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Potassium Depletion Stimulates Beta-Subunit of Colonic H+-K+-ATPase in Mice

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DOI: 10.4236/ijcm.2013.45043    2,495 Downloads   3,689 Views   Citations

ABSTRACT

H+-K+-ATPase (HKA) is composed of two different subunits: an alpha and a beta subunit. Previous studies have shown that in the kidney gastric HKA (HKA alpha 1) predominates under normal dietary conditions while colonic HKA (HKA alpha 2) predominates under potassium depleted conditions [1]. The purpose of the current study was to elucidate the association between the beta and different alpha subunits from stomach, colon and kidney under normal and potassium depleted conditions. Black Swiss mice were fed a potassium-free diet for 2 weeks, beta subunit expression of HKA in stomach mucosae, colon mucosae and renal outer medulla was examined and compared between normal diet and potassium depleted diet. In wild type (WT) mice, the concentrations of the beta subunit under potassium deficient conditions were found significantly increased compared with normal dietary conditions in colon mucosae (8.27 ± 0.73 vs 6.62 ± 0.55 μg/μl, n = 7, p = 0.0416), whereas in cHKA (HKA alpha 2) mice colon mucosae, the concentrations of the beta subunit were statistically the same (5.05 ± 0.31 vs 4.76 ± 0.37 μg/μl, n = 13, p = 0.2833), and the concentration of the beta subunit stayed the same in renal outer medulla and stomach mucosae as well. The data indicate that potassium deficiency results in a significant increase in the levels of HKA beta subunit concentration in the colonic tissue of WT mice. The results indicate that the HKA beta subunit associates with the cHKA (HKA alpha 2) in order to mediate bicarbonate reabsorption under potassium depletion (hypokalemia)

Conflicts of Interest

The authors declare no conflicts of interest.

Cite this paper

G. Wei, J. Ravellette and S. Nakamura, "Potassium Depletion Stimulates Beta-Subunit of Colonic H+-K+-ATPase in Mice," International Journal of Clinical Medicine, Vol. 4 No. 5, 2013, pp. 244-250. doi: 10.4236/ijcm.2013.45043.

References

[1] S. Nakamura, “H+-ATPase Activity in Selective Disruption of H+K+-ATPase Alpha 1 Gene of Mice under Normal and K-Depleted Conditions,” Journal of Laboratory and Clinical Medicine, Vol. 147, No. 1, 2006, pp. 45-51. doi:10.1016/j.lab.2005.08.013
[2] C. Winter, N. Schulz, G. Giebisch, J. Geibel and C. Wagner, “Nongenomic Stimulation of Vacuolar H+-ATPases in Intercalated Renal Tubule Cells by Aldosterone,” Proceedings of the National Academy of Sciences of the United States of America, Vol. 101, No. 8, 2004, pp. 2636-2641. doi:10.1073/pnas.0307321101
[3] P. L. Pedersen and E. Carafoli, “Ion Motive ATPase. II,” Trends in Biochemical Sciences, Vol. 12, 1987, pp. 186-189.
[4] M. L. Gumz, D. Duda, R. McKenna, C. S. Wingo and B. D. Cain, “Molecular Modeling of the Rabbit Colonic (HKα2a) H+ K+ ATPase,” Journal of Molecular Modeling, Vol. 9, 2003, pp. 283-289. doi:10.1007/s00894-003-0140-2
[5] M. L. Gumz, I. J. Lynch, M. M. Greenlee, B. D. Cain and C. S. Wingo, “The Renal H+-K+-ATPases: Physiology, Regulation, and Structure,” Renal Physiology: American Journal of Physiology, Vol. 298, No. 1, 2010, pp. F12-F21. doi:10.1152/ajprenal.90723.2008
[6] P. Meneton, P. Schultheis, J. Greeb, et al., “Increased Sensitivity to K+ Deprivation in Colonic H,K-ATPase Deficient Mice,” Journal of Clinical Investigation, Vol. 101, No. 3, 1998, pp. 536-542. doi:10.1172/JCI1720
[7] S. Nakamura, H. Amlal, M. Soleimani and J. H. Galla, “Pathways for HCO3-Reabsorption in Mouse Medullary Collecting Duct Segments,” Journal of Laboratory and Clinical Medicine, Vol. 136, No. 3, 2000, pp. 218-223. doi:10.1067/mlc.2000.108750
[8] B. Bastani, “Co-Localization of H-ATPase and H,K-ATPase Immunoreactivity in the Rat Kidney,” Journal of the American Society of Nephrology, Vol. 5, 1995, pp. 1476-1482.
[9] C. S. Wingo, K. M. Madsen, A, Smolka and C. C. Tisher, “H+-K+-ATPase Immnoreactivity in Cortical and Outer Medullary Collecting Duct,” Kidney International, Vol. 38, 1995, pp. 985-990. doi:10.1038/ki.1990.302
[10] D. Yan, Y. Hu, S. Li and M. Cheng, “A Model of 3DStructure of H+K+-ATPase Catalytic Subunit Derived by Homology Modeling,” Acta Pharmacologica Sinica, Vol. 25, No. 4, 2004, pp. 474-479.
[11] K. Abe, K. Tani, T. Nishizawa and Y. Fujiyoshi, “InterSubunit Interaction of Gastric H+,K+-ATPase Prevents Reverse Reaction of the Transport Cycle,” The EMBO Journal, Vol. 28, No. 11, 2009, pp. 1637-1643. doi:10.1038/emboj.2009.102
[12] H. Thangarajah, A. Wong, D. C. Chow, J. M. Crothers and J. G. Forte, “Gastric H+-K+-ATPase and Acid-Resistant Surface Proteins,” American Journal of Physiology —Gastrointestinal and Liver Physiology, Vol. 282, 2002, pp. G953-G961.
[13] S. Nakamura, H. Amlal, M. Soleimani and J. H. Galla, “Colonic H+-K+-ATPase Is Induced and Mediates Increased HCO3-Reabsorption in Inner Medullary Collecing Duct in Potassium Depletion,” Kidney International, Vol. 54, No. 4, 1998, pp. 1233-1239. doi:10.1046/j.1523-1755.1998.00105.x
[14] S. Nakamura, Z. Wang, J. H. Galla and M. Soleimani, “K+ Depletion Increases HCO3-Reabsorption in OMCD by Activation of Colonic H+-K+-ATPase,” American Journal of Physiology, Vol. 274, No. 4, 1998, pp. F687-F692.
[15] Z. Spicer, M. L. Miller, A. Andringa, T. M. Riddle, J. J. Duffy, T. Doetschman and G. E. Shull, “Stomachs of Mice Lacking the Gastric H,K-ATPase Alpha-Subunit Have Achlorhydria, Abnormal Parietal Cells, and Ciliated Metaplasia,” The Journal of Biological Chemistry, Vol. 275, No. 28, 2000, pp. 21555-21565. doi:10.1074/jbc.M001558200
[16] P, Meneton, P. J. Schultheis, J. Greeb, M. L. Nieman, L. H. Liu, L. L. Clark, J. J. Duffy, T. Doetschman, J. N. Lorenz and G. E. Shull, “Increased Sensitivity to K+ Deprivation in Colonic H,K-ATPase-Deficient Mice,” Journal of Clinical Investigation, Vol. 101, No. 1, 1998, pp. 536-542. doi:10.1172/JCI1720
[17] P. Sangan, S. S. Kolla, V. M. Rajendran, M. Kashgarian amd H. J. Binder, “Colonic H+-K+-ATPase Beta-Subunit: Identification in Apical Membranes and Regulation by Dietary K Depletion,” American Journal of Physiology— Cell Physiology, Vol. 276, 1999, pp. C350-C360.
[18] J. Codina, J. T. Delmas-Mata and T. J. DuBose, “The Alpha-Subunit of the Colonic H+,K+-ATPase Assembles with Beta1-Subunits of Na+,K+-ATPase in Kidney and Distal Colon,” Journal of Biological Chemistry, Vol. 273, 1998, pp. 7894-7899. doi:10.1074/jbc.273.14.7894
[19] P. Chen, P. Mathews, P. Good, B. Rossier and K. Geering, “Unusual Degredation of α-β Complexes in Xenopus Oocytes by β-Subunits of Xenopus Gastric H-K-ATPase,” American Journal of Physiology, Vol. 275, No. 1, 1998, pp. C139-C145.
[20] A. V. Grishin, J. Reinhard, L. A. Dunbar, et al., “Nongastric H+,K+-ATPase: Cell Biologic and Functional Properties,” Seminars in Nephrology, Vol. 19, No. 5, 1999, pp. 421-430.
[21] V. M. Rajendran, P. Sangan, J. Geibel and H. J. Binder, “Oubain-Sensitive H,K-ATPase Functions as Na,K-ATPase in Apical Membranes of the Rat Distal Colon,” The Journal of Biological Chemistry, Vol. 275, 2000, pp. 13035-13040. doi:10.1074/jbc.275.17.13035
[22] M. S. Crowson and G. E. Shull, “Isolation and Characterization of a cDNA Encoding the Putative Distal Colon H,K-ATPase. Similarity of Deduced Amino Acid Sequence to Gastric H+-K+-ATPase and Na+-K+-ATPase, and mRNA Expression in Distal Colon, Kidney and Uterus,” Journal of Biological Chemistry, Vol. 167, 1992, pp. 13740-13748.
[23] J. A. Kraut, J. Hiura, M. Besancon, A. Smolka, G. Sachs and D. Scott, “Effect of Hypokalemia on the Abundance of HKalpha1 and HKalpha2 Protein in the Rat Kidney,” American Journal of Physiology, Vol. 272, No. 6, 1997, pp. F744-F750.
[24] T. D. Dubose, J. Codina, A. Burges and T. A. Pressley, “Regulation of H-K-ATPase Expression in the Kidney,” American Journal of Physiology, Vol. 269, 1995, pp. F500-F507.
[25] J. R. Dubose, D. Thomas, J. Codina and L Jian, “Molecular Diversity and Regulatory Heterogeneity of the H+-K+-ATPase in Kidney,” Mechanisms and Consequences of Proton Transport, 2002, pp. 53-58.
[26] A. V. Grishin, M. O. Bevensee, N. N. Modyanov, V. Rajendran, W. F. Boron and M. J. Caplan, “Functional Expression of the cDNA Encoded by the Human ATP1AL1 Gene,” American Journal of Physiology, Vol. 271, 1996, pp. F539-F551.
[27] G. Crambert, J. D. Horisberger, N. N. Modyanov and K. Geering, “Human Nongastric H+-K+-ATPase: Transport Properties of ATP1al1 Assembled with Different BetaSubunits,” Cell Physiology: American Journal of Physiology, Vol. 283, No. 1, 2002, pp. C305-C314.
[28] R. B. Silver and M. Soleimani, “H+-K+-ATPase: Regulation and Role in Pathophysiological States,” Renal Physiology: American Journal of Physiology, Vol. 276, 1999, pp. F799-F811.
[29] J. A. Kraut, J. Hiura, J. M. Shin, A. Smolka, G. Sachs and D. Scott, “The Na+K+ ATPase Beta 1 Subunit Is Associated with the HK Alpha 2 Protein in the Rat Kidney,” Kidney International, Vol. 53, No. 4, 1998, pp. 958-962. doi:10.1111/j.1523-1755.1998.00841.x

  
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