Intraluminal autocrine purinergic signaling within cysts: implications for the progression of diseases that involve encapsulated cyst formation.
Intraluminal autocrine purinergic signaling within cysts: implications for the progression of diseases that involve encapsulated cyst formation.
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囊肿内的腔内自分泌嘌呤能信号传导：对涉及囊肿形成的疾病进展的影响。
DOI：
10.1152/ajprenal.00291.2006
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发表时间：
2007
期刊：
影响因子：
--
通讯作者：
Schwiebert,ErikM
中科院分区：
文献类型：
--
作者：
Olteanu,Dragos;Hovater,MichaelB;Schwiebert,ErikM
嘌呤能配体是神经递质、自分泌因子或旁分泌因子（5，7-10，12，16，47-49，51，63，70）。细胞外核苷酸和核苷在生理学和病理生理学中的作用已经研究了几十年（5，7-10，12，16）。然而，由于对作为细胞内生化燃料的ATP的损失的担忧，这是缓慢的认识（9，12，16）。在对嘌呤能配体从细胞中的释放进行广泛而系统的研究之前，多种类型的核苷酸受体（ATP、UTP、UDP、ADP等）被认为是嘌呤能配体的受体。和核苷（腺苷等）出现了分子克隆（1，14，27，41，49）。嘌呤能配体对细胞功能的影响的研究最近已经爆炸，嘌呤能配体的释放和这些配体与P2（核苷酸）和P1（核苷）受体的结合的研究也是如此。最近出版的杂志《嘌呤能信号》谈到了这一革命（6）。关于嘌呤能信号，现在已经全面认识到：1）所有细胞都从占细胞内ATP总含量0.1%或更少的小的“可释放”池中释放ATP（5-10 mM总细胞内ATP中高达10 μM的可检测分泌ATP）（1，4，5，7-10，12，16，47-50，51，61，63，70）; 2）所有细胞表达ATP门控P2 X受体通道、ATP敏感P2 Y G蛋白偶联受体的一种或多种亚型，和腺苷敏感P1 G蛋白偶联受体（1、4、5、7-10、12、16、26、30、33、36、47-50、51、56、60、62-64、70、74、75）;嘌呤能配体通过这些受体以相似和不同的方式影响所有细胞（1、4、5、7-10、12、16、26、30、33、36、47-50、51、56、60、62-65、70、74、75）。Turner et al.的早期文章(64)直接说明了大鼠肾单位节段中相同细胞上存在多个P2 Y和P2 X受体的概念。这篇论文在肾嘌呤能领域也是一个开创性的和有帮助的研究。体内嘌呤能激动剂作为血源性介质无效（5，7-9，12，16，47-51）。ATP在体循环中通过多种膜结合和分泌的胞外ATP酶快速降解（5，7-9，12，16，47-51）。腺苷通过核苷转运蛋白再循环回细胞，用于ATP再合成（5，7-9，12，16，47-51）。普遍认为，嘌呤能配体活性是短暂的，ATP或腺苷与其许多细胞表面受体结合并通过其发出信号的能力在组织“微环境”中最强大。Burnstock（5，7-9）和Gordon（16）已经对这一概念进行了优雅的回顾;这一概念也将在2007年发表在《嘌呤信号传导》特刊上的一系列小型回顾中重新讨论，主题是“核苷酸释放的生理学”。
PURINERGIC LIGANDS ARE LOCAL mediators, autacoids, or paracrine factors (5, 7–10, 12, 16, 47–49, 51, 63, 70). The role of extracellular nucleotides and nucleosides in physiology and pathophysiology has been studied for decades (5, 7–10, 12, 16). However, it was slow to be appreciated because of trepidations with regard to the loss of ATP as an intracellular biochemical fuel (9, 12, 16). Before the release of purinergic ligands from cells was studied extensively and systematically, multiple types of receptors for nucleotides (ATP, UTP, UDP, ADP, etc.) and nucleosides (adenosine, etc.) emerged from molecular cloning (1, 14, 27, 41, 49). The study of purinergic ligand’s effects on cell function has exploded recently, as has the study of purinergic ligand release and the binding of these ligands to P2 (nucleotide) and P1 (nucleoside) receptors. A recently launched journal, Purinergic Signalling, speaks to this revolution (6).With regard to purinergic signaling, it is now comprehensively appreciated that 1) all cells release ATP from small “releasable” pools that account for 0.1% or less of the total intracellular ATP content (up to 10 μM detectable secreted ATP from 5–10 mM total intracellular ATP)(1, 4, 5, 7–10, 12, 16, 47–50, 51, 61, 63, 70); 2) all cells express one or more subtypes of the ATP-gated P2X receptor channels, ATP-sensing P2Y G protein-coupled receptors, and adenosine-sensing P1 G protein-coupled receptors (1, 4, 5, 7–10, 12, 16, 26, 30, 33, 36, 47–50, 51, 56, 60, 62–64, 70, 74, 75); and 3) all cells are influenced by purinergic ligands via these receptors in similar and different ways (1, 4, 5, 7–10, 12, 16, 26, 30, 33, 36, 47–50, 51, 56, 60, 62–65, 70, 74, 75). An earlier article by Turner et al.(64) speaks directly to the concept of multiple P2Y and P2X receptors on the same cells in segments of the rat nephron. This paper, too, was a seminal and helpful study in the renal purinergic field. Purinergic agonists in vivo are not efficient as blood-borne mediators (5, 7–9, 12, 16, 47–51). ATP is degraded rapidly in the general circulation via multiple membrane-bound and secreted ecto-ATPases (5, 7–9, 12, 16, 47–51). Adenosine is recycled back into cells via nucleoside transporters to be used for ATP resynthesis (5, 7–9, 12, 16, 47–51). There is general agreement that purinergic ligand activity is short-lived and the ability of ATP or adenosine to bind to and signal via its many cell surface receptors is most robust in tissue “microenvironments.” Such a concept has been reviewed elegantly by Burnstock (5, 7–9) and by Gordon (16); this concept is also being revisited in a series of minireviews to be published in a special issue of Purinergic Signalling in 2007 on the “Physiology of Nucleotide Release.”
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加压素和 cAMP 刺激 IMCD 细胞系中的电化学氯化物分泌。
DOI：
10.1152/ajprenal.1995.268.5.f854
发表时间：
1995
期刊：
The American journal of physiology.
影响因子：
--
作者：
Kizer,NL;Vandorpe,D;Lewis,B;Bunting,B;Russell,J;Stanton,BA
通讯作者：
Stanton,BA
影响因子：
--
作者：
F. Edwin;G. Wiepz;Rakesh K. Singh;Chimera R. Peet;Deepti Chaturvedi;P. Bertics;T. Patel
通讯作者：
F. Edwin;G. Wiepz;Rakesh K. Singh;Chimera R. Peet;Deepti Chaturvedi;P. Bertics;T. Patel
肾脏和乳房囊肿：液体的比较研究。
影响因子：
2.5
作者：
Davis K. Hurley;Steven M. Bandy;Robert H. Glew;Don M. Morris;Kenneth D. Gardner
通讯作者：
Kenneth D. Gardner
影响因子：
158.5
作者：
KNOWLES, MR;CLARKE, LL;BOUCHER, RC
通讯作者：
BOUCHER, RC
上皮 P2X 嘌呤能受体通道的表达和功能。
DOI：
10.1172/jci7270
发表时间：
1999
期刊：
The Journal of clinical investigation
影响因子：
--
作者：
A. Taylor;L. Schwiebert;J. J. Smith;C. King;J. R. Jones;E. Sorscher;E. Schwiebert
通讯作者：
E. Schwiebert