Deficiency of WFS1 leads to the impairment of AVP secretion under dehydration in male mice.


Journal

Pituitary
ISSN: 1573-7403
Titre abrégé: Pituitary
Pays: United States
ID NLM: 9814578

Informations de publication

Date de publication:
Aug 2021
Historique:
accepted: 08 02 2021
pubmed: 6 3 2021
medline: 15 12 2021
entrez: 5 3 2021
Statut: ppublish

Résumé

Wolfram syndrome (WS) is mainly caused by mutations in the WFS1 gene and characterized by diabetes mellitus, optic atrophy, hearing loss, and central diabetes insipidus (CDI). WFS1 is an endoplasmic reticulum (ER)-resident transmembrane protein, and Wfs1 knockout (Wfs1-/-) mice, which have been used as a mouse model for WS, reportedly manifested impairment of glucose tolerance due to pancreatic β-cell loss. In the present study, we examined water balance, arginine vasopressin (AVP) secretion, and ER stress in AVP neurons of the hypothalamus in Wfs1-/- mice. There were no differences in urine volumes between Wfs1-/- and wild-type mice with free access to water. Conversely, when mice were subjected to intermittent water deprivation (WD) for 20 weeks, during which water was unavailable for 2 days a week, urine volumes were larger in Wfs1-/- mice, accompanied by lower urine AVP concentrations and urine osmolality, compared to wild-type mice. The mRNA expression of immunoglobulin heavy chain binding protein, a marker of ER stress, was significantly increased in the supraoptic nucleus and paraventricular nuclei in Wfs1-/- mice compared to wild-type mice after WD. Our results thus showed that Wfs1 knockout leads to a decrease in AVP secretion during dehydration, which could explain in part the mechanisms by which Wfs1 mutations cause CDI in humans.

Identifiants

pubmed: 33666833
doi: 10.1007/s11102-021-01135-6
pii: 10.1007/s11102-021-01135-6
doi:

Substances chimiques

Membrane Proteins 0
wolframin protein 0
Water 059QF0KO0R

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

582-588

Informations de copyright

© 2021. The Author(s), under exclusive licence to Springer Science+Business Media, LLC part of Springer Nature.

Références

Sano R, Reed JC (2013) ER stress-induced cell death mechanisms. Biochim Biophys Acta Mol Cell Res 1833:3460–3470. https://doi.org/10.1016/j.bbamcr.2013.06.028
doi: 10.1016/j.bbamcr.2013.06.028
Zhang IX, Raghavan M, Satin LS (2020) The endoplasmic reticulum and calcium homeostasis in pancreatic beta cells. Endocrinol (United States) 161:1–14. https://doi.org/10.1210/endocr/bqz028
doi: 10.1210/endocr/bqz028
Haze K, Yoshida H, Yanagi H et al (1999) Mammalian transcription factor ATF6 is synthesized as a transmembrane protein and activated by proteolysis in response to endoplasmic reticulum stress. Mol Biol Cell 10:3787–3799. https://doi.org/10.1091/mbc.10.11.3787
doi: 10.1091/mbc.10.11.3787 pubmed: 10564271 pmcid: 25679
Yoshida H, Okada T, Haze K et al (2000) ATF6 activated by proteolysis binds in the presence of NF-Y (CBF) directly to the cis-acting element responsible for the mammalian unfolded protein response. Mol Cell Biol 20:6755–6767. https://doi.org/10.1128/mcb.20.18.6755-6767.2000
doi: 10.1128/mcb.20.18.6755-6767.2000 pubmed: 10958673 pmcid: 86199
Wang M, Wey S, Zhang Y et al (2009) Role of the unfolded protein response regulator GRP78/BiP in development, cancer, and neurological disorders. Antioxidants Redox Signal 11:2307–2316. https://doi.org/10.1089/ars.2009.2485
doi: 10.1089/ars.2009.2485
Bisset GW, Chowdrey HS (1988) Control of release of vasopressin by neuroendocrine reflexes. Q J Exp Physiol 73:811–872. https://doi.org/10.1113/expphysiol.1988.sp003223
doi: 10.1113/expphysiol.1988.sp003223 pubmed: 2907166
Hagiwara D, Arima H, Morishita Y et al (2012) BiP mRNA expression is upregulated by dehydration in vasopressin neurons in the hypothalamus in mice. Peptides 33:346–350. https://doi.org/10.1016/j.peptides.2011.12.011
doi: 10.1016/j.peptides.2011.12.011 pubmed: 22230548
Arima H, Azuma Y, Morishita Y, Hagiwara D (2016) Central diabetes insipidus. Nagoya J Med Sci 78:349–357. https://doi.org/10.18999/nagjms.78.4.349
doi: 10.18999/nagjms.78.4.349 pubmed: 28008190 pmcid: 5159460
Hayashi M, Arima H, Ozaki N et al (2009) Progressive polyuria without vasopressin neuron loss in a mouse model for familial neurohypophysial diabetes insipidus. Am J Physiol Regul Integr Comp Physiol 296:1641–1649. https://doi.org/10.1152/ajpregu.00034.2009
doi: 10.1152/ajpregu.00034.2009
Hagiwara D, Arima H, Morishita Y et al (2014) Arginine vasopressin neuronal loss results from autophagy-associated cell death in a mouse model for familial neurohypophysial diabetes insipidus. Cell Death Dis. https://doi.org/10.1038/cddis.2014.124
doi: 10.1038/cddis.2014.124 pubmed: 24675466 pmcid: 3973212
Hagiwara D, Grinevich V, Arima H (2019) A novel mechanism of autophagy-associated cell death of vasopressin neurons in familial neurohypophysial diabetes insipidus. Cell Tissue Res 375:259–266. https://doi.org/10.1007/s00441-018-2872-4
doi: 10.1007/s00441-018-2872-4 pubmed: 29961215
Davies J, Murphy D (2002) Autophagy in hypothalamic neurones of rats expressing a familial neurohypophysical diabetes insipidus transgene. J Neuroendocrinol 14:629–637. https://doi.org/10.1046/j.1365-2826.2002.00822.x
doi: 10.1046/j.1365-2826.2002.00822.x pubmed: 12153465
Russell TA, Ito M, Ito M et al (2003) A murine model of autosomal dominant neurohypophyseal diabetes insipidus reveals progressive loss of vasopressin-producing neurons. J Clin Invest 112:1697–1706. https://doi.org/10.1172/JCI200318616
doi: 10.1172/JCI200318616 pubmed: 14660745 pmcid: 281642
Inoue H, Tanizawa Y, Wasson J et al (1998) A gene encoding a transmembrane protein is mutated in patients with diabetes mellitus and optic atrophy (Wolfram syndrome). Nat Genet 20:143–148. https://doi.org/10.1038/2441
doi: 10.1038/2441 pubmed: 9771706
Strom TM, Hörtnagel K, Hofmann S et al (1998) Diabetes insipidus, diabetes mellitus, optic atrophy and deafness (DIDMOAD) caused by mutations in a novel gene (wolframin) coding for a predicted transmembrane protein. Hum Mol Genet 7:2021–2028. https://doi.org/10.1093/hmg/7.13.2021
doi: 10.1093/hmg/7.13.2021 pubmed: 9817917
Takeda K, Inoue H, Tanizawa Y et al (2001) WFS1 (Wolfram syndrome 1) gene product: predominant subcellular localization to endoplasmic reticulum in cultured cells and neuronal expression in rat brain. Hum Mol Genet 10:477–484. https://doi.org/10.1093/hmg/10.5.477
doi: 10.1093/hmg/10.5.477 pubmed: 11181571
Ueda K, Kawano J, Takeda K et al (2005) Endoplasmic reticulum stress induces Wfs1 gene expression in pancreatic β-cells via transcriptional activation. Eur J Endocrinol 153:167–176. https://doi.org/10.1530/eje.1.01945
doi: 10.1530/eje.1.01945 pubmed: 15994758
Fonseca SG, Ishigaki S, Oslowski CM et al (2010) Wolfram syndrome 1 gene negatively regulates ER stress signaling in rodent and human cells. J Clin Invest 120:744–755. https://doi.org/10.1172/JCI39678
doi: 10.1172/JCI39678 pubmed: 20160352 pmcid: 2827948
Angebault C, Fauconnier J, Patergnani S et al (2018) ER-mitochondria cross-talk is regulated by the Ca
doi: 10.1126/scisignal.aaq1380 pubmed: 30352948
Bundey SEMAFBT (1995) Neurodegeneration and diabetes: UK nationwide study of Wolfram (DIDMOAD) syndrome. Lancet 346:1458–1463. https://doi.org/10.1016/S0140-6736(95)92473-6
doi: 10.1016/S0140-6736(95)92473-6 pubmed: 7490992
Smith CJA, Crock PA, King BR et al (2004) Phenotype-genotype correlations in a series of Wolfram syndrome families. Diabetes Care 27:2003–2009. https://doi.org/10.2337/diacare.27.8.2003
doi: 10.2337/diacare.27.8.2003 pubmed: 15277431
Matsunaga K, Tanabe K, Inoue H et al (2014) Wolfram syndrome in the japanese population; molecular analysis of wfs1 gene and characterization of clinical features. PLoS ONE. https://doi.org/10.1371/journal.pone.0106906
doi: 10.1371/journal.pone.0106906 pubmed: 25211237 pmcid: 4161373
Medlej R, Wasson J, Baz P et al (2004) Diabetes mellitus and optic atrophy: a study of Wolfram syndrome in the Lebanese population. J Clin Endocrinol Metab 89:1656–1661. https://doi.org/10.1210/jc.2002-030015
doi: 10.1210/jc.2002-030015 pubmed: 15070927
Ishihara H, Takeda S, Tamura A et al (2004) Disruption of the WFS1 gene in mice causes progressive β-cell loss and impaired stimulus—secretion coupling in insulin secretion. Hum Mol Genet 13:1159–1170. https://doi.org/10.1093/hmg/ddh125
doi: 10.1093/hmg/ddh125 pubmed: 15056606
Plaas M, Seppa K, Reimets R et al (2017) Wfs1-deficient rats develop primary symptoms of Wolfram syndrome: insulin-dependent diabetes, optic nerve atrophy and medullary degeneration. Sci Rep. https://doi.org/10.1038/s41598-017-09392-x
doi: 10.1038/s41598-017-09392-x pubmed: 28860598 pmcid: 5579261
Akiyama M, Hatanaka M, Ohta Y et al (2009) Increased insulin demand promotes while pioglitazone prevents pancreatic beta cell apoptosis in Wfs1 knockout mice. Diabetologia 52:653–663. https://doi.org/10.1007/s00125-009-1270-6
doi: 10.1007/s00125-009-1270-6 pubmed: 19190890
Kawaguchi Y, Hagiwara D, Miyata T et al (2020) Endoplasmic reticulum chaperone BiP/GRP78 knockdown leads to autophagy and cell death of arginine vasopressin neurons in mice. Sci Rep. https://doi.org/10.1038/s41598-020-76839-z
doi: 10.1038/s41598-020-76839-z pubmed: 33339950 pmcid: 7749174
Azuma Y, Hagiwara D, Lu W et al (2014) Activating transcription factor 6α is required for the vasopressin neuron system to maintain water balance under dehydration in male mice. Endocrinology 155:4905–4914. https://doi.org/10.1210/en.2014-1522
doi: 10.1210/en.2014-1522 pubmed: 25203138
Tochiya M, Hagiwara D, Azuma Y et al (2018) Chemical chaperone 4-phenylbutylate reduces mutant protein accumulation in the endoplasmic reticulum of arginine vasopressin neurons in a mouse model for familial neurohypophysial diabetes insipidus. Neurosci Lett 682:50–55. https://doi.org/10.1016/j.neulet.2018.06.013
doi: 10.1016/j.neulet.2018.06.013 pubmed: 29886132
Cryns K, Thys S, Van Laer L et al (2003) The WFS1 gene, responsible for low frequency sensorineural hearing loss and Wolfram syndrome, is expressed in a variety of inner ear cells. Histochem Cell Biol 119:247–256. https://doi.org/10.1007/s00418-003-0495-6
doi: 10.1007/s00418-003-0495-6 pubmed: 12649740
Ben-Barak Y, Russell JT, Whitnall M et al (1984) Phylogenetic cross-reactivities of monoclonal antibodies produced against rat neurophysin. Cell Mol Neurobiol 4:339–349. https://doi.org/10.1007/BF00733596
doi: 10.1007/BF00733596 pubmed: 6085284
Ben-Barak Y, Russell JT, Whitnall MH et al (1985) Neurophysin in the hypothalamo-neurohypophysial system. I. Production and characterization of monoclonal antibodies. J Neurosci 5:81–97. https://doi.org/10.1523/jneurosci.05-01-00081.1985
doi: 10.1523/jneurosci.05-01-00081.1985 pubmed: 3880813 pmcid: 6565074
Kõks S, Soomets U, Paya-Cano JL et al (2009) Wfs1 gene deletion causes growth retardation in mice and interferes with the growth hormone pathway. Physiol Genom 37:249–259. https://doi.org/10.1152/physiolgenomics.90407.2008.-The
doi: 10.1152/physiolgenomics.90407.2008.-The
Kawano J, Tanizawa Y, Shinoda K (2008) Wolfram syndrome 1 (WFS1) gene expression in the normal mouse visual system. J Comp Neurol 510:1–23. https://doi.org/10.1002/cne.21734
doi: 10.1002/cne.21734 pubmed: 18613120
Kawano J, Fujinaga R, Yamamoto-Hanada K et al (2009) Wolfram syndrome 1 (Wfs1) mRNA expression in the normal mouse brain during postnatal development. Neurosci Res 64:213–230. https://doi.org/10.1016/j.neures.2009.03.005
doi: 10.1016/j.neures.2009.03.005 pubmed: 19428703
Babey M, Kopp P, Robertson GL (2011) Familial forms of diabetes insipidus: clinical and molecular characteristics. Nat Rev Endocrinol 7:701–714. https://doi.org/10.1038/nrendo.2011.100
doi: 10.1038/nrendo.2011.100 pubmed: 21727914
Bonnet Wersinger D, Benkafadar N, Jagodzinska J et al (2014) Impairment of visual function and retinal ER stress activation in Wfs1-deficient mice. PLoS ONE. https://doi.org/10.1371/journal.pone.0097222
doi: 10.1371/journal.pone.0097222 pubmed: 24823368 pmcid: 4019519
Riggs AC, Bernal-Mizrachi E, Ohsugi M et al (2005) Mice conditionally lacking the Wolfram gene in pancreatic islet beta cells exhibit diabetes as a result of enhanced endoplasmic reticulum stress and apoptosis. Diabetologia 48:2313–2321. https://doi.org/10.1007/s00125-005-1947-4
doi: 10.1007/s00125-005-1947-4 pubmed: 16215705
Lee AS (2001) The glucose-regulated proteins: stress induction and clinical applications. Trends Biochem Sci 26:504–510. https://doi.org/10.1016/S0968-0004(01)01908-9
doi: 10.1016/S0968-0004(01)01908-9 pubmed: 11504627
Lee AS (2005) The ER chaperone and signaling regulator GRP78/BiP as a monitor of endoplasmic reticulum stress. Methods 35:373–381. https://doi.org/10.1016/j.ymeth.2004.10.010
doi: 10.1016/j.ymeth.2004.10.010 pubmed: 15804610

Auteurs

Junki Kurimoto (J)

Department of Endocrinology and Diabetes, Nagoya University Graduate School of Medicine, 65 Tsurumai-cho, Showa-ku, Nagoya, 466-8550, Japan.

Hiroshi Takagi (H)

Department of Endocrinology and Diabetes, Nagoya University Graduate School of Medicine, 65 Tsurumai-cho, Showa-ku, Nagoya, 466-8550, Japan.

Takashi Miyata (T)

Department of Endocrinology and Diabetes, Nagoya University Graduate School of Medicine, 65 Tsurumai-cho, Showa-ku, Nagoya, 466-8550, Japan.

Yuichi Hodai (Y)

Department of Endocrinology and Diabetes, Nagoya University Graduate School of Medicine, 65 Tsurumai-cho, Showa-ku, Nagoya, 466-8550, Japan.

Yohei Kawaguchi (Y)

Department of Endocrinology and Diabetes, Nagoya University Graduate School of Medicine, 65 Tsurumai-cho, Showa-ku, Nagoya, 466-8550, Japan.

Daisuke Hagiwara (D)

Department of Endocrinology and Diabetes, Nagoya University Graduate School of Medicine, 65 Tsurumai-cho, Showa-ku, Nagoya, 466-8550, Japan.

Hidetaka Suga (H)

Department of Endocrinology and Diabetes, Nagoya University Graduate School of Medicine, 65 Tsurumai-cho, Showa-ku, Nagoya, 466-8550, Japan.

Tomoko Kobayashi (T)

Department of Endocrinology and Diabetes, Nagoya University Graduate School of Medicine, 65 Tsurumai-cho, Showa-ku, Nagoya, 466-8550, Japan.

Mariko Sugiyama (M)

Department of Endocrinology and Diabetes, Nagoya University Graduate School of Medicine, 65 Tsurumai-cho, Showa-ku, Nagoya, 466-8550, Japan.

Takeshi Onoue (T)

Department of Endocrinology and Diabetes, Nagoya University Graduate School of Medicine, 65 Tsurumai-cho, Showa-ku, Nagoya, 466-8550, Japan.

Yoshihiro Ito (Y)

Department of Endocrinology and Diabetes, Nagoya University Graduate School of Medicine, 65 Tsurumai-cho, Showa-ku, Nagoya, 466-8550, Japan.

Shintaro Iwama (S)

Department of Endocrinology and Diabetes, Nagoya University Graduate School of Medicine, 65 Tsurumai-cho, Showa-ku, Nagoya, 466-8550, Japan.

Ryoichi Banno (R)

Department of Endocrinology and Diabetes, Nagoya University Graduate School of Medicine, 65 Tsurumai-cho, Showa-ku, Nagoya, 466-8550, Japan.
Research Center of Health, Physical Fitness and Sports, Nagoya University, Nagoya, 464-8601, Japan.

Katsuya Tanabe (K)

Division of Endocrinology, Metabolism, Hematological Sciences and Therapeutics, Yamaguchi University Graduate School of Medicine, Ube, 755-8505, Japan.

Yukio Tanizawa (Y)

Division of Endocrinology, Metabolism, Hematological Sciences and Therapeutics, Yamaguchi University Graduate School of Medicine, Ube, 755-8505, Japan.

Hiroshi Arima (H)

Department of Endocrinology and Diabetes, Nagoya University Graduate School of Medicine, 65 Tsurumai-cho, Showa-ku, Nagoya, 466-8550, Japan. arima105@med.nagoya-u.ac.jp.

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