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Original Article

Calneuron 1 Increased Ca2+ in the Endoplasmic Reticulum and Aldosterone Production in Aldosterone-Producing AdenomaNovelty and Significance

Kazuhiro Kobuke, Kenji Oki, Celso E. Gomez-Sanchez, Elise P. Gomez-Sanchez, Haruya Ohno, Kiyotaka Itcho, Yoko Yoshii, Masayasu Yoneda, Noboru Hattori
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https://doi.org/10.1161/HYPERTENSIONAHA.117.10205
Hypertension. 2018;71:125-133
Originally published November 6, 2017
Kazuhiro Kobuke
From the Department of Molecular and Internal Medicine, Graduate School of Biomedical and Health Sciences, Hiroshima University, Japan (K.K., K.O., H.O., K.I., Y.Y., M.Y., N.H.); Division of Endocrinology, G.V. (Sonny) Montgomery VA Medical Center, Jackson, MS (C.E.G.-S., E.P.G.-S.); and University of Mississippi Medical Center, Jackson (C.E.G.-S., E.P.G.-S.).
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Kenji Oki
From the Department of Molecular and Internal Medicine, Graduate School of Biomedical and Health Sciences, Hiroshima University, Japan (K.K., K.O., H.O., K.I., Y.Y., M.Y., N.H.); Division of Endocrinology, G.V. (Sonny) Montgomery VA Medical Center, Jackson, MS (C.E.G.-S., E.P.G.-S.); and University of Mississippi Medical Center, Jackson (C.E.G.-S., E.P.G.-S.).
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Celso E. Gomez-Sanchez
From the Department of Molecular and Internal Medicine, Graduate School of Biomedical and Health Sciences, Hiroshima University, Japan (K.K., K.O., H.O., K.I., Y.Y., M.Y., N.H.); Division of Endocrinology, G.V. (Sonny) Montgomery VA Medical Center, Jackson, MS (C.E.G.-S., E.P.G.-S.); and University of Mississippi Medical Center, Jackson (C.E.G.-S., E.P.G.-S.).
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Elise P. Gomez-Sanchez
From the Department of Molecular and Internal Medicine, Graduate School of Biomedical and Health Sciences, Hiroshima University, Japan (K.K., K.O., H.O., K.I., Y.Y., M.Y., N.H.); Division of Endocrinology, G.V. (Sonny) Montgomery VA Medical Center, Jackson, MS (C.E.G.-S., E.P.G.-S.); and University of Mississippi Medical Center, Jackson (C.E.G.-S., E.P.G.-S.).
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Haruya Ohno
From the Department of Molecular and Internal Medicine, Graduate School of Biomedical and Health Sciences, Hiroshima University, Japan (K.K., K.O., H.O., K.I., Y.Y., M.Y., N.H.); Division of Endocrinology, G.V. (Sonny) Montgomery VA Medical Center, Jackson, MS (C.E.G.-S., E.P.G.-S.); and University of Mississippi Medical Center, Jackson (C.E.G.-S., E.P.G.-S.).
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Kiyotaka Itcho
From the Department of Molecular and Internal Medicine, Graduate School of Biomedical and Health Sciences, Hiroshima University, Japan (K.K., K.O., H.O., K.I., Y.Y., M.Y., N.H.); Division of Endocrinology, G.V. (Sonny) Montgomery VA Medical Center, Jackson, MS (C.E.G.-S., E.P.G.-S.); and University of Mississippi Medical Center, Jackson (C.E.G.-S., E.P.G.-S.).
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Yoko Yoshii
From the Department of Molecular and Internal Medicine, Graduate School of Biomedical and Health Sciences, Hiroshima University, Japan (K.K., K.O., H.O., K.I., Y.Y., M.Y., N.H.); Division of Endocrinology, G.V. (Sonny) Montgomery VA Medical Center, Jackson, MS (C.E.G.-S., E.P.G.-S.); and University of Mississippi Medical Center, Jackson (C.E.G.-S., E.P.G.-S.).
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Masayasu Yoneda
From the Department of Molecular and Internal Medicine, Graduate School of Biomedical and Health Sciences, Hiroshima University, Japan (K.K., K.O., H.O., K.I., Y.Y., M.Y., N.H.); Division of Endocrinology, G.V. (Sonny) Montgomery VA Medical Center, Jackson, MS (C.E.G.-S., E.P.G.-S.); and University of Mississippi Medical Center, Jackson (C.E.G.-S., E.P.G.-S.).
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Noboru Hattori
From the Department of Molecular and Internal Medicine, Graduate School of Biomedical and Health Sciences, Hiroshima University, Japan (K.K., K.O., H.O., K.I., Y.Y., M.Y., N.H.); Division of Endocrinology, G.V. (Sonny) Montgomery VA Medical Center, Jackson, MS (C.E.G.-S., E.P.G.-S.); and University of Mississippi Medical Center, Jackson (C.E.G.-S., E.P.G.-S.).
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  • RE: Mitochondria Are Not to be Forgotten.
    Kenji Oki, Kazuhiro Kobuke, Elise P. Gomez-Sanchez and Celso E. Gomez-Sanchez
    Published on January 8, 2018
  • RE: Calneuron 1 Increased Ca2+ in the Endoplasmic Reticulum and Aldosterone Production in Aldosterone-Producing Adenoma: Mitochondria Are Not to be Forgotten.
    Verdiana Ravarotto, Sofia Zanin and GianPaolo Rossi
    Published on December 13, 2017
  • Published on January 8, 2018
    RE: Mitochondria Are Not to be Forgotten.
    • Kenji Oki, Assistant Professor, Department of Molecular and Internal Medicine, Hiroshima University
    • Other Contributors:
      • Kazuhiro Kobuke, Graduate school student, Department of Molecular and Internal Medicine
      • Elise P. Gomez-Sanchez, Professor, Department of Pharmacology & Toxicology
      • Celso E. Gomez-Sanchez, Professor, Division of Endocrinology

    We appreciate the chance to discuss the letter of Ravarotto et al regarding to our paper 1. They raise the issue of hyperparathyroidism secondary to increased calcium excretion in hyperaldosteronism 2 and its potential influence on intracellular Ca2+. Administration of aldosterone Na+ excess to rats increases urinary calcium, decreases serum Ca2+, increases parathyroid hormone, and increases cytosolic Ca2+ in the heart and other tissues 3. By extrapolation, cytosolic calcium in adrenal cells may also be increased, though this was not studied. Parathyroid hormone also increases angiotensin II- and potassium-stimulated aldosterone biosynthesis in bovine zona glomerulosa cells and produces a mild increase in cytosolic calcium 4. As Ravarotto, et al. stated, stored Ca2+ in endoplasmic reticulum (ER) is transferred to mitochondria, thus the ER network has a pivotal role in the maintenance of multiple vital Ca2+-dependent processes 5. Rapid release of Ca2+ from the ER results in transient Ca2+ increases in the mitochondria stimulates activity of the CYP11B2 enzyme in adrenal glomerulosa cells and has pro-survival effects 6-8. Excessive increases in mitochondrial Ca2+ concentration for a prolonged time induce the opening of the mitochondrial permeability transition pore, and induces apoptotic or necrotic cell death. Stored Ca2+ in ER is also released to the nuclei and cytosol 9. Our study focused on cytosolic Ca2+ and clarified that increased Ca2+ leads to a sequence of eve...

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    We appreciate the chance to discuss the letter of Ravarotto et al regarding to our paper 1. They raise the issue of hyperparathyroidism secondary to increased calcium excretion in hyperaldosteronism 2 and its potential influence on intracellular Ca2+. Administration of aldosterone Na+ excess to rats increases urinary calcium, decreases serum Ca2+, increases parathyroid hormone, and increases cytosolic Ca2+ in the heart and other tissues 3. By extrapolation, cytosolic calcium in adrenal cells may also be increased, though this was not studied. Parathyroid hormone also increases angiotensin II- and potassium-stimulated aldosterone biosynthesis in bovine zona glomerulosa cells and produces a mild increase in cytosolic calcium 4. As Ravarotto, et al. stated, stored Ca2+ in endoplasmic reticulum (ER) is transferred to mitochondria, thus the ER network has a pivotal role in the maintenance of multiple vital Ca2+-dependent processes 5. Rapid release of Ca2+ from the ER results in transient Ca2+ increases in the mitochondria stimulates activity of the CYP11B2 enzyme in adrenal glomerulosa cells and has pro-survival effects 6-8. Excessive increases in mitochondrial Ca2+ concentration for a prolonged time induce the opening of the mitochondrial permeability transition pore, and induces apoptotic or necrotic cell death. Stored Ca2+ in ER is also released to the nuclei and cytosol 9. Our study focused on cytosolic Ca2+ and clarified that increased Ca2+ leads to a sequence of events that increase CYP11B2 transcription 1. This is compatible with data demonstrating that increased Ca2+ availability via the ER-mitochondria network and mitochondrial NADPH-Ca2+ stimulates CYP11B2 activity, resulting in aldosterone synthesis 6.
    Thus, based on the results of our study, we suggest that increased CALN1 expression in APA is associated with elevated Ca2+ storage in ER, leading to a sequence of events that culminate in stimulating CYP11B2 transcription and aldosterone overproduction. Thus CALN1 would be a potential therapeutic target for excess of aldosterone production.

    References
    1. Kobuke K, Oki K, Gomez-Sanchez CE, Gomez-Sanchez EP, Ohno H, Itcho K, Yoshii Y, Yoneda M, Hattori N. Calneuron 1 increased ca(2+) in the endoplasmic reticulum and aldosterone production in aldosterone-producing adenoma. Hypertension. 2018;71:125-133.
    2. Rossi GP, Ragazzo F, Seccia TM, Maniero C, Barisa M, Calo LA, Frigo AC, Fassina A, Pessina AC. Hyperparathyroidism can be useful in the identification of primary aldosteronism due to aldosterone-producing adenoma. Hypertension. 2012;60:431-436.
    3. Chhokar VS, Sun Y, Bhattacharya SK, Ahokas RA, Myers LK, Xing Z, Smith RA, Gerling IC, Weber KT. Hyperparathyroidism and the calcium paradox of aldosteronism. Circulation. 2005;111:871-878.
    4. Isales CM, Barrett PQ, Brines M, Bollag W, Rasmussen H. Parathyroid hormone modulates angiotensin ii-induced aldosterone secretion from the adrenal glomerulosa cell. Endocrinology. 1991;129:489-495.
    5. Rowland AA, Chitwood PJ, Phillips MJ, Voeltz GK. Er contact sites define the position and timing of endosome fission. Cell. 2014;159:1027-1041.
    6. Spat A, Szanda G. Special features of mitochondrial ca(2)(+) signalling in adrenal glomerulosa cells. Pflugers Arch. 2012;464:43-50.
    7. Bonora M, Morganti C, Morciano G, Pedriali G, Lebiedzinska-Arciszewska M, Aquila G, Giorgi C, Rizzo P, Campo G, Ferrari R, Kroemer G, Wieckowski MR, Galluzzi L, Pinton P. Mitochondrial permeability transition involves dissociation of f1fo atp synthase dimers and c-ring conformation. EMBO Rep. 2017;18:1077-1089.
    8. Bonora M, Giorgi C, Bononi A, Marchi S, Patergnani S, Rimessi A, Rizzuto R, Pinton P. Subcellular calcium measurements in mammalian cells using jellyfish photoprotein aequorin-based probes. Nat Protoc. 2013;8:2105-2118.
    9. Kaufman RJ, Malhotra JD. Calcium trafficking integrates endoplasmic reticulum function with mitochondrial bioenergetics. Biochim Biophys Acta. 2014;1843:2233-2239.

    Show Less
    Competing Interests: None declared.
  • Published on December 13, 2017
    RE: Calneuron 1 Increased Ca2+ in the Endoplasmic Reticulum and Aldosterone Production in Aldosterone-Producing Adenoma: Mitochondria Are Not to be Forgotten.
    • Verdiana Ravarotto, Post-doc, Department of Medicine DIMED, University of Padova
    • Other Contributors:
      • Sofia Zanin, Post-doc
      • GianPaolo Rossi, Professor

    Kobuke and coworkers should be commended for pinpointing the role of Ca2+ in the endoplasmic reticulum (ER) and the importance of the Ca2+ binding protein Calneuron 1 (CALN1) in the over production of aldosterone in aldosterone producing adenoma (APA), one of the most common cause of human primary aldosteronism (PA) 1. Although the role of Ca2+ in aldosterone biosynthesis is unambiguously known, their findings deserve some comments. Rats made aldosteronemic develop hypercalciuria, with ensuing decrease of hypocalcemia and hyperparathyroidism 2. Likewise, APA patients have low serum Ca2+, with ensuing secondary hyperparathyroidism, both of which corrected by adrenalectomy 3–5. The increase in CALN1 can thus be an adaptive response of APA cells to the chronic hypercalcemia. Moreover, the final step of aldosterone synthesis occurs in the mitochondria, because such organelles contain the NADPH-Ca2+-dependent aldosterone synthase and generate the reactive oxygen species, which are necessary for conversion of deoxycorticosterone to aldosterone. This fact would be difficult to reconcile with the role of CALN1 in increasing Ca2+ stores in the ER if there weren’t specialized regions 6,7 of contact between ER and mitochondria. In the last decades, compelling experimental evidences shed light on the functions of qualified ER-mitochondria contact sites, known as mitochondrial-associated membrane (MAMs). MAMs are dynamics structures that play a fundamental role in coordinating lipid s...

    Show More

    Kobuke and coworkers should be commended for pinpointing the role of Ca2+ in the endoplasmic reticulum (ER) and the importance of the Ca2+ binding protein Calneuron 1 (CALN1) in the over production of aldosterone in aldosterone producing adenoma (APA), one of the most common cause of human primary aldosteronism (PA) 1. Although the role of Ca2+ in aldosterone biosynthesis is unambiguously known, their findings deserve some comments. Rats made aldosteronemic develop hypercalciuria, with ensuing decrease of hypocalcemia and hyperparathyroidism 2. Likewise, APA patients have low serum Ca2+, with ensuing secondary hyperparathyroidism, both of which corrected by adrenalectomy 3–5. The increase in CALN1 can thus be an adaptive response of APA cells to the chronic hypercalcemia. Moreover, the final step of aldosterone synthesis occurs in the mitochondria, because such organelles contain the NADPH-Ca2+-dependent aldosterone synthase and generate the reactive oxygen species, which are necessary for conversion of deoxycorticosterone to aldosterone. This fact would be difficult to reconcile with the role of CALN1 in increasing Ca2+ stores in the ER if there weren’t specialized regions 6,7 of contact between ER and mitochondria. In the last decades, compelling experimental evidences shed light on the functions of qualified ER-mitochondria contact sites, known as mitochondrial-associated membrane (MAMs). MAMs are dynamics structures that play a fundamental role in coordinating lipid synthesis, mitochondria metabolism, and Ca2+ transfer regulating key cellular processes, namely mitochondrial morphology, reactive oxygen species (ROS)-induced cell stress, autophagy, and apoptosis 8. Accordingly, disruptions in the ER-mitochondria tethers network has recently been involved in the pathogenesis of several diseases. By pointing to CALN1 in ER and cellular Ca2+ handling, Kobuke et al. findings strongly support a connection via MAMs between ER Ca2+ accumulation and activation of aldosterone biosynthesis through increased mitochondrial Ca2+.
    1. Rossi GP, Bernini G, Caliumi C, Desideri G, Fabris B, Ferri C, Ganzaroli C, Giachetti G, Letizia C, Maccario M, et al. A prospective study of the prevalence of primary aldosteronism in 1,125 hypertensive patients. J Am Coll Cardiol. 2006;48:2293-300
    2. Chhokar VS, Sun Y, Bhattacharya SK, Ahokas RA, Myers LK, Xing Z, Smith RA, Gerling IC, Weber KT. Hyperparathyroidism and the calcium paradox of aldosteronism. Circulation. 2005;111:871–878.
    3. Maniero C, Fassina A, Seccia TM, Toniato A, Iacobone M, Plebani M, Caro R De, Calo LA, Pessina AC, Rossi GP. Mild hyperparathyroidism: a novel surgically correctable feature of primary aldosteronism. J Hypertens. 2012;30:390–395.
    4. Maniero C, Fassina A, Guzzardo V, Lenzini L, Amadori G, Pelizzo MR, Gomez-Sanchez C, Rossi GP. Primary hyperparathyroidism with concurrent primary aldosteronism. Hypertension. 2011;58:341–346.
    5. Rossi GP, Ragazzo F, Seccia TM, Maniero C, Barisa M, Calo LA, Frigo AC, Fassina A, Pessina AC. Hyperparathyroidism can be useful in the identification of primary aldosteronism due to aldosterone-producing adenoma. Hypertension. 2012;60:431–436.
    6. Giorgi C, De Stefani D, Bononi A, Rizzuto R, Pinton P. Structural and functional link between the mitochondrial network and the endoplasmic reticulum. Int J Biochem Cell Biol. 2009;41:1817-1827
    7. Hayashi T, Rizzuto R, Hajnoczky G, Su TP. MAM: more than just a housekeeper. Trends Cell Biol. 2009;19(2):81-88
    8. Rodríguez-Arribas M, Yakhine-DiopJ SMS, Bravo-San Pedro JM, Gómez-Suaga P, Gómez-Sánchez R, Martínez-Chacón G, Fuentes JM, González-Polo RA, Niso-Santano M. Mitochondria-Associated Membranes (MAMs): Overview and its role in Parkinson’s disease. Molecular Neurobiology.2016; 54:6287-6303

    Show Less
    Competing Interests: None declared.
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    Calneuron 1 Increased Ca2+ in the Endoplasmic Reticulum and Aldosterone Production in Aldosterone-Producing AdenomaNovelty and Significance
    Kazuhiro Kobuke, Kenji Oki, Celso E. Gomez-Sanchez, Elise P. Gomez-Sanchez, Haruya Ohno, Kiyotaka Itcho, Yoko Yoshii, Masayasu Yoneda and Noboru Hattori
    Hypertension. 2018;71:125-133, originally published November 6, 2017
    https://doi.org/10.1161/HYPERTENSIONAHA.117.10205

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    Calneuron 1 Increased Ca2+ in the Endoplasmic Reticulum and Aldosterone Production in Aldosterone-Producing AdenomaNovelty and Significance
    Kazuhiro Kobuke, Kenji Oki, Celso E. Gomez-Sanchez, Elise P. Gomez-Sanchez, Haruya Ohno, Kiyotaka Itcho, Yoko Yoshii, Masayasu Yoneda and Noboru Hattori
    Hypertension. 2018;71:125-133, originally published November 6, 2017
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