PTH regulates expression of ClC.5 chloride channel in the kidney

American Journal of Physiology - Renal Physiology

Volumn 278, Issue 2 47-2, 2000, Pages

  Silva, Ian V ^b   Blaisdell, Carol J ^a   Guggino, Sandra E ^a   Guggino, William B ^a  

^a JOHNS HOPKINS UNIVERSITY SCHOOL OF MEDICINE   (United States)

^b School of Medicine ^*

Author keywords

Chloride channels; Kidney stones; Nephrolithiasis

Indexed keywords

CALCITRIOL; CALCIUM; CHLORIDE; CHLORIDE CHANNEL; MESSENGER RNA; PARATHYROID HORMONE;

ANIMAL CELL; ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; ARTICLE; CALCIUM HOMEOSTASIS; CONTROLLED STUDY; FEMALE; GENE MUTATION; HORMONAL REGULATION; KIDNEY CORTEX; KIDNEY MEDULLA; KIDNEY TUBULE ABSORPTION; MALE; NEPHROLITHIASIS; NONHUMAN; PRIORITY JOURNAL; RAT; THYROPARATHYROIDECTOMY; VITAMIN D DEFICIENCY;

EID: 0034056746     PISSN: 1931857X     EISSN: 15221466     Source Type: Journal    
DOI: 10.1152/ajprenal.2000.278.2.f238     Document Type: Article

References (40)

1. + exchanger NHE-3 isoform in renal cells (OK) via dual signaling cassette involving protein kinase A and C. J. Biol. Chem. 270: 20004-20010, 1995.
2. Bushinsky, D. A., M. D. Grynpas, E. L. Nilsson, Y. Nakagawa, and F. L. Coe. Stone formation in genetic hypercalciuric rats. Kidney Int. 48: 1705-1713, 1995.
3. Coe, F. L., and D. A. Bushinsky. Pathophysiology of hypercalciuria. Am. J. Physiol. Renal Fluid Electrolyte Physiol. 247: F1-F14, 1984.
4. 3 levels in patients with idiopathic hypercalciuria and normal subjects. Am. J. Med. 72: 25-31, 1982.
5. Devuyst, O., P. T. Christie, P. J. Courtoy, R. Beauwens, and R. V Thakker. Intra-renal and subcellular distribution of human chloride channel, ClC-5, reveals a pathophysiological basis for Dent's disease. Hum. Mol. Genet. 8: 247-257, 1999.
6. Fisher, S. E., G. C. M. Black, S. E. Lloyd, E. Hatchwell, O. Wrong, R. V. Thakker, and I. W. Craig. Isolation and partial characterization of a chloride channel gene which is expressed in kidney and is a candidate for Dent's disease (an X-linked hereditary nephrolithiasis) Hum. Mol. Genet. 3 : 2053-2059, 1994.
7. Gesek, F. A., and P. A. Friedman. Calcitonin stimulates calcium transport in distal convoluted tubule cells. Am. J. Physiol. Renal Fluid Electrolyte Physiol. 264: F744-F751, 1993.
8. Gunther, W., A. Luchow, F. Cluzeaud, A. Vandewalle, and T. J. Jentsch. ClC-5, the chloride channel mutated in Dent's disease, co-localizes with the proton pump in endocytotically active kidney cells. Proc. Natl. Acad. Sci. USA 95: 8075-8080, 1998.
9. Hebert, S. C. Crystal-clear chloride channels. Nature Lond. 379: 398-399, 1996.
10. Hoopes, R. R., Jr., P. A. Hueber, R. J. Reid, Jr., G. L. Braden, P. R. Goodyer, A. R. Melnyk, M. P. Midgley, D. I. Moel, A. M. Neu, S. K. VanWhy, and S. J. Scheinman. CLC-5 chloride-channel mutations in six new North American families with X-linked nephrolithiasis. Kidney Int. 54: 698-7051, 1998.
11. 3. Am. J. Physiol. Renal Fluid Electrolyte Physiol. 236: F349-F356, 1979.
12. Jentsch, T. J. Structure and function of ClC chloride channels. Jpn. J. Physiol. 44: S1-S2, 1994.
13. Jentsch, T. J., W. Gunther, M. Pusch, and B. Schwappach. Properties of voltage-gated chloride channels of the ClC gene family. J. Physiol. (Lond.) 482: 19S-25S, 1995.
14. Kelleher, C. L., V. M. Buckalew, E. D. Frederickson, D. J. Rhodes, D. A. Conner, and J. G. Seidman. CLC-5 mutation Ser244Leu is associated with X-linked renal failure without X-linked recessive hypophosphatemic rickets. Kidney Int. 53: 31-37, 1998.
15. Kiebzak, G. M., B. A. Roos, and R. A. Meyer, Jr. Secondary hyperparathyroidism in X-linked hypophosphatemic mice. Endocrinology. 111: 650-652, 1982.
16. Khan, S. R., and P. A. Glenton. Deposition of calcium phosphate and calcium oxalate crystals in the kidney. J. Urol. 153: 811-817, 1995.
17. Knudtzon, J., J. Halse, E. Monn, A, Nesland, K. P. Nordal, P. Paus, M. Seip, S. Sund, and G. Sodal. Autonomous hyperparathyroidism in X-linked hypophosphataemia. Clin. Endocrinol. (Oxf.) 42: 199-203, 1995.
18. Kok, D. J., and S. R. Khan. Calcium oxalate nephrolithiasis, a free or fixed particle disease. Kidney Int. 46: 847-854, 1994.
19. Kumar, R. ClC-5 chloride channels and renal disease. Kidney Int. 53: 228-229, 1998.
20. Lieske, J. C., H. Swift, T. Martin, B. Patterson, and F. G. Toback. Renal epithelial cells rapidly bind and internalize calcium oxalate monohydrate crystals. Proc. Natl. Acad. Sci. USA 91: 6987-6991, 1994.
21. - channel from the renal cell line A6. Am. J. Physiol. Cell Physiol. 273: C1176-C1185, 1997.
22. Lloyd, S. E., W. Gunther, S. H. Pearce, A. Thomson, M. L. Bianchi, M. Bosio, I. W. Craig, S. E. Fisher, S. J. Scheinman, O. Wrong, T. J. Jentsch, and R. V. Thakker. Characterization of renal chloride channel, CLC-5, mutations in hypercalciuric nephrolithiasis (kidney stones) disorders. Hum. Mol. Genet. 6: 1233-1239, 1997.
23. Lloyd, S. E., S. H. Pearce, S. E. Fisher, K. Steinmeyer, B. Schwappach, S. J. Scheinman, B. Harding, A. Bolino, M. Devoto, P. Goodyer, S. P. Rigden, O. Wrong, T. J. Jentsch, I. W. Craig, and R. V. Thakker. A common molecular basis for three inherited kidney stone diseases. Nature 379: 445-449, 1996.
24. 2+ channels sensitive to dihydropyridines, and activated by hyperpolarizing voltages. Am. J. Physiol. Cell Physiol. 267: C157-C165, 1994.
25. Morimoto, T., S. Uchida, H. Sakamoto, Y. Kondo, H., Hanamizu, M. Fukui, Y. Tomino, N. Nagano, S. Sasaki, and F. Marumo. Mutations in CLC-5 chloride channel in Japanese patients with low molecular weight proteinuria. J. Am. Soc. Nephrol. 9: 811-818, 1998.
26. Obermuller, N. N. Gretz, W. Kris, R. F. Reilly, and R. Witxgall. The swelling-activated chloride channel ClC-2, the chloride channel ClC-3, and ClC-5 a chloride channel mutated in kidney stone disease, are expressed in distinct subpopulations of renal epithelial cells. J. Clin. Invest. 101: 635-642, 1998.
27. Ominato, M., T. Satoh, and A. I. Katz. Regulation of Na-K-ATPase activity in the proximal tubule: role of the protein kinase C pathway and of eicosanoids. J. Membr. Biol. 152: 235-243, 1996.
28. i cotransporter. Proc. Natl. Acad. Sci. USA 95: 1909-1914, 1998.
29. Reinhart, S. C., A. G. W. Nordem, M. Lapsley, R. V. Thakker, J. Pang, A. M. Moses, P. A. Frymoyer, M. J. Favus, J. A. Hoepner, and S. J. Scheinman. Characterization of carrier females and affected males with X-linked recessive nephrolithiasis. J. Am S. Nephr. 5: 1451-1461, 1993.
30. Rivkees, S. A., G. El-Hajj-Fuleihan, E. M. Brown, and J. D. Crawford. Tertiary hyperparathyroidism during high phosphate therapy of familial hypophosphatemic rickets. J. Clin. Endocrinol. Metab. 75: 1514-1518, 1992.
31. - channels. J. Biol. Chem. 271: 10210-10216, 1996.
32. Sasaki, S., S. Uchida, M. Kawasaki, S. Sasaki, S. Adachi, and F. Marumo. ClC family in the Kidney. Jpn. J. Physiol. 44: S3-S8, 1994.
33. Scheinman, S. J. X-linked hypercalciuric nephrolithiasis: clinical syndromes and chloride channel mutations. Kidney Int. 53: 3-17, 1998.
34. Shapiro, L. J. The genetic basis of X-linked nephrolithiasis: leaving no stone unturned (Abstract). J. Clin. Invest. 91: 2339, 1993.
35. Steinmeyer, K., B. Schwappach, M. Bens, A. Vandewalle, and T. J. Jentsch. Cloning and functional expression of rat ClC-5, a chloride channel related to kidney disease. J. Biol. Chem. 270: 31172-31177, 1995.
36. Stirn, J. A., A. A. Bernardo, and J. A. Arruda. The role of parathyroid hormone and vitamin D in acid excretion and extrarenal buffer mobilization. Miner. Electrolyte. Metab. 20: 60-71, 1994.
37. Strange, K., F. Emma, and P. S. Jackson. Cellular and molecular physiology of volume-sensitive anion channels. Am. J. Physiol. Cell Physiol. 270: C711-C730, 1996.
38. Strohmaier, W. L., R. D. Seeger, H. Osswald, and K. H. Bichler. Reduction of vitamin D induced stone formation by calcium. Urol. Res. 22: 301-303, 1994.
39. Suzuki, M., T. Morita, K. Hanaoka, Y. Kawagushi, and O. Sakai. A Cl- channel activated by parathyroid hormone in rabbit renal proximal tubule cells. J. Clin. Invest. 88: 735-742, 1991.
40. Thakker, R. V. The role of renal chloride channels mutations in kidney stone disease and nephrocalcinosis. Curr. Opin. Nephrol. Hypertens. 7: 385-388, 1998.