SLC16A2 Membrane Protein Introduction

Introduction of SLC16A2

SLC16A2 is also known as Monocarboxylate transporter 8, Monocarboxylate transporter 7 (MCT7), Solute carrier family 16 member 2 and X-linked PEST-containing transporter (XPCT). It belongs to the monocarboxylate transporters (MCTs), encoded by the SLC16 gene family. The family consists of 14 members, of which SLC16A2 (encoded by SLC16A2) and MCT10 (encoded by SLC16A10) are two homologous 12 transmembrane helical proteins responsible for thyroid hormones transport and play vital roles during mammalian embryonic brain development.

Function of SLC16A2 Membrane Protein

The SLC16A2 gene located on the X chromosome encodes the SLC16A2 protein, a 63 kDa transmembrane protein which is a well-established thyroid hormones transporter. Injection of rat SLC16A2 mRNA into Xenopus oocytes resulted in a 10-fold increase in thyroxine (T4) and triiodothyronine (T3) uptake, whilst the transfection of human SLC16A2 cDNA into COS1 and JEG3 cells have little or no endogenous SLC16A2, more than doubled the uptake of T3. SLC16A2 mutations result in X-linked severe global neurodevelopmental delay associated with low circulating T4, high T3 and normal or slightly elevated thyroid stimulating hormone (TSH). Reports of a hyperplastic thyroid lesion in a male patient carrying an SLC16A2 mutation and papillary hyperplasia in SLC16A2 knockout mice suggest that SLC16A2 suppresses thyrocyte cell turnover in vivo. Meanwhile, SLC16A2 suppresses the proliferation of JEG-3 (a choriocarcinoma cell line) and N-Tera-2 (a neuronal precursor cell line) cells in a T3-independent manner, just as SLC16A2 decreased the viability of non-proliferating primary term cytotrophoblast.

Fig.1 Structural model of SLC16A2 membrane protein. (Fischer, 2015)

Application of SLC16A2 Membrane Protein in Literature

1. Fischer J., et al. Modulation of monocarboxylate transporter 8 oligomerization by specific pathogenic mutations. Journal of Molecular Endocrinology. 2015, 54(1):39-50. PubMed ID: 25527620
   
   

   The results of this article add a new link between the functions (substrate transport) and protein dimerization of SLC16A2 and might be of relevance for other members of the major facilitator superfamily.

2. Vasilopoulou E., et al. Monocarboxylate Transporter 8 Modulates the Viability and Invasive Capacity of Human Placental Cells and Fetoplacental Growth in Mice. PLOS ONE. 2013, 8(6):e65402. PubMed ID: 23776477
   
   

   This article investigates the effect of altering SLC16A2 expression in human trophoblast in vitro and in a SLC16A2 knockout mouse model. Silencing of endogenous SLC16A2 reduced T3 uptake into human extravillous trophoblast-like cells and SLC16A2 over-expression transiently increased T3 uptake.

3. Lee J.Y., et al. Overcoming Monocarboxylate Transporter 8 (MCT8)-Deficiency to Promote Human Oligodendrocyte Differentiation and Myelination. EBioMedicine. 2017, 25:122-135. PubMed ID: 29111262
   
   

   The results of this article highlight the potential role of SLC16A2 in TH transport for human oligodendrocytes development and may implicate DITPA (an SLC16A2 independent thyroid hormone analog) as a promising treatment for developmentally-regulated myelination in X-linked-inherited psychomotor retardation and hypomyelination disorder, Allan-Herndon-Dudley syndrome.

4. Friesema E.C.H., et al. Identification of Monocarboxylate Transporter 8 as a Specific Thyroid Hormone Transporter. J. Biol. Chem. 2013, 278(41):40128-40135. PubMed ID: 12871948
   
   

   Authors in this article clone rat SLC16A2 and apply immunohistochemistry to show that SLC16A2 is highly expressed in liver, kidney, brain, and heart. More importantly, the results of this article demonstrate that SLC16A2 is a very active and specific thyroid hormone transporter.

5. Trajkovic-Arsic M., et al. Consequences of Monocarboxylate Transporter 8 Deficiency for Renal Transport and Metabolism of Thyroid Hormones in Mice. Endocrinology. 2010, 151(2):802-809. PubMed ID: 19996182
   
   

   This article proposes that the renal alterations in thyroid hormone metabolism observed in SLC16A2 null mice represent an important pathogenic mechanism by which serum T4 is decreased and serum T3 levels are further stimulated.

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Reference

1. Fischer J., et al. (2015) Modulation of monocarboxylate transporter 8 oligomerization by specific pathogenic mutations. Journal of Molecular Endocrinology. 54(1):39-50.

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