fluid phase endocytosis and led to dramatic cell swelling. In contrast, pCMBS did not affect receptor-mediated endocytosis via the mannose receptor. These findings indicate that aquaporins represent essential elements of a volume control mechanism that allows DCs to concentrate macrosolutes taken up via macropinocytosis.     

<Emphasis Type="Italic">In vitro</Emphasis> study of the role of lenticular epithelial calcium channels and aquaporins in the development of cataract

The role of calcium and water channels (aquaporins) in the pathogenesis of cataract was studied in vitro. Aquaporin blockade caused opacity of the lens sooner than changes in calcium ion concentration in culture medium. __________ Translated from Byulleten’ Eksperimental’noi Biologii i Meditsiny, Vol. 145, No. 2, pp. 144–147, February, 2008     

Chitosan promotes aquaporin formation and inhibits mucociliary differentiation of nasal epithelial cells through increased TGF‐β1 production

Although endoscopic sinus surgery is the mainstay surgical treatment for chronic rhinosinusitis, over 15% of patients require a repeat operation wherein postoperative adhesion formation is one of the main causes of failure. Several recently proposed chitosan‐based biomaterials promote mucosal healing, reduce postoperative adhesion formation and restore mucociliary function of sinonasal mucosa. However, the effects of chitosan on cellular morphology, re‐epithelization, and mucociliary differentiation of nasal epithelial cells (NECs) during the wound healing process have not been thoroughly investigated. The present study investigates the direct effects of chitosan on cellular growth, cellular migration, mucociliary differentiation and aquaporin (AQP) formation of NECs to elucidate the role of chitosan in sinonasal applications. Wound healing assay reveals that proliferation and migration of NECs are inhibited by incubation of chitosan. The NECs become irregular in shape without formation of tight junction and mucociliary differentiation of NECs is inhibited during a culture period with incubation of chitosan. However, AQP3 and AQP5 formation in NECs is significantly higher in chitosan groups than in control groups. Further, expressions of transforming growth factor (TGF)‐β1, Smad2, and Smad3 are significantly higher in the chitosan groups compared with controls. The results of the comparison indicate that chitosan inhibits proliferation, migration and mucociliary differentiation of NECs through increasing production of TGF‐β1. Copyright © 2016 John Wiley & Sons, Ltd.     

地塞米松对大鼠肝脏Mrp2和AQP1表达的影响

【目的】探讨地塞米松（Dex）对Wistar大鼠肝胆系统多药耐药相关蛋白2（Mrp2）和水通道蛋白1（AQPt）的调节作用。【方法】20只Wistar大鼠随机分为空白对照组和Dex干预组，观测1h胆汁流量、直接胆红素（DBIL），用免疫组织化学的方法观测Mrp2和AQP1的表达。【结果】干预组较之对照组胆汁量增加（P〈0．05），血清DBIL明显下降（P〈0．01），胆汁DBIL差异无显著性（P〉0．05），Mrp2和AQP1免疫组化切片光密度值增加（P〈0．01）。【结论】Dex可增加大鼠肝胆系统Mrp2和AQP1的表达。血清DBIL下降，胆汁分泌量增加，与Mrp2和AQP1的表达相关。