کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10767224 | 1050718 | 2007 | 7 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Apical P2XR contribute to [Ca2+]i signaling and Isc in mouse renal MCD
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کلمات کلیدی
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: Apical P2XR contribute to [Ca2+]i signaling and Isc in mouse renal MCD Apical P2XR contribute to [Ca2+]i signaling and Isc in mouse renal MCD](/preview/png/10767224.png)
چکیده انگلیسی
We examined P2X receptor expression and distribution in the mouse collecting duct (CD) and their functional role in Ca2+ signaling. Both P2X1 and P2X4 were detected by RT-PCR and Western blot. Immunohistochemistry demonstrated apical P2X1 and P2X4 immunoreactivity in principal cells in the outer medullary CD (OMCD) and inner medullary CD (IMCD). Luminal ATP induced an increase in Ca2+ signaling in native medullary CD (MCD) as measured by fluorescence imaging. ATP also induced an increase in Ca2+ signaling in MCD cells grown in primary culture but not in the presence of P2XR antagonist PPNDS. Short circuit current (Isc) measurement with mouse IMCD cells showed that P2XR agonist BzATP induced a larger Isc than did P2YR agonist UTP in the apical membrane. Our data reveal for the first time that P2X1 and P2X4 are cell-specific with prominent immunoreactivity in the apical area of MCD cells. The finding that P2XR blockade inhibits ATP-induced Ca2+ signaling suggests that activation of P2XR is a key step in Ca2+-dependent purinergic signaling. The result that activation of P2XR produces large Isc indicates the necessity of P2XR in renal CD ion transport.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biochemical and Biophysical Research Communications - Volume 359, Issue 3, 3 August 2007, Pages 438-444
Journal: Biochemical and Biophysical Research Communications - Volume 359, Issue 3, 3 August 2007, Pages 438-444
نویسندگان
Liuzhe Li, I. Jeanette Lynch, Wencui Zheng, Melanie N. Cash, Xueling Teng, Charles S. Wingo, Jill W. Verlander, Shen-Ling Xia,