Natural Autoimmunity to Selenoprotein P Impairs Selenium Transport in Hashimoto’s Thyroiditis

The essential trace element selenium (Se) is needed for the biosynthesis of selenocysteine-containing selenoproteins, including the secreted enzyme glutathione peroxidase 3 (GPX3) and the Se-transporter selenoprotein P (SELENOP). Both are found in blood and thyroid colloid, where they serve protecti...
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Autor*in:	Qian Sun [verfasserIn] Sebastian Mehl [verfasserIn] Kostja Renko [verfasserIn] Petra Seemann [verfasserIn] Christian L. Görlich [verfasserIn] Julian Hackler [verfasserIn] Waldemar B. Minich [verfasserIn] George J. Kahaly [verfasserIn] Lutz Schomburg [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2021

Schlagwörter:	antioxidative defense autoantibody glutathione peroxidase Hashimoto’s thyroiditis trace element

Übergeordnetes Werk:	In: International Journal of Molecular Sciences - MDPI AG, 2003, 22(2021), 23, p 13088
Übergeordnetes Werk:	volume:22 ; year:2021 ; number:23, p 13088

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc Journal toc

DOI / URN:	10.3390/ijms222313088

Katalog-ID:	DOAJ051469111

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520			\|a The essential trace element selenium (Se) is needed for the biosynthesis of selenocysteine-containing selenoproteins, including the secreted enzyme glutathione peroxidase 3 (GPX3) and the Se-transporter selenoprotein P (SELENOP). Both are found in blood and thyroid colloid, where they serve protective functions. Serum SELENOP derives mainly from hepatocytes, whereas the kidney contributes most serum GPX3. Studies using transgenic mice indicated that renal GPX3 biosynthesis depends on Se supply by hepatic SELENOP, which is produced in protein variants with varying Se contents. Low Se status is an established risk factor for autoimmune thyroid disease, and thyroid autoimmunity generates novel autoantigens. We hypothesized that natural autoantibodies to SELENOP are prevalent in thyroid patients, impair Se transport, and negatively affect GPX3 biosynthesis. Using a newly established quantitative immunoassay, SELENOP autoantibodies were particularly prevalent in Hashimoto’s thyroiditis as compared with healthy control subjects (6.6% versus 0.3%). Serum samples rich in SELENOP autoantibodies displayed relatively high total Se and SELENOP concentrations in comparison with autoantibody-negative samples ([Se]; 85.3 vs. 77.1 µg/L, <i<p</i< = 0.0178, and [SELENOP]; 5.1 vs. 3.5 mg/L, <i<p</i< = 0.001), while GPX3 activity was low and correlated inversely to SELENOP autoantibody concentrations. In renal cells in culture, antibodies to SELENOP inhibited Se uptake. Our results indicate an impairment of SELENOP-dependent Se transport by natural SELENOP autoantibodies, suggesting that the characterization of health risk from Se deficiency may need to include autoimmunity to SELENOP as additional biomarker of Se status.
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allfields	10.3390/ijms222313088 doi (DE-627)DOAJ051469111 (DE-599)DOAJ1e19cd40e33e43a4abf75b7577486f66 DE-627 ger DE-627 rakwb eng QH301-705.5 QD1-999 Qian Sun verfasserin aut Natural Autoimmunity to Selenoprotein P Impairs Selenium Transport in Hashimoto’s Thyroiditis 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier The essential trace element selenium (Se) is needed for the biosynthesis of selenocysteine-containing selenoproteins, including the secreted enzyme glutathione peroxidase 3 (GPX3) and the Se-transporter selenoprotein P (SELENOP). Both are found in blood and thyroid colloid, where they serve protective functions. Serum SELENOP derives mainly from hepatocytes, whereas the kidney contributes most serum GPX3. Studies using transgenic mice indicated that renal GPX3 biosynthesis depends on Se supply by hepatic SELENOP, which is produced in protein variants with varying Se contents. Low Se status is an established risk factor for autoimmune thyroid disease, and thyroid autoimmunity generates novel autoantigens. We hypothesized that natural autoantibodies to SELENOP are prevalent in thyroid patients, impair Se transport, and negatively affect GPX3 biosynthesis. Using a newly established quantitative immunoassay, SELENOP autoantibodies were particularly prevalent in Hashimoto’s thyroiditis as compared with healthy control subjects (6.6% versus 0.3%). Serum samples rich in SELENOP autoantibodies displayed relatively high total Se and SELENOP concentrations in comparison with autoantibody-negative samples ([Se]; 85.3 vs. 77.1 µg/L, <i<p</i< = 0.0178, and [SELENOP]; 5.1 vs. 3.5 mg/L, <i<p</i< = 0.001), while GPX3 activity was low and correlated inversely to SELENOP autoantibody concentrations. In renal cells in culture, antibodies to SELENOP inhibited Se uptake. Our results indicate an impairment of SELENOP-dependent Se transport by natural SELENOP autoantibodies, suggesting that the characterization of health risk from Se deficiency may need to include autoimmunity to SELENOP as additional biomarker of Se status. antioxidative defense autoantibody glutathione peroxidase Hashimoto’s thyroiditis trace element Biology (General) Chemistry Sebastian Mehl verfasserin aut Kostja Renko verfasserin aut Petra Seemann verfasserin aut Christian L. Görlich verfasserin aut Julian Hackler verfasserin aut Waldemar B. Minich verfasserin aut George J. Kahaly verfasserin aut Lutz Schomburg verfasserin aut In International Journal of Molecular Sciences MDPI AG, 2003 22(2021), 23, p 13088 (DE-627)316340715 (DE-600)2019364-6 14220067 nnns volume:22 year:2021 number:23, p 13088 https://doi.org/10.3390/ijms222313088 kostenfrei https://doaj.org/article/1e19cd40e33e43a4abf75b7577486f66 kostenfrei https://www.mdpi.com/1422-0067/22/23/13088 kostenfrei https://doaj.org/toc/1661-6596 Journal toc kostenfrei https://doaj.org/toc/1422-0067 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 22 2021 23, p 13088
spelling	10.3390/ijms222313088 doi (DE-627)DOAJ051469111 (DE-599)DOAJ1e19cd40e33e43a4abf75b7577486f66 DE-627 ger DE-627 rakwb eng QH301-705.5 QD1-999 Qian Sun verfasserin aut Natural Autoimmunity to Selenoprotein P Impairs Selenium Transport in Hashimoto’s Thyroiditis 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier The essential trace element selenium (Se) is needed for the biosynthesis of selenocysteine-containing selenoproteins, including the secreted enzyme glutathione peroxidase 3 (GPX3) and the Se-transporter selenoprotein P (SELENOP). Both are found in blood and thyroid colloid, where they serve protective functions. Serum SELENOP derives mainly from hepatocytes, whereas the kidney contributes most serum GPX3. Studies using transgenic mice indicated that renal GPX3 biosynthesis depends on Se supply by hepatic SELENOP, which is produced in protein variants with varying Se contents. Low Se status is an established risk factor for autoimmune thyroid disease, and thyroid autoimmunity generates novel autoantigens. We hypothesized that natural autoantibodies to SELENOP are prevalent in thyroid patients, impair Se transport, and negatively affect GPX3 biosynthesis. Using a newly established quantitative immunoassay, SELENOP autoantibodies were particularly prevalent in Hashimoto’s thyroiditis as compared with healthy control subjects (6.6% versus 0.3%). Serum samples rich in SELENOP autoantibodies displayed relatively high total Se and SELENOP concentrations in comparison with autoantibody-negative samples ([Se]; 85.3 vs. 77.1 µg/L, <i<p</i< = 0.0178, and [SELENOP]; 5.1 vs. 3.5 mg/L, <i<p</i< = 0.001), while GPX3 activity was low and correlated inversely to SELENOP autoantibody concentrations. In renal cells in culture, antibodies to SELENOP inhibited Se uptake. Our results indicate an impairment of SELENOP-dependent Se transport by natural SELENOP autoantibodies, suggesting that the characterization of health risk from Se deficiency may need to include autoimmunity to SELENOP as additional biomarker of Se status. antioxidative defense autoantibody glutathione peroxidase Hashimoto’s thyroiditis trace element Biology (General) Chemistry Sebastian Mehl verfasserin aut Kostja Renko verfasserin aut Petra Seemann verfasserin aut Christian L. Görlich verfasserin aut Julian Hackler verfasserin aut Waldemar B. Minich verfasserin aut George J. Kahaly verfasserin aut Lutz Schomburg verfasserin aut In International Journal of Molecular Sciences MDPI AG, 2003 22(2021), 23, p 13088 (DE-627)316340715 (DE-600)2019364-6 14220067 nnns volume:22 year:2021 number:23, p 13088 https://doi.org/10.3390/ijms222313088 kostenfrei https://doaj.org/article/1e19cd40e33e43a4abf75b7577486f66 kostenfrei https://www.mdpi.com/1422-0067/22/23/13088 kostenfrei https://doaj.org/toc/1661-6596 Journal toc kostenfrei https://doaj.org/toc/1422-0067 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 22 2021 23, p 13088
allfields_unstemmed	10.3390/ijms222313088 doi (DE-627)DOAJ051469111 (DE-599)DOAJ1e19cd40e33e43a4abf75b7577486f66 DE-627 ger DE-627 rakwb eng QH301-705.5 QD1-999 Qian Sun verfasserin aut Natural Autoimmunity to Selenoprotein P Impairs Selenium Transport in Hashimoto’s Thyroiditis 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier The essential trace element selenium (Se) is needed for the biosynthesis of selenocysteine-containing selenoproteins, including the secreted enzyme glutathione peroxidase 3 (GPX3) and the Se-transporter selenoprotein P (SELENOP). Both are found in blood and thyroid colloid, where they serve protective functions. Serum SELENOP derives mainly from hepatocytes, whereas the kidney contributes most serum GPX3. Studies using transgenic mice indicated that renal GPX3 biosynthesis depends on Se supply by hepatic SELENOP, which is produced in protein variants with varying Se contents. Low Se status is an established risk factor for autoimmune thyroid disease, and thyroid autoimmunity generates novel autoantigens. We hypothesized that natural autoantibodies to SELENOP are prevalent in thyroid patients, impair Se transport, and negatively affect GPX3 biosynthesis. Using a newly established quantitative immunoassay, SELENOP autoantibodies were particularly prevalent in Hashimoto’s thyroiditis as compared with healthy control subjects (6.6% versus 0.3%). Serum samples rich in SELENOP autoantibodies displayed relatively high total Se and SELENOP concentrations in comparison with autoantibody-negative samples ([Se]; 85.3 vs. 77.1 µg/L, <i<p</i< = 0.0178, and [SELENOP]; 5.1 vs. 3.5 mg/L, <i<p</i< = 0.001), while GPX3 activity was low and correlated inversely to SELENOP autoantibody concentrations. In renal cells in culture, antibodies to SELENOP inhibited Se uptake. Our results indicate an impairment of SELENOP-dependent Se transport by natural SELENOP autoantibodies, suggesting that the characterization of health risk from Se deficiency may need to include autoimmunity to SELENOP as additional biomarker of Se status. antioxidative defense autoantibody glutathione peroxidase Hashimoto’s thyroiditis trace element Biology (General) Chemistry Sebastian Mehl verfasserin aut Kostja Renko verfasserin aut Petra Seemann verfasserin aut Christian L. Görlich verfasserin aut Julian Hackler verfasserin aut Waldemar B. Minich verfasserin aut George J. Kahaly verfasserin aut Lutz Schomburg verfasserin aut In International Journal of Molecular Sciences MDPI AG, 2003 22(2021), 23, p 13088 (DE-627)316340715 (DE-600)2019364-6 14220067 nnns volume:22 year:2021 number:23, p 13088 https://doi.org/10.3390/ijms222313088 kostenfrei https://doaj.org/article/1e19cd40e33e43a4abf75b7577486f66 kostenfrei https://www.mdpi.com/1422-0067/22/23/13088 kostenfrei https://doaj.org/toc/1661-6596 Journal toc kostenfrei https://doaj.org/toc/1422-0067 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 22 2021 23, p 13088
allfieldsGer	10.3390/ijms222313088 doi (DE-627)DOAJ051469111 (DE-599)DOAJ1e19cd40e33e43a4abf75b7577486f66 DE-627 ger DE-627 rakwb eng QH301-705.5 QD1-999 Qian Sun verfasserin aut Natural Autoimmunity to Selenoprotein P Impairs Selenium Transport in Hashimoto’s Thyroiditis 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier The essential trace element selenium (Se) is needed for the biosynthesis of selenocysteine-containing selenoproteins, including the secreted enzyme glutathione peroxidase 3 (GPX3) and the Se-transporter selenoprotein P (SELENOP). Both are found in blood and thyroid colloid, where they serve protective functions. Serum SELENOP derives mainly from hepatocytes, whereas the kidney contributes most serum GPX3. Studies using transgenic mice indicated that renal GPX3 biosynthesis depends on Se supply by hepatic SELENOP, which is produced in protein variants with varying Se contents. Low Se status is an established risk factor for autoimmune thyroid disease, and thyroid autoimmunity generates novel autoantigens. We hypothesized that natural autoantibodies to SELENOP are prevalent in thyroid patients, impair Se transport, and negatively affect GPX3 biosynthesis. Using a newly established quantitative immunoassay, SELENOP autoantibodies were particularly prevalent in Hashimoto’s thyroiditis as compared with healthy control subjects (6.6% versus 0.3%). Serum samples rich in SELENOP autoantibodies displayed relatively high total Se and SELENOP concentrations in comparison with autoantibody-negative samples ([Se]; 85.3 vs. 77.1 µg/L, <i<p</i< = 0.0178, and [SELENOP]; 5.1 vs. 3.5 mg/L, <i<p</i< = 0.001), while GPX3 activity was low and correlated inversely to SELENOP autoantibody concentrations. In renal cells in culture, antibodies to SELENOP inhibited Se uptake. Our results indicate an impairment of SELENOP-dependent Se transport by natural SELENOP autoantibodies, suggesting that the characterization of health risk from Se deficiency may need to include autoimmunity to SELENOP as additional biomarker of Se status. antioxidative defense autoantibody glutathione peroxidase Hashimoto’s thyroiditis trace element Biology (General) Chemistry Sebastian Mehl verfasserin aut Kostja Renko verfasserin aut Petra Seemann verfasserin aut Christian L. Görlich verfasserin aut Julian Hackler verfasserin aut Waldemar B. Minich verfasserin aut George J. Kahaly verfasserin aut Lutz Schomburg verfasserin aut In International Journal of Molecular Sciences MDPI AG, 2003 22(2021), 23, p 13088 (DE-627)316340715 (DE-600)2019364-6 14220067 nnns volume:22 year:2021 number:23, p 13088 https://doi.org/10.3390/ijms222313088 kostenfrei https://doaj.org/article/1e19cd40e33e43a4abf75b7577486f66 kostenfrei https://www.mdpi.com/1422-0067/22/23/13088 kostenfrei https://doaj.org/toc/1661-6596 Journal toc kostenfrei https://doaj.org/toc/1422-0067 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 22 2021 23, p 13088
allfieldsSound	10.3390/ijms222313088 doi (DE-627)DOAJ051469111 (DE-599)DOAJ1e19cd40e33e43a4abf75b7577486f66 DE-627 ger DE-627 rakwb eng QH301-705.5 QD1-999 Qian Sun verfasserin aut Natural Autoimmunity to Selenoprotein P Impairs Selenium Transport in Hashimoto’s Thyroiditis 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier The essential trace element selenium (Se) is needed for the biosynthesis of selenocysteine-containing selenoproteins, including the secreted enzyme glutathione peroxidase 3 (GPX3) and the Se-transporter selenoprotein P (SELENOP). Both are found in blood and thyroid colloid, where they serve protective functions. Serum SELENOP derives mainly from hepatocytes, whereas the kidney contributes most serum GPX3. Studies using transgenic mice indicated that renal GPX3 biosynthesis depends on Se supply by hepatic SELENOP, which is produced in protein variants with varying Se contents. Low Se status is an established risk factor for autoimmune thyroid disease, and thyroid autoimmunity generates novel autoantigens. We hypothesized that natural autoantibodies to SELENOP are prevalent in thyroid patients, impair Se transport, and negatively affect GPX3 biosynthesis. Using a newly established quantitative immunoassay, SELENOP autoantibodies were particularly prevalent in Hashimoto’s thyroiditis as compared with healthy control subjects (6.6% versus 0.3%). Serum samples rich in SELENOP autoantibodies displayed relatively high total Se and SELENOP concentrations in comparison with autoantibody-negative samples ([Se]; 85.3 vs. 77.1 µg/L, <i<p</i< = 0.0178, and [SELENOP]; 5.1 vs. 3.5 mg/L, <i<p</i< = 0.001), while GPX3 activity was low and correlated inversely to SELENOP autoantibody concentrations. In renal cells in culture, antibodies to SELENOP inhibited Se uptake. Our results indicate an impairment of SELENOP-dependent Se transport by natural SELENOP autoantibodies, suggesting that the characterization of health risk from Se deficiency may need to include autoimmunity to SELENOP as additional biomarker of Se status. antioxidative defense autoantibody glutathione peroxidase Hashimoto’s thyroiditis trace element Biology (General) Chemistry Sebastian Mehl verfasserin aut Kostja Renko verfasserin aut Petra Seemann verfasserin aut Christian L. Görlich verfasserin aut Julian Hackler verfasserin aut Waldemar B. Minich verfasserin aut George J. Kahaly verfasserin aut Lutz Schomburg verfasserin aut In International Journal of Molecular Sciences MDPI AG, 2003 22(2021), 23, p 13088 (DE-627)316340715 (DE-600)2019364-6 14220067 nnns volume:22 year:2021 number:23, p 13088 https://doi.org/10.3390/ijms222313088 kostenfrei https://doaj.org/article/1e19cd40e33e43a4abf75b7577486f66 kostenfrei https://www.mdpi.com/1422-0067/22/23/13088 kostenfrei https://doaj.org/toc/1661-6596 Journal toc kostenfrei https://doaj.org/toc/1422-0067 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 22 2021 23, p 13088
language	English
source	In International Journal of Molecular Sciences 22(2021), 23, p 13088 volume:22 year:2021 number:23, p 13088
sourceStr	In International Journal of Molecular Sciences 22(2021), 23, p 13088 volume:22 year:2021 number:23, p 13088
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	antioxidative defense autoantibody glutathione peroxidase Hashimoto’s thyroiditis trace element Biology (General) Chemistry
isfreeaccess_bool	true
container_title	International Journal of Molecular Sciences
authorswithroles_txt_mv	Qian Sun @@aut@@ Sebastian Mehl @@aut@@ Kostja Renko @@aut@@ Petra Seemann @@aut@@ Christian L. Görlich @@aut@@ Julian Hackler @@aut@@ Waldemar B. Minich @@aut@@ George J. Kahaly @@aut@@ Lutz Schomburg @@aut@@
publishDateDaySort_date	2021-01-01T00:00:00Z
hierarchy_top_id	316340715
id	DOAJ051469111
language_de	englisch
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callnumber-first	Q - Science
author	Qian Sun
spellingShingle	Qian Sun misc QH301-705.5 misc QD1-999 misc antioxidative defense misc autoantibody misc glutathione peroxidase misc Hashimoto’s thyroiditis misc trace element misc Biology (General) misc Chemistry Natural Autoimmunity to Selenoprotein P Impairs Selenium Transport in Hashimoto’s Thyroiditis
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topic_title	QH301-705.5 QD1-999 Natural Autoimmunity to Selenoprotein P Impairs Selenium Transport in Hashimoto’s Thyroiditis antioxidative defense autoantibody glutathione peroxidase Hashimoto’s thyroiditis trace element
topic	misc QH301-705.5 misc QD1-999 misc antioxidative defense misc autoantibody misc glutathione peroxidase misc Hashimoto’s thyroiditis misc trace element misc Biology (General) misc Chemistry
topic_unstemmed	misc QH301-705.5 misc QD1-999 misc antioxidative defense misc autoantibody misc glutathione peroxidase misc Hashimoto’s thyroiditis misc trace element misc Biology (General) misc Chemistry
topic_browse	misc QH301-705.5 misc QD1-999 misc antioxidative defense misc autoantibody misc glutathione peroxidase misc Hashimoto’s thyroiditis misc trace element misc Biology (General) misc Chemistry
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title	Natural Autoimmunity to Selenoprotein P Impairs Selenium Transport in Hashimoto’s Thyroiditis
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title_full	Natural Autoimmunity to Selenoprotein P Impairs Selenium Transport in Hashimoto’s Thyroiditis
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author_browse	Qian Sun Sebastian Mehl Kostja Renko Petra Seemann Christian L. Görlich Julian Hackler Waldemar B. Minich George J. Kahaly Lutz Schomburg
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author-letter	Qian Sun
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title_sort	natural autoimmunity to selenoprotein p impairs selenium transport in hashimoto’s thyroiditis
callnumber	QH301-705.5
title_auth	Natural Autoimmunity to Selenoprotein P Impairs Selenium Transport in Hashimoto’s Thyroiditis
abstract	The essential trace element selenium (Se) is needed for the biosynthesis of selenocysteine-containing selenoproteins, including the secreted enzyme glutathione peroxidase 3 (GPX3) and the Se-transporter selenoprotein P (SELENOP). Both are found in blood and thyroid colloid, where they serve protective functions. Serum SELENOP derives mainly from hepatocytes, whereas the kidney contributes most serum GPX3. Studies using transgenic mice indicated that renal GPX3 biosynthesis depends on Se supply by hepatic SELENOP, which is produced in protein variants with varying Se contents. Low Se status is an established risk factor for autoimmune thyroid disease, and thyroid autoimmunity generates novel autoantigens. We hypothesized that natural autoantibodies to SELENOP are prevalent in thyroid patients, impair Se transport, and negatively affect GPX3 biosynthesis. Using a newly established quantitative immunoassay, SELENOP autoantibodies were particularly prevalent in Hashimoto’s thyroiditis as compared with healthy control subjects (6.6% versus 0.3%). Serum samples rich in SELENOP autoantibodies displayed relatively high total Se and SELENOP concentrations in comparison with autoantibody-negative samples ([Se]; 85.3 vs. 77.1 µg/L, <i<p</i< = 0.0178, and [SELENOP]; 5.1 vs. 3.5 mg/L, <i<p</i< = 0.001), while GPX3 activity was low and correlated inversely to SELENOP autoantibody concentrations. In renal cells in culture, antibodies to SELENOP inhibited Se uptake. Our results indicate an impairment of SELENOP-dependent Se transport by natural SELENOP autoantibodies, suggesting that the characterization of health risk from Se deficiency may need to include autoimmunity to SELENOP as additional biomarker of Se status.
abstractGer	The essential trace element selenium (Se) is needed for the biosynthesis of selenocysteine-containing selenoproteins, including the secreted enzyme glutathione peroxidase 3 (GPX3) and the Se-transporter selenoprotein P (SELENOP). Both are found in blood and thyroid colloid, where they serve protective functions. Serum SELENOP derives mainly from hepatocytes, whereas the kidney contributes most serum GPX3. Studies using transgenic mice indicated that renal GPX3 biosynthesis depends on Se supply by hepatic SELENOP, which is produced in protein variants with varying Se contents. Low Se status is an established risk factor for autoimmune thyroid disease, and thyroid autoimmunity generates novel autoantigens. We hypothesized that natural autoantibodies to SELENOP are prevalent in thyroid patients, impair Se transport, and negatively affect GPX3 biosynthesis. Using a newly established quantitative immunoassay, SELENOP autoantibodies were particularly prevalent in Hashimoto’s thyroiditis as compared with healthy control subjects (6.6% versus 0.3%). Serum samples rich in SELENOP autoantibodies displayed relatively high total Se and SELENOP concentrations in comparison with autoantibody-negative samples ([Se]; 85.3 vs. 77.1 µg/L, <i<p</i< = 0.0178, and [SELENOP]; 5.1 vs. 3.5 mg/L, <i<p</i< = 0.001), while GPX3 activity was low and correlated inversely to SELENOP autoantibody concentrations. In renal cells in culture, antibodies to SELENOP inhibited Se uptake. Our results indicate an impairment of SELENOP-dependent Se transport by natural SELENOP autoantibodies, suggesting that the characterization of health risk from Se deficiency may need to include autoimmunity to SELENOP as additional biomarker of Se status.
abstract_unstemmed	The essential trace element selenium (Se) is needed for the biosynthesis of selenocysteine-containing selenoproteins, including the secreted enzyme glutathione peroxidase 3 (GPX3) and the Se-transporter selenoprotein P (SELENOP). Both are found in blood and thyroid colloid, where they serve protective functions. Serum SELENOP derives mainly from hepatocytes, whereas the kidney contributes most serum GPX3. Studies using transgenic mice indicated that renal GPX3 biosynthesis depends on Se supply by hepatic SELENOP, which is produced in protein variants with varying Se contents. Low Se status is an established risk factor for autoimmune thyroid disease, and thyroid autoimmunity generates novel autoantigens. We hypothesized that natural autoantibodies to SELENOP are prevalent in thyroid patients, impair Se transport, and negatively affect GPX3 biosynthesis. Using a newly established quantitative immunoassay, SELENOP autoantibodies were particularly prevalent in Hashimoto’s thyroiditis as compared with healthy control subjects (6.6% versus 0.3%). Serum samples rich in SELENOP autoantibodies displayed relatively high total Se and SELENOP concentrations in comparison with autoantibody-negative samples ([Se]; 85.3 vs. 77.1 µg/L, <i<p</i< = 0.0178, and [SELENOP]; 5.1 vs. 3.5 mg/L, <i<p</i< = 0.001), while GPX3 activity was low and correlated inversely to SELENOP autoantibody concentrations. In renal cells in culture, antibodies to SELENOP inhibited Se uptake. Our results indicate an impairment of SELENOP-dependent Se transport by natural SELENOP autoantibodies, suggesting that the characterization of health risk from Se deficiency may need to include autoimmunity to SELENOP as additional biomarker of Se status.
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container_issue	23, p 13088
title_short	Natural Autoimmunity to Selenoprotein P Impairs Selenium Transport in Hashimoto’s Thyroiditis
url	https://doi.org/10.3390/ijms222313088 https://doaj.org/article/1e19cd40e33e43a4abf75b7577486f66 https://www.mdpi.com/1422-0067/22/23/13088 https://doaj.org/toc/1661-6596 https://doaj.org/toc/1422-0067
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