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Jitendra Vishwakarma Developmental Toxicology Laboratory, Systems Toxicology & Health Risk Assessment Group, CSIR-Indian Institute of Toxicology Research (CSIR-IITR), Vishvigyan Bhawan, 31, Mahatma Gandhi Marg, Lucknow-226001, Uttar Pradesh, India
Academy of Scientific and Innovative Research (AcSIR), Ghaziabad, 201002, India

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Keerti Gupta Developmental Toxicology Laboratory, Systems Toxicology & Health Risk Assessment Group, CSIR-Indian Institute of Toxicology Research (CSIR-IITR), Vishvigyan Bhawan, 31, Mahatma Gandhi Marg, Lucknow-226001, Uttar Pradesh, India
Academy of Scientific and Innovative Research (AcSIR), Ghaziabad, 201002, India

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Juhi Mishra Developmental Toxicology Laboratory, Systems Toxicology & Health Risk Assessment Group, CSIR-Indian Institute of Toxicology Research (CSIR-IITR), Vishvigyan Bhawan, 31, Mahatma Gandhi Marg, Lucknow-226001, Uttar Pradesh, India

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Asmita Garg Developmental Toxicology Laboratory, Systems Toxicology & Health Risk Assessment Group, CSIR-Indian Institute of Toxicology Research (CSIR-IITR), Vishvigyan Bhawan, 31, Mahatma Gandhi Marg, Lucknow-226001, Uttar Pradesh, India
Academy of Scientific and Innovative Research (AcSIR), Ghaziabad, 201002, India

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Rafat Malik Developmental Toxicology Laboratory, Systems Toxicology & Health Risk Assessment Group, CSIR-Indian Institute of Toxicology Research (CSIR-IITR), Vishvigyan Bhawan, 31, Mahatma Gandhi Marg, Lucknow-226001, Uttar Pradesh, India

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Amit Kashyap Developmental Toxicology Laboratory, Systems Toxicology & Health Risk Assessment Group, CSIR-Indian Institute of Toxicology Research (CSIR-IITR), Vishvigyan Bhawan, 31, Mahatma Gandhi Marg, Lucknow-226001, Uttar Pradesh, India

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Manoj Shukla Department of Endocrinology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow-226014, Uttar Pradesh, India

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Dhirendra Singh Central Pathology Laboratory, Regulatory Toxicology Group, CSIR-Indian Institute of Toxicology Research (CSIR–IITR), Vishvigyan Bhawan, 31, Mahatma Gandhi Marg, Lucknow-226001, Uttar Pradesh, India

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Sanghamitra Bandyopadhyay Developmental Toxicology Laboratory, Systems Toxicology & Health Risk Assessment Group, CSIR-Indian Institute of Toxicology Research (CSIR-IITR), Vishvigyan Bhawan, 31, Mahatma Gandhi Marg, Lucknow-226001, Uttar Pradesh, India
Academy of Scientific and Innovative Research (AcSIR), Ghaziabad, 201002, India

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Introduction Thyroid hormones (TH), triiodothyronine (T3) and thyroxine (T4), are essential for brain functioning from developmental stages to adulthood ( Salazar et al. 2019 , Bernal 2000 ). On the other hand, TH deficiency, i

Article Type:
Research Article
DOI:
https://doi.org/10.1530/JOE-22-0338
Volume/Issue:
Volume 257: Issue 1
Restricted access
R Singh
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G Upadhyay
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MM Godbole
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Thyroid hormone (TH) deficiency leads to extensive apoptosis during cerebellar development, but the mechanism still remains unclear. Different signals also converge on mitochondria during apoptosis to induce the release of apoptogenic proteins that activate proteolytic cascade through specific enzymes called caspases. Here we studied the effect of hypothyroidism on alterations in mitochondrial structure and translocation of apoptogenic molecules during rat cerebellar development. Structural analysis of mitochondria was studied by electron microscopy. The translocation of apoptogenic molecules was analyzed by Western blotting. TH deficiency led to vacuolization, enlargement and decrease in the number of cristae. The majority of the proapoptotic molecule, Bax, was localized in mitochondria under hypothyroid conditions whereas a limited presence of Bax was detected in the euthyroid state. Translocation of cytochrome c, apoptosis-inducing factor (AIF) and second mitochondrial-derived activator of caspases (SMAC) from mitochondria to cytosol was detected primarily in early developmental stages in the hypothyroid condition. These experimental results demonstrate that TH maintains mitochondrial architecture and inhibits the release of apoptogenic molecules to prevent excess apoptosis during cerebellar development.

Article Type:
Other
DOI:
https://doi.org/10.1677/joe.0.1760321
Volume/Issue:
Volume 176: Issue 3
Free access
R Singh
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G Upadhyay
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S Kumar
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A Kapoor
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A Kumar
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M Tiwari
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MM Godbole
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Thyroid hormone (TH) deficiency results in delayed proliferation and migration of cerebellar granule cells. Although extensive cell loss during the development of the cerebellum under hypothyroid conditions is known, its nature and its mechanism are poorly understood. Bcl-2 family gene expression is known to determine the fate of cells to undergo apoptosis. We evaluated the effect of hypothyroidism on Bcl-2 family gene expression in the developing rat cerebellum. Electrophoresis and Western blotting were used to analyze DNA fragmentation and expression of DNA fragmentation factor (DFF-45), Bcl-2, Bcl-xL and Bax genes respectively. In the hypothyroid condition, extensive DNA fragmentation and enhanced cleavage of DFF-45 were seen throughout development (postnatal day 0 to day 24) and adulthood whereas they were absent in the euthyroid state. The anti-apoptotic genes Bcl-2 and Bcl-xL were down-regulated and the pro-apoptotic gene Bax was expressed at higher levels compared with the euthyroid state. These results suggest that normal levels of TH prevent cerebellar apoptosis to a large extent, whereas hypothyroidism not only increases the extent but also the duration of apoptosis by down-regulating the anti-apoptotic genes and maintaining a high level of the pro-apoptotic gene Bax.

Article Type:
Other
DOI:
https://doi.org/10.1677/joe.0.1760039
Volume/Issue:
Volume 176: Issue 1
Free access
Aline Cordeiro
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Luana Lopes de Souza
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Lorraine Soares Oliveira
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Larissa Costa Faustino
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Letícia Aragão Santiago
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Flavia Fonseca Bloise
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Tania Maria Ortiga-Carvalho
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Norma Aparecida dos Santos Almeida Biophysics Institute Carlos Chagas Filho, Department of Physiological Sciences, Federal University of Rio de Janeiro, Cidade Universitária - Ilha do Fundão, Avenida Carlos Chagas Filho, 373, Centro de Ciências da Saúde, Bloco G, CEP: 21941-902, Rio de Janeiro, RJ, Brazil

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Carmen Cabanelas Pazos-Moura
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and hypothyroid groups ( Fig. 2 D, P <0.01). Therefore, the protein expression of SIRT1 was downregulated by TH in tissues such as liver and BAT and upregulated by TH deficiency in the liver. As hepatic SIRT1 expression was differently altered in the

Article Type:
Research Article
DOI:
https://doi.org/10.1530/JOE-12-0420
Volume/Issue:
Volume 216: Issue 2
Free access
Shiao Y Chan School of Clinical and Experimental Medicine, Department of Pathology, Fetal Medicine Centre, College of Medical and Dental Sciences, University of Birmingham, Edgbaston, Birmingham B15 2TT, UK

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Laura A Hancox School of Clinical and Experimental Medicine, Department of Pathology, Fetal Medicine Centre, College of Medical and Dental Sciences, University of Birmingham, Edgbaston, Birmingham B15 2TT, UK

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Azucena Martín-Santos School of Clinical and Experimental Medicine, Department of Pathology, Fetal Medicine Centre, College of Medical and Dental Sciences, University of Birmingham, Edgbaston, Birmingham B15 2TT, UK

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Laurence S Loubière School of Clinical and Experimental Medicine, Department of Pathology, Fetal Medicine Centre, College of Medical and Dental Sciences, University of Birmingham, Edgbaston, Birmingham B15 2TT, UK

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Merlin N M Walter School of Clinical and Experimental Medicine, Department of Pathology, Fetal Medicine Centre, College of Medical and Dental Sciences, University of Birmingham, Edgbaston, Birmingham B15 2TT, UK

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Ana-Maria González School of Clinical and Experimental Medicine, Department of Pathology, Fetal Medicine Centre, College of Medical and Dental Sciences, University of Birmingham, Edgbaston, Birmingham B15 2TT, UK

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Phillip M Cox School of Clinical and Experimental Medicine, Department of Pathology, Fetal Medicine Centre, College of Medical and Dental Sciences, University of Birmingham, Edgbaston, Birmingham B15 2TT, UK

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Ann Logan School of Clinical and Experimental Medicine, Department of Pathology, Fetal Medicine Centre, College of Medical and Dental Sciences, University of Birmingham, Edgbaston, Birmingham B15 2TT, UK

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Christopher J McCabe School of Clinical and Experimental Medicine, Department of Pathology, Fetal Medicine Centre, College of Medical and Dental Sciences, University of Birmingham, Edgbaston, Birmingham B15 2TT, UK

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Jayne A Franklyn School of Clinical and Experimental Medicine, Department of Pathology, Fetal Medicine Centre, College of Medical and Dental Sciences, University of Birmingham, Edgbaston, Birmingham B15 2TT, UK

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Mark D Kilby School of Clinical and Experimental Medicine, Department of Pathology, Fetal Medicine Centre, College of Medical and Dental Sciences, University of Birmingham, Edgbaston, Birmingham B15 2TT, UK
School of Clinical and Experimental Medicine, Department of Pathology, Fetal Medicine Centre, College of Medical and Dental Sciences, University of Birmingham, Edgbaston, Birmingham B15 2TT, UK

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, reduced neuronal migration, or increased cell death in IUGR is not known. In rats, abnormal neuronal migration in the fetal CNS in both IUGR ( Sasaki et al . 2000 ) and TH deficiency ( Auso et al . 2004 ) has been reported. Maternal TH deficiency in rats

Article Type:
Research Article
DOI:
https://doi.org/10.1530/JOE-13-0400
Volume/Issue:
Volume 220: Issue 2
Open access
A Santillo Dipartimento di Scienze e Tecnologie Ambientali, Biologiche e Farmaceutiche, Seconda Università degli Studi di Napoli, via Vivaldi, 43, 81100 Caserta, Italy

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L Burrone Dipartimento di Scienze e Tecnologie Ambientali, Biologiche e Farmaceutiche, Seconda Università degli Studi di Napoli, via Vivaldi, 43, 81100 Caserta, Italy

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S Falvo Dipartimento di Scienze e Tecnologie Ambientali, Biologiche e Farmaceutiche, Seconda Università degli Studi di Napoli, via Vivaldi, 43, 81100 Caserta, Italy

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R Senese Dipartimento di Scienze e Tecnologie Ambientali, Biologiche e Farmaceutiche, Seconda Università degli Studi di Napoli, via Vivaldi, 43, 81100 Caserta, Italy

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A Lanni Dipartimento di Scienze e Tecnologie Ambientali, Biologiche e Farmaceutiche, Seconda Università degli Studi di Napoli, via Vivaldi, 43, 81100 Caserta, Italy

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G Chieffi Baccari Dipartimento di Scienze e Tecnologie Ambientali, Biologiche e Farmaceutiche, Seconda Università degli Studi di Napoli, via Vivaldi, 43, 81100 Caserta, Italy

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). Nuclear receptors for triiodothyronine (T 3 ) have been observed in the HG of the golden hamster ( Vilchis & Perez-Pelacios 1989 ). TH injections lead to an increase in porphyrin content in hamster HG, an effect that is reversed under conditions of TH

Article Type:
Research Article
DOI:
https://doi.org/10.1530/JOE-13-0127
Volume/Issue:
Volume 219: Issue 1
Free access
Praveen Kumar Department of Molecular Medicine and Biotechnology, Department of Biochemistry and Biophysics, Cardiovascular and Metabolic Disorder Program, Sanjay Gandhi Post Graduate Institute of Medical Sciences, Lucknow 226014, India

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Vishwa Mohan Department of Molecular Medicine and Biotechnology, Department of Biochemistry and Biophysics, Cardiovascular and Metabolic Disorder Program, Sanjay Gandhi Post Graduate Institute of Medical Sciences, Lucknow 226014, India

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Rohit Anthony Sinha Department of Molecular Medicine and Biotechnology, Department of Biochemistry and Biophysics, Cardiovascular and Metabolic Disorder Program, Sanjay Gandhi Post Graduate Institute of Medical Sciences, Lucknow 226014, India

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Megha Chagtoo Department of Molecular Medicine and Biotechnology, Department of Biochemistry and Biophysics, Cardiovascular and Metabolic Disorder Program, Sanjay Gandhi Post Graduate Institute of Medical Sciences, Lucknow 226014, India

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Madan M Godbole Department of Molecular Medicine and Biotechnology, Department of Biochemistry and Biophysics, Cardiovascular and Metabolic Disorder Program, Sanjay Gandhi Post Graduate Institute of Medical Sciences, Lucknow 226014, India

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other epigenetic mechanism such as DNA methylation and miRNAs involved in unliganded TR action. Since TH deficiency during pregnancy and birth is still a major health concern globally, our results raise an intriguing possibility as to whether HDAC

Article Type:
Research Article
DOI:
https://doi.org/10.1530/JOE-15-0168
Volume/Issue:
Volume 227: Issue 2
Free access
Joachim M Weitzel Institute of Reproductive Biology, Leibniz Institute for Farm Animal Biology (FBN), Dummerstorf, Germany

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Torsten Viergutz Institute of Reproductive Biology, Leibniz Institute for Farm Animal Biology (FBN), Dummerstorf, Germany

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Dirk Albrecht Institute of Microbiology, Ernst-Moritz-Arndt-University, Greifswald, Germany

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Rupert Bruckmaier Veterinary Physiology, Vetsuisse Faculty, University of Bern, Bern, Switzerland

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Marion Schmicke Clinic for Cattle, Endocrinology Laboratory, University of Veterinary Medicine Hannover, Hannover, Germany

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Armin Tuchscherer Institute of Genetics and Biometry, Leibniz Institute for Farm Animal Biology (FBN), Dummerstorf, Germany

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Franziska Koch Institute of Nutritional Physiology ‘Oskar Kellner’, Leibniz Institute for Farm Animal Biology (FBN), Dummerstorf, Germany

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Björn Kuhla Institute of Nutritional Physiology ‘Oskar Kellner’, Leibniz Institute for Farm Animal Biology (FBN), Dummerstorf, Germany

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a TH deficiency (hypothyroidism) is associated with a decrease in body temperature ( Mullur et al. 2014 ). Both statuses are accomplished by accelerated and dampened metabolic activities, respectively. Further, alterations in important thyroid

Article Type:
Research Article
DOI:
https://doi.org/10.1530/JOE-17-0066
Volume/Issue:
Volume 234: Issue 2
Open access
H A Sterle Instituto de Investigaciones Biomédicas (BIOMED), Centro de Estudios Farmacológicos y Botánicos (CEFYBO), Laboratorio de Radioisótopos, Area de Investigación, Departamento de Química Biológica, Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET), Facultad de Ciencias Médicas, Pontificia Universidad Católica Argentina (UCA), Av. A. Moreau de Justo 1600, 3er piso, 1107AFF Buenos Aires, Argentina

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E Valli Instituto de Investigaciones Biomédicas (BIOMED), Centro de Estudios Farmacológicos y Botánicos (CEFYBO), Laboratorio de Radioisótopos, Area de Investigación, Departamento de Química Biológica, Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET), Facultad de Ciencias Médicas, Pontificia Universidad Católica Argentina (UCA), Av. A. Moreau de Justo 1600, 3er piso, 1107AFF Buenos Aires, Argentina

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F Cayrol Instituto de Investigaciones Biomédicas (BIOMED), Centro de Estudios Farmacológicos y Botánicos (CEFYBO), Laboratorio de Radioisótopos, Area de Investigación, Departamento de Química Biológica, Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET), Facultad de Ciencias Médicas, Pontificia Universidad Católica Argentina (UCA), Av. A. Moreau de Justo 1600, 3er piso, 1107AFF Buenos Aires, Argentina

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M A Paulazo Instituto de Investigaciones Biomédicas (BIOMED), Centro de Estudios Farmacológicos y Botánicos (CEFYBO), Laboratorio de Radioisótopos, Area de Investigación, Departamento de Química Biológica, Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET), Facultad de Ciencias Médicas, Pontificia Universidad Católica Argentina (UCA), Av. A. Moreau de Justo 1600, 3er piso, 1107AFF Buenos Aires, Argentina

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D J Martinel Lamas Instituto de Investigaciones Biomédicas (BIOMED), Centro de Estudios Farmacológicos y Botánicos (CEFYBO), Laboratorio de Radioisótopos, Area de Investigación, Departamento de Química Biológica, Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET), Facultad de Ciencias Médicas, Pontificia Universidad Católica Argentina (UCA), Av. A. Moreau de Justo 1600, 3er piso, 1107AFF Buenos Aires, Argentina

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M C Diaz Flaqué Instituto de Investigaciones Biomédicas (BIOMED), Centro de Estudios Farmacológicos y Botánicos (CEFYBO), Laboratorio de Radioisótopos, Area de Investigación, Departamento de Química Biológica, Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET), Facultad de Ciencias Médicas, Pontificia Universidad Católica Argentina (UCA), Av. A. Moreau de Justo 1600, 3er piso, 1107AFF Buenos Aires, Argentina

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A J Klecha Instituto de Investigaciones Biomédicas (BIOMED), Centro de Estudios Farmacológicos y Botánicos (CEFYBO), Laboratorio de Radioisótopos, Area de Investigación, Departamento de Química Biológica, Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET), Facultad de Ciencias Médicas, Pontificia Universidad Católica Argentina (UCA), Av. A. Moreau de Justo 1600, 3er piso, 1107AFF Buenos Aires, Argentina

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L Colombo Instituto de Investigaciones Biomédicas (BIOMED), Centro de Estudios Farmacológicos y Botánicos (CEFYBO), Laboratorio de Radioisótopos, Area de Investigación, Departamento de Química Biológica, Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET), Facultad de Ciencias Médicas, Pontificia Universidad Católica Argentina (UCA), Av. A. Moreau de Justo 1600, 3er piso, 1107AFF Buenos Aires, Argentina

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V A Medina Instituto de Investigaciones Biomédicas (BIOMED), Centro de Estudios Farmacológicos y Botánicos (CEFYBO), Laboratorio de Radioisótopos, Area de Investigación, Departamento de Química Biológica, Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET), Facultad de Ciencias Médicas, Pontificia Universidad Católica Argentina (UCA), Av. A. Moreau de Justo 1600, 3er piso, 1107AFF Buenos Aires, Argentina

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G A Cremaschi Instituto de Investigaciones Biomédicas (BIOMED), Centro de Estudios Farmacológicos y Botánicos (CEFYBO), Laboratorio de Radioisótopos, Area de Investigación, Departamento de Química Biológica, Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET), Facultad de Ciencias Médicas, Pontificia Universidad Católica Argentina (UCA), Av. A. Moreau de Justo 1600, 3er piso, 1107AFF Buenos Aires, Argentina
Instituto de Investigaciones Biomédicas (BIOMED), Centro de Estudios Farmacológicos y Botánicos (CEFYBO), Laboratorio de Radioisótopos, Area de Investigación, Departamento de Química Biológica, Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET), Facultad de Ciencias Médicas, Pontificia Universidad Católica Argentina (UCA), Av. A. Moreau de Justo 1600, 3er piso, 1107AFF Buenos Aires, Argentina

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M L Barreiro Arcos Instituto de Investigaciones Biomédicas (BIOMED), Centro de Estudios Farmacológicos y Botánicos (CEFYBO), Laboratorio de Radioisótopos, Area de Investigación, Departamento de Química Biológica, Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET), Facultad de Ciencias Médicas, Pontificia Universidad Católica Argentina (UCA), Av. A. Moreau de Justo 1600, 3er piso, 1107AFF Buenos Aires, Argentina
Instituto de Investigaciones Biomédicas (BIOMED), Centro de Estudios Farmacológicos y Botánicos (CEFYBO), Laboratorio de Radioisótopos, Area de Investigación, Departamento de Química Biológica, Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET), Facultad de Ciencias Médicas, Pontificia Universidad Católica Argentina (UCA), Av. A. Moreau de Justo 1600, 3er piso, 1107AFF Buenos Aires, Argentina

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area of the tumors. This is probably a result of TH deficiency. In fact, THs are necessary growth factors involved in T cell lymphoma proliferative and survival signals ( Barreiro Arcos et al . 2006 , 2011 ), hence the lack of THs would induce cell

Article Type:
Research Article
DOI:
https://doi.org/10.1530/JOE-14-0159
Volume/Issue:
Volume 222: Issue 2
Free access
Joke Delbaere Laboratory of Comparative Endocrinology, Department of Biology, KU Leuven, Leuven, Belgium

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Pieter Vancamp Laboratory of Comparative Endocrinology, Department of Biology, KU Leuven, Leuven, Belgium

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Stijn L J Van Herck Laboratory of Comparative Endocrinology, Department of Biology, KU Leuven, Leuven, Belgium

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Nele M A Bourgeois Laboratory of Comparative Endocrinology, Department of Biology, KU Leuven, Leuven, Belgium

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Mary J Green Medical Research Council Centre for Developmental Neurobiology, King’s College London, London, UK

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Richard J T Wingate Medical Research Council Centre for Developmental Neurobiology, King’s College London, London, UK

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Veerle M Darras Laboratory of Comparative Endocrinology, Department of Biology, KU Leuven, Leuven, Belgium

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demonstrate the impact of TH deficiency on distinct neurodevelopmental processes, they have not addressed the underlying mechanisms of TH action in the developing brain. As a prerequisite for TH action, intracellular concentrations of THs are tightly

Article Type:
Research Article
DOI:
https://doi.org/10.1530/JOE-16-0323
Volume/Issue:
Volume 232: Issue 2
Free access