P2X6 knockout mice exhibit normal electrolyte homeostasis
ATP-mediated signaling is an important regulator of electrolyte transport in the kidney. The purinergic cation channel P2X6 has been previously localized to the distal convoluted tubule (DCT), a nephron segment important for Mg2+ and Na+ reabsorption, but its role in ion transport remains unknown. I...
| Main Authors: | , , , , , |
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| Format: | Journal article |
| Language: | English |
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Public Library of Science
2016
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| _version_ | 1826256530555535360 |
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| author | De Baaij, J Kompatscher, A Viering, D Bos, C Bindels, R Hoenderop, J |
| author_facet | De Baaij, J Kompatscher, A Viering, D Bos, C Bindels, R Hoenderop, J |
| author_sort | De Baaij, J |
| collection | OXFORD |
| description | ATP-mediated signaling is an important regulator of electrolyte transport in the kidney. The purinergic cation channel P2X6 has been previously localized to the distal convoluted tubule (DCT), a nephron segment important for Mg2+ and Na+ reabsorption, but its role in ion transport remains unknown. In this study, P2x6 knockout (P2x6-/-) mice were generated to investigate the role of P2X6 in renal electrolyte transport. The P2x6-/- animals displayed a normal phenotype and did not differ physiologically from wild type mice. Differences in serum concentration and 24-hrs urine excretion of Na+, K+, Mg2+ and Ca2+ were not detected between P2x6+/+, P2x6+/- and P2x6-/- mice. Quantitative PCR was applied to examine potential compensatory changes in renal expression levels of other P2x subunits and electrolyte transporters, including P2x1-5, P2x7, Trpm6, Ncc, Egf, Cldn16, Scnn1, Slc12a3, Slc41a1, Slc41a3, Cnnm2, Kcnj10 and Fxyd2. Additionally, protein levels of P2X2 and P2X4 were assessed in P2x6+/+ and P2x6-/- mouse kidneys. However, significant changes in expression were not detected. Furthermore, no compensatory changes in gene expression could be demonstrated in heart material isolated from P2x6-/- mice. Except for a significant (P<0.05) upregulation of P2x2 in the heart of P2x6-/- mice compared to the P2x6+/+ mice. Thus, our data suggests that purinergic signaling via P2X6 is not significantly involved in the regulation of renal electrolyte handling under normal physiological conditions. |
| first_indexed | 2024-03-06T18:03:41Z |
| format | Journal article |
| id | oxford-uuid:00b0043b-9dcb-4c1f-ad6d-9dba7ef2dc76 |
| institution | University of Oxford |
| language | English |
| last_indexed | 2024-03-06T18:03:41Z |
| publishDate | 2016 |
| publisher | Public Library of Science |
| record_format | dspace |
| spelling | oxford-uuid:00b0043b-9dcb-4c1f-ad6d-9dba7ef2dc762022-03-26T08:30:53ZP2X6 knockout mice exhibit normal electrolyte homeostasisJournal articlehttp://purl.org/coar/resource_type/c_dcae04bcuuid:00b0043b-9dcb-4c1f-ad6d-9dba7ef2dc76EnglishSymplectic Elements at OxfordPublic Library of Science2016De Baaij, JKompatscher, AViering, DBos, CBindels, RHoenderop, JATP-mediated signaling is an important regulator of electrolyte transport in the kidney. The purinergic cation channel P2X6 has been previously localized to the distal convoluted tubule (DCT), a nephron segment important for Mg2+ and Na+ reabsorption, but its role in ion transport remains unknown. In this study, P2x6 knockout (P2x6-/-) mice were generated to investigate the role of P2X6 in renal electrolyte transport. The P2x6-/- animals displayed a normal phenotype and did not differ physiologically from wild type mice. Differences in serum concentration and 24-hrs urine excretion of Na+, K+, Mg2+ and Ca2+ were not detected between P2x6+/+, P2x6+/- and P2x6-/- mice. Quantitative PCR was applied to examine potential compensatory changes in renal expression levels of other P2x subunits and electrolyte transporters, including P2x1-5, P2x7, Trpm6, Ncc, Egf, Cldn16, Scnn1, Slc12a3, Slc41a1, Slc41a3, Cnnm2, Kcnj10 and Fxyd2. Additionally, protein levels of P2X2 and P2X4 were assessed in P2x6+/+ and P2x6-/- mouse kidneys. However, significant changes in expression were not detected. Furthermore, no compensatory changes in gene expression could be demonstrated in heart material isolated from P2x6-/- mice. Except for a significant (P<0.05) upregulation of P2x2 in the heart of P2x6-/- mice compared to the P2x6+/+ mice. Thus, our data suggests that purinergic signaling via P2X6 is not significantly involved in the regulation of renal electrolyte handling under normal physiological conditions. |
| spellingShingle | De Baaij, J Kompatscher, A Viering, D Bos, C Bindels, R Hoenderop, J P2X6 knockout mice exhibit normal electrolyte homeostasis |
| title | P2X6 knockout mice exhibit normal electrolyte homeostasis |
| title_full | P2X6 knockout mice exhibit normal electrolyte homeostasis |
| title_fullStr | P2X6 knockout mice exhibit normal electrolyte homeostasis |
| title_full_unstemmed | P2X6 knockout mice exhibit normal electrolyte homeostasis |
| title_short | P2X6 knockout mice exhibit normal electrolyte homeostasis |
| title_sort | p2x6 knockout mice exhibit normal electrolyte homeostasis |
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