{"id":{"repo_id":"birmingham","oai_identifier":"oai:etheses.bham.ac.uk:1195"},"canonical_url":"https://search.dev.ndltd.org/etd/birmingham/oai:etheses.bham.ac.uk:1195","repository":{"repo_id":"birmingham","name":"University of Birmingham","base_url":"https://etheses.bham.ac.uk/cgi/oai2"},"display":{"title":"The role of Thyroid hormone Transporters Monocarboxylate Transporter 10 (MCT10) and Monocarboxylate Transporter 8 (MCT8) in extravillous trophoblasts.","abstract":"Thyroid hormones (TH) are important for fetal and placental development. Monocarboxylate transporters 8 and 10 (MCT8, MCT10) are effective plasma membrane TH transporters expressed in the human placenta from 6 weeks of gestation. Both have been localized to human villous trophoblasts and extravillous trophoblasts (EVTs). Aims: Using HTR-8/SVneo cells as a model of 1st trimester EVTs, we assessed 1) Triiodothyronine (T3) effects on gene expression and cell proliferation; 2) the effect of altered MCT8 or MCT10 expression on proliferation and apoptosis; and whether effects were T3-mediated. Methods: 1) Cell proliferation was assessed by the MTT assay at 24-96hrs. Gene expression was assessed by quantitative QPCR (2-48h). 2) MCT8 was down-regulated using siRNA, and MCT8 and MCT10 were over-expressed by plasmid transfection. Effects of altering expression were assessed by MTT assay (Proliferation) and Caspase3/7 activity (Apoptosis). Results: We observed that T3 treatment did not affect HTR-8/SVneo proliferation nor alter the mRNA expressions of TH responsive gene, Connexin43 (Cx43) and the pre-receptor regulators of T3 action, deiodinases 2 and 3 (D2, D3), nor its own transporters, MCT8 and MCT10. However, T3 treatment was observed to decrease the expression of TH receptor β1 (TRβ1) (ANOVA p<0.05). Over-expression of MCT8 or MCT10 reduced cell proliferation by 36% and 29% respectively (ANOVA p<0.05) in the presence of T3. Apoptosis was reduced, independently of T3 treatment, by 24 and 31% (+/- T3 respectively) following overexpression of MCT8, and by 12 and 19% (+/- T3 respectively) following overexpression of MCT10, respectively (ANOVA p<0.005). Conversely, down-regulation of MCT8 resulted in increased apoptosis independently of T3 (p<0.003). Conclusions: HTR-8/SVneo cell proliferation does not change with T3 treatment. In addition, MCT8 and MCT10 may have both T3-dependent (suppress proliferation) and T3-independent (apoptosis) effects in EVTs. This suggests an important role for MCT8 and MCT10 in human placental development.","abstract_html":"Thyroid hormones (TH) are important for fetal and placental development. Monocarboxylate transporters 8 and 10 (MCT8, MCT10) are effective plasma membrane TH transporters expressed in the human placenta from 6 weeks of gestation. Both have been localized to human villous trophoblasts and extravillous trophoblasts (EVTs). Aims: Using HTR-8/SVneo cells as a model of 1st trimester EVTs, we assessed 1) Triiodothyronine (T3) effects on gene expression and cell proliferation; 2) the effect of altered MCT8 or MCT10 expression on proliferation and apoptosis; and whether effects were T3-mediated. Methods: 1) Cell proliferation was assessed by the MTT assay at 24-96hrs. Gene expression was assessed by quantitative QPCR (2-48h). 2) MCT8 was down-regulated using siRNA, and MCT8 and MCT10 were over-expressed by plasmid transfection. Effects of altering expression were assessed by MTT assay (Proliferation) and Caspase3/7 activity (Apoptosis). Results: We observed that T3 treatment did not affect HTR-8/SVneo proliferation nor alter the mRNA expressions of TH responsive gene, Connexin43 (Cx43) and the pre-receptor regulators of T3 action, deiodinases 2 and 3 (D2, D3), nor its own transporters, MCT8 and MCT10. However, T3 treatment was observed to decrease the expression of TH receptor β1 (TRβ1) (ANOVA p&lt;0.05). Over-expression of MCT8 or MCT10 reduced cell proliferation by 36% and 29% respectively (ANOVA p&lt;0.05) in the presence of T3. Apoptosis was reduced, independently of T3 treatment, by 24 and 31% (+/- T3 respectively) following overexpression of MCT8, and by 12 and 19% (+/- T3 respectively) following overexpression of MCT10, respectively (ANOVA p&lt;0.005). Conversely, down-regulation of MCT8 resulted in increased apoptosis independently of T3 (p&lt;0.003). Conclusions: HTR-8/SVneo cell proliferation does not change with T3 treatment. In addition, MCT8 and MCT10 may have both T3-dependent (suppress proliferation) and T3-independent (apoptosis) effects in EVTs. This suggests an important role for MCT8 and MCT10 in human placental development.","abstract_has_math":false,"creators":["Choudhury, Juhela"],"institution":"University of Birmingham","degree_name":"m_ph","degree_level":"m_ph","degree_discipline":null,"degree_department":null,"school":null,"contributors":[],"advisors":[],"committee_chairs":[],"committee_members":[],"year":2010,"date_issued":"2010-12","date_published":"2010-12","updated_at":"2026-07-24T01:11:23Z","subjects":["RC Internal medicine","RJ Pediatrics"],"languages":[],"rights":[],"rights_urls":[],"identifier_entries":[]},"links":{"outbound_url":null,"outbound_label":null,"outbound_source":null},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:contributor.sponsor","label":"Sponsor","values":["na"]},{"key":"dc:creator","label":"Author","values":["Choudhury, Juhela"]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"dc:date","label":"Dc Date","values":["2010-12"]},{"key":"dc:date.issued","label":"Date","values":["2010-12"]},{"key":"dc:publisher.department","label":"Dc Publisher Department","values":["College of Medical & Dental Sciences","School of Clinical and Experimental Medicine"]},{"key":"dc:publisher.institution","label":"Dc Publisher Institution","values":["University of Birmingham"]},{"key":"dc:relation.isreferencedby","label":"Dc Relation Isreferencedby","values":["http://etheses.bham.ac.uk//id/eprint/1195/"]},{"key":"dc:type","label":"Dc Type","values":["Thesis"]},{"key":"dc:type.qualificationlevel","label":"Dc Type Qualificationlevel","values":["m_ph"]},{"key":"dc:type.qualificationname","label":"Dc Type Qualificationname","values":["m_ph"]}]},{"id":"subjects_keywords","label":"Subjects and Keywords","entries":[{"key":"dc:subject","label":"Dc Subject","values":["RC Internal medicine","RJ Pediatrics"]}]},{"id":"identifiers","label":"Identifiers","entries":[{"key":"dc:identifier.uri","label":"Identifier URI","values":["http://etheses.bham.ac.uk//id/eprint/1195/1/Choudhury_10_MPhil.pdf","http://etheses.bham.ac.uk//id/eprint/1195/2/Decl_IS_Choudhury_10_MPhil.pdf"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description.abstract","label":"Abstract","values":["Thyroid hormones (TH) are important for fetal and placental development. Monocarboxylate transporters 8 and 10 (MCT8, MCT10) are effective plasma membrane TH transporters expressed in the human placenta from 6 weeks of gestation. Both have been localized to human villous trophoblasts and extravillous trophoblasts (EVTs). Aims: Using HTR-8/SVneo cells as a model of 1st trimester EVTs, we assessed 1) Triiodothyronine (T3) effects on gene expression and cell proliferation; 2) the effect of altered MCT8 or MCT10 expression on proliferation and apoptosis; and whether effects were T3-mediated. Methods: 1) Cell proliferation was assessed by the MTT assay at 24-96hrs. Gene expression was assessed by quantitative QPCR (2-48h). 2) MCT8 was down-regulated using siRNA, and MCT8 and MCT10 were over-expressed by plasmid transfection. Effects of altering expression were assessed by MTT assay (Proliferation) and Caspase3/7 activity (Apoptosis). Results: We observed that T3 treatment did not affect HTR-8/SVneo proliferation nor alter the mRNA expressions of TH responsive gene, Connexin43 (Cx43) and the pre-receptor regulators of T3 action, deiodinases 2 and 3 (D2, D3), nor its own transporters, MCT8 and MCT10. However, T3 treatment was observed to decrease the expression of TH receptor β1 (TRβ1) (ANOVA p<0.05). Over-expression of MCT8 or MCT10 reduced cell proliferation by 36% and 29% respectively (ANOVA p<0.05) in the presence of T3. Apoptosis was reduced, independently of T3 treatment, by 24 and 31% (+/- T3 respectively) following overexpression of MCT8, and by 12 and 19% (+/- T3 respectively) following overexpression of MCT10, respectively (ANOVA p<0.005). Conversely, down-regulation of MCT8 resulted in increased apoptosis independently of T3 (p<0.003). Conclusions: HTR-8/SVneo cell proliferation does not change with T3 treatment. In addition, MCT8 and MCT10 may have both T3-dependent (suppress proliferation) and T3-independent (apoptosis) effects in EVTs. This suggests an important role for MCT8 and MCT10 in human placental development."]},{"key":"dc:format","label":"Dc Format","values":["application/pdf"]},{"key":"dc:title","label":"Title","values":["The role of Thyroid hormone Transporters Monocarboxylate Transporter 10 (MCT10) and Monocarboxylate Transporter 8 (MCT8) in extravillous trophoblasts."]}]}],"canonical_facts":{"dc:contributor.sponsor":["na"],"dc:creator":["Choudhury, Juhela"],"dc:date":["2010-12"],"dc:date.issued":["2010-12"],"dc:description.abstract":["Thyroid hormones (TH) are important for fetal and placental development. Monocarboxylate transporters 8 and 10 (MCT8, MCT10) are effective plasma membrane TH transporters expressed in the human placenta from 6 weeks of gestation. Both have been localized to human villous trophoblasts and extravillous trophoblasts (EVTs). Aims: Using HTR-8/SVneo cells as a model of 1st trimester EVTs, we assessed 1) Triiodothyronine (T3) effects on gene expression and cell proliferation; 2) the effect of altered MCT8 or MCT10 expression on proliferation and apoptosis; and whether effects were T3-mediated. Methods: 1) Cell proliferation was assessed by the MTT assay at 24-96hrs. Gene expression was assessed by quantitative QPCR (2-48h). 2) MCT8 was down-regulated using siRNA, and MCT8 and MCT10 were over-expressed by plasmid transfection. Effects of altering expression were assessed by MTT assay (Proliferation) and Caspase3/7 activity (Apoptosis). Results: We observed that T3 treatment did not affect HTR-8/SVneo proliferation nor alter the mRNA expressions of TH responsive gene, Connexin43 (Cx43) and the pre-receptor regulators of T3 action, deiodinases 2 and 3 (D2, D3), nor its own transporters, MCT8 and MCT10. However, T3 treatment was observed to decrease the expression of TH receptor β1 (TRβ1) (ANOVA p<0.05). Over-expression of MCT8 or MCT10 reduced cell proliferation by 36% and 29% respectively (ANOVA p<0.05) in the presence of T3. Apoptosis was reduced, independently of T3 treatment, by 24 and 31% (+/- T3 respectively) following overexpression of MCT8, and by 12 and 19% (+/- T3 respectively) following overexpression of MCT10, respectively (ANOVA p<0.005). Conversely, down-regulation of MCT8 resulted in increased apoptosis independently of T3 (p<0.003). Conclusions: HTR-8/SVneo cell proliferation does not change with T3 treatment. In addition, MCT8 and MCT10 may have both T3-dependent (suppress proliferation) and T3-independent (apoptosis) effects in EVTs. This suggests an important role for MCT8 and MCT10 in human placental development."],"dc:format":["application/pdf"],"dc:identifier.uri":["http://etheses.bham.ac.uk//id/eprint/1195/1/Choudhury_10_MPhil.pdf","http://etheses.bham.ac.uk//id/eprint/1195/2/Decl_IS_Choudhury_10_MPhil.pdf"],"dc:publisher.department":["College of Medical & Dental Sciences","School of Clinical and Experimental Medicine"],"dc:publisher.institution":["University of Birmingham"],"dc:relation.isreferencedby":["http://etheses.bham.ac.uk//id/eprint/1195/"],"dc:subject":["RC Internal medicine","RJ Pediatrics"],"dc:title":["The role of Thyroid hormone Transporters Monocarboxylate Transporter 10 (MCT10) and Monocarboxylate Transporter 8 (MCT8) in extravillous trophoblasts."],"dc:type":["Thesis"],"dc:type.qualificationlevel":["m_ph"],"dc:type.qualificationname":["m_ph"]},"updated_at":"2026-07-24T01:11:23Z"}