Implications of Na+/I- Symporter transport to the plasma membrane for thyroid hormonogenesis and radioiodide therapy
- Autores
- Martín, Mariano; Geysels, Romina Celeste; Peyret, Victoria; Bernal Barquero, Carlos Eduardo; Masini-Repiso, Ana María; Nicola, Juan Pablo
- Año de publicación
- 2019
- Idioma
- inglés
- Tipo de recurso
- artículo
- Estado
- versión publicada
- Descripción
- Iodine is a crucial component of thyroid hormones; therefore, a key requirement for thyroid hormone biosynthesis is that iodide (I2) be actively accumulated in the thyroid follicular cell. The ability of the thyroid epithelia to concentrate I2 is ultimately dependent on functional Na+/ I2 symporter (NIS) expression at the plasma membrane. Underscoring the significance of NIS for thyroid physiology, loss-of-function mutations in the NIS-coding SLC5A5 gene cause an I2 transport defect, resulting in dyshormonogenic congenital hypothyroidism. Moreover, I2 accumulation in the thyroid cell constitutes the cornerstone for radioiodide ablation therapy for differentiated thyroid carcinoma. However, differentiated thyroid tumors often exhibit reduced (or even undetectable) I2 transport compared with normal thyroid tissue, and they are diagnosed as cold nodules on thyroid scintigraphy. Paradoxically, immunohistochemistry analysis revealed that cold thyroid nodules do not express NIS or express normal, or even higher NIS levels compared with adjacent normal tissue, but NIS is frequently intracellularly retained, suggesting the presence of posttranslational abnormalities in the transport of the protein to the plasma membrane. Ultimately, a thorough comprehension of the mechanisms that regulate NIS transport to the plasma membrane would have multiple implications for radioiodide therapy, opening the possibility to identify new molecular targets to treat radioiodide-refractory thyroid tumors. Therefore, in this review, we discuss the current knowledge regarding posttranslational mechanisms that regulate NIS transport to the plasma membrane under physiological and pathological conditions affecting the thyroid follicular cell, a topic of great interest in the thyroid cancer field.
Fil: Martín, Mariano. Universidad Nacional de Córdoba. Facultad de Ciencias Químicas; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Córdoba. Centro de Investigaciones en Bioquímica Clínica e Inmunología; Argentina
Fil: Geysels, Romina Celeste. Universidad Nacional de Córdoba. Facultad de Ciencias Químicas; Argentina
Fil: Peyret, Victoria. Universidad Nacional de Córdoba. Facultad de Ciencias Químicas. Departamento de Bioquímica Clínica; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Bernal Barquero, Carlos Eduardo. Universidad Nacional de Córdoba. Facultad de Ciencias Químicas; Argentina
Fil: Masini-Repiso, Ana María. Universidad Nacional de Córdoba. Facultad de Ciencias Químicas. Departamento de Bioquímica Clínica; Argentina
Fil: Nicola, Juan Pablo. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Córdoba. Centro de Investigaciones en Bioquímica Clínica e Inmunología; Argentina - Materia
-
CONGENITAL HYPOTHYROIDISM
DIFFERENTIATED THYROID CANCER
I2 DEFICIENCY DISORDERS
I2 TRANSPORT DEFECT
NA+/I2 SYMPORTER
RADIOIODINE THERAPY - Nivel de accesibilidad
- acceso abierto
- Condiciones de uso
- https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
- Repositorio
- Institución
- Consejo Nacional de Investigaciones Científicas y Técnicas
- OAI Identificador
- oai:ri.conicet.gov.ar:11336/128769
Ver los metadatos del registro completo
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Implications of Na+/I- Symporter transport to the plasma membrane for thyroid hormonogenesis and radioiodide therapyMartín, MarianoGeysels, Romina CelestePeyret, VictoriaBernal Barquero, Carlos EduardoMasini-Repiso, Ana MaríaNicola, Juan PabloCONGENITAL HYPOTHYROIDISMDIFFERENTIATED THYROID CANCERI2 DEFICIENCY DISORDERSI2 TRANSPORT DEFECTNA+/I2 SYMPORTERRADIOIODINE THERAPYhttps://purl.org/becyt/ford/1.6https://purl.org/becyt/ford/1Iodine is a crucial component of thyroid hormones; therefore, a key requirement for thyroid hormone biosynthesis is that iodide (I2) be actively accumulated in the thyroid follicular cell. The ability of the thyroid epithelia to concentrate I2 is ultimately dependent on functional Na+/ I2 symporter (NIS) expression at the plasma membrane. Underscoring the significance of NIS for thyroid physiology, loss-of-function mutations in the NIS-coding SLC5A5 gene cause an I2 transport defect, resulting in dyshormonogenic congenital hypothyroidism. Moreover, I2 accumulation in the thyroid cell constitutes the cornerstone for radioiodide ablation therapy for differentiated thyroid carcinoma. However, differentiated thyroid tumors often exhibit reduced (or even undetectable) I2 transport compared with normal thyroid tissue, and they are diagnosed as cold nodules on thyroid scintigraphy. Paradoxically, immunohistochemistry analysis revealed that cold thyroid nodules do not express NIS or express normal, or even higher NIS levels compared with adjacent normal tissue, but NIS is frequently intracellularly retained, suggesting the presence of posttranslational abnormalities in the transport of the protein to the plasma membrane. Ultimately, a thorough comprehension of the mechanisms that regulate NIS transport to the plasma membrane would have multiple implications for radioiodide therapy, opening the possibility to identify new molecular targets to treat radioiodide-refractory thyroid tumors. Therefore, in this review, we discuss the current knowledge regarding posttranslational mechanisms that regulate NIS transport to the plasma membrane under physiological and pathological conditions affecting the thyroid follicular cell, a topic of great interest in the thyroid cancer field.Fil: Martín, Mariano. Universidad Nacional de Córdoba. Facultad de Ciencias Químicas; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Córdoba. Centro de Investigaciones en Bioquímica Clínica e Inmunología; ArgentinaFil: Geysels, Romina Celeste. Universidad Nacional de Córdoba. Facultad de Ciencias Químicas; ArgentinaFil: Peyret, Victoria. Universidad Nacional de Córdoba. Facultad de Ciencias Químicas. Departamento de Bioquímica Clínica; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Bernal Barquero, Carlos Eduardo. Universidad Nacional de Córdoba. Facultad de Ciencias Químicas; ArgentinaFil: Masini-Repiso, Ana María. Universidad Nacional de Córdoba. Facultad de Ciencias Químicas. Departamento de Bioquímica Clínica; ArgentinaFil: Nicola, Juan Pablo. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Córdoba. Centro de Investigaciones en Bioquímica Clínica e Inmunología; ArgentinaOxford University Press2019-01info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/128769Martín, Mariano; Geysels, Romina Celeste; Peyret, Victoria; Bernal Barquero, Carlos Eduardo; Masini-Repiso, Ana María; et al.; Implications of Na+/I- Symporter transport to the plasma membrane for thyroid hormonogenesis and radioiodide therapy; Oxford University Press; Journal of the Endocrine Society; 3; 1; 1-2019; 222-2342472-1972CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/url/https://academic.oup.com/jes/article/3/1/222/5230905info:eu-repo/semantics/altIdentifier/doi/10.1210/js.2018-00100info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-03T10:04:06Zoai:ri.conicet.gov.ar:11336/128769instacron:CONICETInstitucionalhttp://ri.conicet.gov.ar/Organismo científico-tecnológicoNo correspondehttp://ri.conicet.gov.ar/oai/requestdasensio@conicet.gov.ar; lcarlino@conicet.gov.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:34982025-09-03 10:04:06.902CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse |
dc.title.none.fl_str_mv |
Implications of Na+/I- Symporter transport to the plasma membrane for thyroid hormonogenesis and radioiodide therapy |
title |
Implications of Na+/I- Symporter transport to the plasma membrane for thyroid hormonogenesis and radioiodide therapy |
spellingShingle |
Implications of Na+/I- Symporter transport to the plasma membrane for thyroid hormonogenesis and radioiodide therapy Martín, Mariano CONGENITAL HYPOTHYROIDISM DIFFERENTIATED THYROID CANCER I2 DEFICIENCY DISORDERS I2 TRANSPORT DEFECT NA+/I2 SYMPORTER RADIOIODINE THERAPY |
title_short |
Implications of Na+/I- Symporter transport to the plasma membrane for thyroid hormonogenesis and radioiodide therapy |
title_full |
Implications of Na+/I- Symporter transport to the plasma membrane for thyroid hormonogenesis and radioiodide therapy |
title_fullStr |
Implications of Na+/I- Symporter transport to the plasma membrane for thyroid hormonogenesis and radioiodide therapy |
title_full_unstemmed |
Implications of Na+/I- Symporter transport to the plasma membrane for thyroid hormonogenesis and radioiodide therapy |
title_sort |
Implications of Na+/I- Symporter transport to the plasma membrane for thyroid hormonogenesis and radioiodide therapy |
dc.creator.none.fl_str_mv |
Martín, Mariano Geysels, Romina Celeste Peyret, Victoria Bernal Barquero, Carlos Eduardo Masini-Repiso, Ana María Nicola, Juan Pablo |
author |
Martín, Mariano |
author_facet |
Martín, Mariano Geysels, Romina Celeste Peyret, Victoria Bernal Barquero, Carlos Eduardo Masini-Repiso, Ana María Nicola, Juan Pablo |
author_role |
author |
author2 |
Geysels, Romina Celeste Peyret, Victoria Bernal Barquero, Carlos Eduardo Masini-Repiso, Ana María Nicola, Juan Pablo |
author2_role |
author author author author author |
dc.subject.none.fl_str_mv |
CONGENITAL HYPOTHYROIDISM DIFFERENTIATED THYROID CANCER I2 DEFICIENCY DISORDERS I2 TRANSPORT DEFECT NA+/I2 SYMPORTER RADIOIODINE THERAPY |
topic |
CONGENITAL HYPOTHYROIDISM DIFFERENTIATED THYROID CANCER I2 DEFICIENCY DISORDERS I2 TRANSPORT DEFECT NA+/I2 SYMPORTER RADIOIODINE THERAPY |
purl_subject.fl_str_mv |
https://purl.org/becyt/ford/1.6 https://purl.org/becyt/ford/1 |
dc.description.none.fl_txt_mv |
Iodine is a crucial component of thyroid hormones; therefore, a key requirement for thyroid hormone biosynthesis is that iodide (I2) be actively accumulated in the thyroid follicular cell. The ability of the thyroid epithelia to concentrate I2 is ultimately dependent on functional Na+/ I2 symporter (NIS) expression at the plasma membrane. Underscoring the significance of NIS for thyroid physiology, loss-of-function mutations in the NIS-coding SLC5A5 gene cause an I2 transport defect, resulting in dyshormonogenic congenital hypothyroidism. Moreover, I2 accumulation in the thyroid cell constitutes the cornerstone for radioiodide ablation therapy for differentiated thyroid carcinoma. However, differentiated thyroid tumors often exhibit reduced (or even undetectable) I2 transport compared with normal thyroid tissue, and they are diagnosed as cold nodules on thyroid scintigraphy. Paradoxically, immunohistochemistry analysis revealed that cold thyroid nodules do not express NIS or express normal, or even higher NIS levels compared with adjacent normal tissue, but NIS is frequently intracellularly retained, suggesting the presence of posttranslational abnormalities in the transport of the protein to the plasma membrane. Ultimately, a thorough comprehension of the mechanisms that regulate NIS transport to the plasma membrane would have multiple implications for radioiodide therapy, opening the possibility to identify new molecular targets to treat radioiodide-refractory thyroid tumors. Therefore, in this review, we discuss the current knowledge regarding posttranslational mechanisms that regulate NIS transport to the plasma membrane under physiological and pathological conditions affecting the thyroid follicular cell, a topic of great interest in the thyroid cancer field. Fil: Martín, Mariano. Universidad Nacional de Córdoba. Facultad de Ciencias Químicas; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Córdoba. Centro de Investigaciones en Bioquímica Clínica e Inmunología; Argentina Fil: Geysels, Romina Celeste. Universidad Nacional de Córdoba. Facultad de Ciencias Químicas; Argentina Fil: Peyret, Victoria. Universidad Nacional de Córdoba. Facultad de Ciencias Químicas. Departamento de Bioquímica Clínica; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina Fil: Bernal Barquero, Carlos Eduardo. Universidad Nacional de Córdoba. Facultad de Ciencias Químicas; Argentina Fil: Masini-Repiso, Ana María. Universidad Nacional de Córdoba. Facultad de Ciencias Químicas. Departamento de Bioquímica Clínica; Argentina Fil: Nicola, Juan Pablo. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Córdoba. Centro de Investigaciones en Bioquímica Clínica e Inmunología; Argentina |
description |
Iodine is a crucial component of thyroid hormones; therefore, a key requirement for thyroid hormone biosynthesis is that iodide (I2) be actively accumulated in the thyroid follicular cell. The ability of the thyroid epithelia to concentrate I2 is ultimately dependent on functional Na+/ I2 symporter (NIS) expression at the plasma membrane. Underscoring the significance of NIS for thyroid physiology, loss-of-function mutations in the NIS-coding SLC5A5 gene cause an I2 transport defect, resulting in dyshormonogenic congenital hypothyroidism. Moreover, I2 accumulation in the thyroid cell constitutes the cornerstone for radioiodide ablation therapy for differentiated thyroid carcinoma. However, differentiated thyroid tumors often exhibit reduced (or even undetectable) I2 transport compared with normal thyroid tissue, and they are diagnosed as cold nodules on thyroid scintigraphy. Paradoxically, immunohistochemistry analysis revealed that cold thyroid nodules do not express NIS or express normal, or even higher NIS levels compared with adjacent normal tissue, but NIS is frequently intracellularly retained, suggesting the presence of posttranslational abnormalities in the transport of the protein to the plasma membrane. Ultimately, a thorough comprehension of the mechanisms that regulate NIS transport to the plasma membrane would have multiple implications for radioiodide therapy, opening the possibility to identify new molecular targets to treat radioiodide-refractory thyroid tumors. Therefore, in this review, we discuss the current knowledge regarding posttranslational mechanisms that regulate NIS transport to the plasma membrane under physiological and pathological conditions affecting the thyroid follicular cell, a topic of great interest in the thyroid cancer field. |
publishDate |
2019 |
dc.date.none.fl_str_mv |
2019-01 |
dc.type.none.fl_str_mv |
info:eu-repo/semantics/article info:eu-repo/semantics/publishedVersion http://purl.org/coar/resource_type/c_6501 info:ar-repo/semantics/articulo |
format |
article |
status_str |
publishedVersion |
dc.identifier.none.fl_str_mv |
http://hdl.handle.net/11336/128769 Martín, Mariano; Geysels, Romina Celeste; Peyret, Victoria; Bernal Barquero, Carlos Eduardo; Masini-Repiso, Ana María; et al.; Implications of Na+/I- Symporter transport to the plasma membrane for thyroid hormonogenesis and radioiodide therapy; Oxford University Press; Journal of the Endocrine Society; 3; 1; 1-2019; 222-234 2472-1972 CONICET Digital CONICET |
url |
http://hdl.handle.net/11336/128769 |
identifier_str_mv |
Martín, Mariano; Geysels, Romina Celeste; Peyret, Victoria; Bernal Barquero, Carlos Eduardo; Masini-Repiso, Ana María; et al.; Implications of Na+/I- Symporter transport to the plasma membrane for thyroid hormonogenesis and radioiodide therapy; Oxford University Press; Journal of the Endocrine Society; 3; 1; 1-2019; 222-234 2472-1972 CONICET Digital CONICET |
dc.language.none.fl_str_mv |
eng |
language |
eng |
dc.relation.none.fl_str_mv |
info:eu-repo/semantics/altIdentifier/url/https://academic.oup.com/jes/article/3/1/222/5230905 info:eu-repo/semantics/altIdentifier/doi/10.1210/js.2018-00100 |
dc.rights.none.fl_str_mv |
info:eu-repo/semantics/openAccess https://creativecommons.org/licenses/by-nc-sa/2.5/ar/ |
eu_rights_str_mv |
openAccess |
rights_invalid_str_mv |
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/ |
dc.format.none.fl_str_mv |
application/pdf application/pdf application/pdf application/pdf |
dc.publisher.none.fl_str_mv |
Oxford University Press |
publisher.none.fl_str_mv |
Oxford University Press |
dc.source.none.fl_str_mv |
reponame:CONICET Digital (CONICET) instname:Consejo Nacional de Investigaciones Científicas y Técnicas |
reponame_str |
CONICET Digital (CONICET) |
collection |
CONICET Digital (CONICET) |
instname_str |
Consejo Nacional de Investigaciones Científicas y Técnicas |
repository.name.fl_str_mv |
CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicas |
repository.mail.fl_str_mv |
dasensio@conicet.gov.ar; lcarlino@conicet.gov.ar |
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1842269838023589888 |
score |
13.13397 |