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Cardiac aquaporin expression in humans, rats, and mice.

机译:心脏水通道蛋白在人,大鼠和小鼠中的表达。

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Water accumulation in the heart is important in ischemia-reperfusion injury and operations performed by using cardiopulmonary bypass, with cardiac dysfunction associated with myocardial edema being the principal determinant of clinical outcome. As an initial step in determining the role of aquaporin (AQP) water channels in myocardial edema, we have assessed the myocardial expression of AQPs in humans, rats, and mice. RT-PCR revealed expression of AQP-1, -4, -6, -7, -8, and -11 transcripts in the mouse heart. AQP-1, -6, -7, and -11 mRNAs were found in the rat heart as well as low levels of AQP-4 and -9. Human hearts contained AQP-1, -3, -4, -5, -7, -9, -10, and -11 mRNAs. AQP-1 protein expression was confirmed by Western blot analysis in all three species. AQP-4 protein was detected in the mouse heart but not in the rat or human heart. To determine the potential functional consequences of myocardial AQP expression, water permeability was measured in plasma membrane vesicles from myocardial cells of wild-type versus various AQP knockout mice. Water permeability was reduced by AQP-1 knockout but not by AQP-4 or AQP-8 knockout. With the use of a model of isolated rat heart perfusion, it was found that osmotic and ischemic stresses are not associated with changes in AQP-1 or AQP-4 expression. These studies support a possible functional role of AQP-1 in myocardium but indicate that early adaptations to osmotic and ischemic stress do not involve transcriptional or posttranslational AQP-1 regulation.
机译:心脏中的水积聚在缺血再灌注损伤和通过体外循环进行的手术中很重要,与心肌水肿相关的心脏功能障碍是临床结果的主要决定因素。作为确定水通道蛋白(AQP)水通道在心肌水肿中的作用的第一步,我们评估了AQP在人,大鼠和小鼠中的心肌表达。 RT-PCR显示小鼠心脏中AQP-1,-4,-6,-7,-8和-11转录本的表达。在大鼠心脏中发现了AQP-1,-6,-7和-11 mRNA,以及低水平的AQP-4和-9。人的心脏含有AQP-1,-3,-4,-5,-7,-9,-10和-11 mRNA。通过蛋白质印迹分析在所有三个物种中证实了AQP-1蛋白表达。在小鼠心脏中检测到AQP-4蛋白,但在大鼠或人心脏中未检测到。为了确定心肌AQP表达的潜在功能后果,在野生型与各种AQP敲除小鼠的心肌细胞的质膜囊泡中测量了水渗透性。 AQP-1敲除降低了透水性,但AQP-4或AQP-8敲除并未降低透水性。使用分离的大鼠心脏灌注模型,发现渗透压和局部缺血性应激与AQP-1或AQP-4表达的变化无关。这些研究支持AQP-1在心肌中可能的功能作用,但表明对渗透压和缺血应激的早期适应不涉及转录或翻译后AQP-1调节。

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