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Hipotiroidismo Congénito Central: Correlaciones Clínico-Genéticas E Investigación De Sus Mecanismos Moleculares

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Hipotiroidismo Congénito Central: Correlaciones Clínico-Genéticas E Investigación De Sus Mecanismos Moleculares Universidad Autónoma de Madrid. Departamento de Bioquímica. Hipotiroidismo congénito central: correlaciones clínico-genéticas e investigación de sus mecanismos moleculares Marta García González Madrid, 2017 Departamento de Bioquímica. Facultad de Medicina. Universidad Autónoma de Madrid. Hipotiroidismo congénito central: correlaciones clínico-genéticas e investigación de sus mecanismos moleculares Doctoranda: Marta GARCÍA GONZÁLEZ. Licenciada en Ciencias Biológicas. Universidad Complutense de Madrid. Director: Dr. José Carlos Moreno Navarro. Laboratorio Molecular de Tiroides. Instituto de Genética Médica y Molecular (INGEMM). Hospital Universitario La Paz (Madrid). José Carlos Moreno Navarro, Doctor en Medicina y Director del Laboratorio Molecular de Tiroides en el Instituto de Genética Médica y Molecular (INGEMM) del Hospital Universitario La Paz, Madrid. CERTIFICA: Que Marta García González, Licenciada en Biología y Máster en Bioquímica, Biología Molecular y Biomedicina por la Universidad Complutense de Madrid, ha realizado bajo su dirección el trabajo de investigación titulado: Hipotiroidismo congénito central: correlaciones clínico-genéticas e investigación de sus mecanismos moleculares El que suscribe considera el trabajo realizado satisfactorio y apto para ser presentado como Tesis Doctoral en el Departamento de Bioquímica de la Facultad de Medicina de la Universidad Autónoma de Madrid. Y para que conste donde proceda expiden el presente certificado en Madrid a 19 de Junio de 2017. Fdo. José Carlos Moreno Navarro Marta García González. 2017. RESUMEN Hipotiroidismo congénito central: correlaciones clínico-genéticas e investigación de sus mecanismos moleculares Marta García González. 2017. Hipotiroidismo congénito central: correlaciones clínico-genéticas e investigación de sus mecanismos moleculares Resumen RESUMEN El Hipotiroidismo Congénito Central (HCC) es un grupo heterogéneo de patologías causadas por la disminución de la síntesis, secreción o bioactividad de la hormona tirotropa (TSH), que no consigue estimular correctamente una glándula tiroidea normal. Esta patología no es detectada en el cribado neonatal de hipotiroidismo congénito por TSH realizado en España y en la mayoría de países europeos. Por este motivo suele ser una entidad infra-diagnosticada. En el presente estudio se ha investigado fenotípica y genéticamente la cohorte de pacientes con HCC más amplia conocida hasta la actualidad. Esta serie de pacientes es única por contener una gran proporción de casos con HCC aislado (68%). En la discriminación etiológica de la enfermedad mediante test de TRH se han identificado 5 tipos de respuestas: dos de carácter hipofisario (P1 yP2), dos hipotalámicas (H1 y H2) y un tipo de respuesta normal. En un paciente con respuesta hipotalámica tipo H2 al test de TRH se identificó una hipoplasia hipofisaria e hipotalámica poniendo de manifiesto un origen mixto de la enfermedad. Además, se identificó un paciente con un fenotipo central clínicamente demostrado de hipotiroidismo e hipermetabolismo hipotalámicos con respuesta tipo H1 en el test de TRH. La base molecular del HCC es ampliamente desconocida. En el presente estudio se han identificado mutaciones en tres de los cuatros genes asociados a HCC en humanos: IGSF1, TRHR y TBL1X. Defectos en IGSF1 causaron hipotiroidismo congénito central y un fenotipo no descrito hasta la fecha de sobreestimulación del eje gonadotropo (FSH) durante la minipubertad neonatal, causante del macroorquidismo observado en este paciente, como se ha demostrado en ensayos funcionales in vitro. De este modo, se ha desvelado el mecanismo de actuación de IGSF1 en células tirotropas y gonadotropas: IGSF1 estimula la expresión de TRHR, e indirectamente de síntesis y bioactividad de TSH, por regulación negativa de la vía TGFβ-Smad; y reduce la expresión de FSHB por regulación negativa de la vía Activina-Smad. Además, se ha demostrado la expresión de IGSF1en tiroides pero su función en la glándula aún está por investigar. Se ha identificado un defecto leve en el TRHR en una familia de etnia gitana cuyos portadores heterocigotos muestran por primera vez un fenotipo de Hipertirotropinemia de origen central. También se han descrito nuevas características fenotípicas asociadas a defectos en TBL1X por mutaciones severas: trastorno por déficit de atención e hiperactividad, macrocefalia y malformación de Arnold-Chiari I. Algunas de estas características fenotípicas también se han observado en pacientes con variantes en otros factores integrados en el complejo NCoR-SMRT del que TBL1X forma parte, como son NCOR1 y GPS2. Factores no asociados previamente con HCC en humanos, que abren una nueva línea de investigación para desentrañar su patogenia molecular en la enfermedad. Resumen Resumen ABSTRACT Central Congenital Hypothyroidism (CCH) is a heterogeneous group of pathologies caused by decreased synthesis, secretion or bioactivity of the thyrotropin hormone (TSH), which fails to properly stimulate a normal thyroid gland. This pathology is not detected in the TSH-based neonatal screening program for congenital hypothyroidism performed in Spain as in most European countries. For this reason, it is usually an under-diagnosed entity. In the present study, the cohort of patients with broader central congenital hypothyroidism (CCH) known to date has been genetically and phenotypically investigated. This series of patients is unique because it contains a large proportion of cases with isolated central hypothyroidism (68%). In the aetiological discrimination of the disease by TRH test, 5 types of responses have been identified: two pituitary (P1 and P2), two hypothalamic (H1 and H2) and one normal response type. In a patient with H2 hypothalamic response to the TRH test, pituitary and hypothalamic hypoplasia were identified, revealing a mixed origin of the disease. Moreover, we identified a patient with clinically demonstrated hypothalamic hypothyroidism and hypermetabolism and with hypothalamic H1 type response. The molecular basis of CCH is largely unknown. In the present study, mutations have been identified in three of the four genes associated with CCH in humans: IGSF1, TRHR and TBL1X. Defects in IGSF1 caused CCH and a non-described phenotype to date of over-stimulation of the gonadotropic axis (FSH) during neonatal minipuberty, causing macroorchidism observed in this patient, as demonstrated in functional in vitro assays. Thus, the mechanism of action of IGSF1 in thyrotrophic and gonadotropic cells has been unveiled: IGSF1 stimulates the expression of TRHR, and indirectly of TSH synthesis and bioactivity, by negative regulation of the TGFβ-Smad pathway, and reduces FSHB expression by down-regulation of the Activin-Smad pathway. In addition, the expression of IGSF1 has been demonstrated in the thyroid but its function in the gland has yet to be investigated. A mild defect in TRHR has been identified in family of Roma origin, whose heterozygous carriers show, for the first time, a phenotype of hyperthyrotropinemia. Novel phenotypic characteristics associated with defects in TBL1X have also been described caused by severe mutations: attention deficit hyperactivity disorder, macrocephaly, and Arnold-Chiari type I malformation. Some of these phenotypic characteristics have also been observed in patients with variants in other integrated factors of the NCoR-SMRT complex such as NCOR1 and GPS2, of which TBL1X is part. These factors not previously associated with CCH in humans, open a new line of future research that will unravel its molecular implications in the disease. Resumen Marta García González. 2017. ÍNDICE Hipotiroidismo congénito central: correlaciones clínico-genéticas e investigación de sus mecanismos moleculares Marta García González. 2017. Hipotiroidismo congénito central: correlaciones clínico-genéticas e investigación de sus mecanismos moleculares Índice ÍNDICE ABREVIATURAS ……………………………………………………………………………………………… 1 INTRODUCCIÓN ……………………………………………………………………………………………… 5 Cribado neonatal de hipotiroidismo congénito ………………………………………………… 7 Control central de la función tiroidea: mecanismos hormonales y moleculares …… 8 Mecanismos hormonales que controlan la acción de la TSH ………………………………. 9 1. Señales estimulatorias de la síntesis y acción de la TSH …………………………………… 9 Síntesis y degradación de TRH ………………………………………………………………. 9 Pulsatilidad de la secreción de TSH y TRH ………………………………………………… 9 Desensibilización de los receptores de TRH (TRHR) hipofisarios al TRH …………… 10 TRH controla la biopotencia de TSH ……………………………………………………….. 10 2. Señales inhibitorias de la acción de la TSH ……………………………………………………. 10 Asa larga de retroalimentación negativa …………………………………………………. 11 Asa corta de retroalimentación negativa …………………………………………………. 11 Asa ultracorta de retroalimentación negativa …………………………………………… 11 Plasticidad de la célula hipofisaria y trans-diferenciación entre tipos celulares …. 12 Dopamina y somatostatina en el hipotálamo …………………………………………… 12 3. Otras señales involucradas en la señalización de TSH ……………………………………… 14 Tiroestimulina …………………………………………………………………………………… 14 Índice Mecanismos moleculares que controlan la acción de la TSH ……………………………… 14 1. En el promotor del gen TRH …………………………………………………………………… 14 Control transcripcional positivo ……………………………………………………………. 14 Control transcripcional negativo …………………………………………………………… 14 2. En el promotor del gen TSHB ……………………………………………………………………. 15 Control transcripcional positivo ……………………………………………………………….. 15 Control transcripcional negativo ………………………………………………………………. 17 Modelos animales
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