دورية أكاديمية
SLC41A1 knockout mice display normal magnesium homeostasis.
| العنوان: | SLC41A1 knockout mice display normal magnesium homeostasis. |
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| المؤلفون: | Ilenwabor BP; Department of Physiology, Radboud Institute for Molecular Life Sciences, Radboud University Medical Center, Nijmegen, The Netherlands., Franken GAC; Department of Physiology, Radboud Institute for Molecular Life Sciences, Radboud University Medical Center, Nijmegen, The Netherlands., Sponder G; Institute of Veterinary Physiology, Freie Universität Berlin, Berlin, Germany., Bos C; Department of Physiology, Radboud Institute for Molecular Life Sciences, Radboud University Medical Center, Nijmegen, The Netherlands., Racay P; Department of Medical Biochemistry, Jessenius Faculty of Medicine, Comenius University in Bratislava, Martin, Slovakia.; Biomedical Center Martin, Jessenius Faculty of Medicine, Comenius University in Bratislava, Martin, Slovakia., Kolisek M; Biomedical Center Martin, Jessenius Faculty of Medicine, Comenius University in Bratislava, Martin, Slovakia., Hoenderop JGJ; Department of Physiology, Radboud Institute for Molecular Life Sciences, Radboud University Medical Center, Nijmegen, The Netherlands., de Baaij JHF; Department of Physiology, Radboud Institute for Molecular Life Sciences, Radboud University Medical Center, Nijmegen, The Netherlands. |
| المصدر: | American journal of physiology. Renal physiology [Am J Physiol Renal Physiol] 2022 Nov 01; Vol. 323 (5), pp. F553-F563. Date of Electronic Publication: 2022 Sep 01. |
| نوع المنشور: | Journal Article; Research Support, Non-U.S. Gov't |
| اللغة: | English |
| بيانات الدورية: | Publisher: American Physiological Society Country of Publication: United States NLM ID: 100901990 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1522-1466 (Electronic) Linking ISSN: 15221466 NLM ISO Abbreviation: Am J Physiol Renal Physiol Subsets: MEDLINE |
| أسماء مطبوعة: | Original Publication: Bethesda, Md. : American Physiological Society, c1997- |
| مواضيع طبية MeSH: | Magnesium*/metabolism , Cation Transport Proteins*/genetics, Animals ; Mice ; Cations ; Cyclins/metabolism ; Homeostasis ; Kidney Tubules, Distal/metabolism ; Mice, Knockout ; Mice, Transgenic ; TRPM Cation Channels/genetics ; TRPM Cation Channels/metabolism |
| مستخلص: | Transcellular Mg 2+ reabsorption in the distal convoluted tubule (DCT) of the kidneys plays an important role in maintaining systemic Mg 2+ homeostasis. SLC41A1 is a Na + /Mg 2+ exchanger that mediates Mg 2+ efflux from cells and is hypothesized to facilitate basolateral extrusion of Mg 2+ in the DCT. In this study, we generated a SLC41A1 knockout mouse model to examine the role of SLC41A1 in Mg 2+ homeostasis. Slc41a1 -/- mice exhibited similar serum and urine Mg 2+ levels as their wild-type littermates. Dietary restriction of Mg 2+ resulted in reduced serum Mg 2+ concentration and urinary Mg 2+ excretion, which was similar in the wild-type and knockout groups. Expression of genes encoding Mg 2+ channels and transporters such as transient receptor potential melastatin 6 ( Trpm6 ), transient receptor potential melastatin 7 ( Trpm7 ), cyclin and CBS domain divalent metal cation transport mediator 2 ( Cnnm2 ), and Slc41a3 were unchanged based on genotype. We investigated the potential redundancy of SLC41A1 and its homolog SLC41A3 by generating a double knockout mouse. Although Slc41a3 -/- knockout mice showed significantly reduced serum Mg 2+ compared with wild-type and Slc41a1 -/- knockout groups, double knockout mice displayed similar serum Mg 2+ levels as Slc41a3 -/- knockout mice. In conclusion, our data show that SLC41A1 is not involved in the regulation of systemic Mg 2+ homeostasis in mice. Our data also demonstrate that SLC41A1 does not compensate for the loss of SLC41A3, suggesting different functions of these SLC41 proteins in vivo. NEW & NOTEWORTHY SLC41A1 has been hypothesized to mediate Mg 2+ extrusion in the distal convoluted tubule and thus regulate Mg 2+ homeostasis. This study investigated the role of SLC41A1 in Mg 2+ homeostasis in vivo using a transgenic mouse model. Our results demonstrate that SLC41A1 is not required to maintain normal Mg 2+ balance in mice. We also show that SLC41A3 is more important than SLC41A1 in regulating systemic Mg 2+ levels. |
| فهرسة مساهمة: | Keywords: SLC41A1; SLC41A3; distal tubule; magnesium transport |
| المشرفين على المادة: | 0 (Cations) 0 (Cyclins) I38ZP9992A (Magnesium) 0 (TRPM Cation Channels) EC 2.7.1.- (Trpm7 protein, mouse) 0 (Slc41a1 protein, mouse) 0 (Cation Transport Proteins) |
| تواريخ الأحداث: | Date Created: 20220901 Date Completed: 20221024 Latest Revision: 20221212 |
| رمز التحديث: | 20231215 |
| DOI: | 10.1152/ajprenal.00101.2022 |
| PMID: | 36049064 |
| قاعدة البيانات: | MEDLINE |
| تدمد: | 1522-1466 |
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| DOI: | 10.1152/ajprenal.00101.2022 |