Molecular Basis for Certain Neuroprotective Effects of Thyroid Hormone
The pathophysiology of brain damage that is common to ischemia-reperfusion inury and brain trauma includes disordered neuronal and glial cell energetics, intracellular acidosis, calcium toxicity, extracellular excitotoxic glutamate accumulation and dysfunction of the cytoskeleton and endoplasmic ret...
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| Format: | Article |
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Frontiers Media S.A.
2011-10-01
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| Series: | Frontiers in Molecular Neuroscience |
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| Online Access: | http://journal.frontiersin.org/Journal/10.3389/fnmol.2011.00029/full |
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| author | Paul eDavis Paul eDavis Hung-Yun eLin Faith B Davis Mary eLuidens Shaker eMousa James eCao Min eZhou |
| author_facet | Paul eDavis Paul eDavis Hung-Yun eLin Faith B Davis Mary eLuidens Shaker eMousa James eCao Min eZhou |
| author_sort | Paul eDavis |
| collection | DOAJ |
| description | The pathophysiology of brain damage that is common to ischemia-reperfusion inury and brain trauma includes disordered neuronal and glial cell energetics, intracellular acidosis, calcium toxicity, extracellular excitotoxic glutamate accumulation and dysfunction of the cytoskeleton and endoplasmic reticulum. Thyroid hormone isoforms, 3, 5, 3'-triiodo-L-thyronine (T3) and L-thyroxine (T4), have nongenomic and genomic actions that are relevant to repair of certain features of the pathophysiology of brain damage. Thyroid hormone can nongenomically repair intracullar H+ accumulation by stimulation of the Na+/H+ exchanger and can support desirably low [Ca2+]i.c. by activation of plasma membrane Ca2+-ATPase. Thyroid hormone nongenomically stimulates astrocyte glutamate uptake, an action that protects both glial cells and neurons. The hormone supports the integrity of the cytoskeleton by its effect on actin. Several proteins linked to thyroid hormone action are also neuroprotective. For example, the hormone stimulates expression of the seladin-1 gene whose gene product is anti-apoptotic and is potentially protection in the setting of neurodegeneration. Transthyretin (TTR) is a serum transport protein for T4 that is important to blood-brain barrier transfer of the hormone and TTR has also been found to be neuroprotective in the setting of ischemia. Finally, the interesting thyronamine derivatives of T4 have been shown to protect against ischemic brain damage through their ability to induce hypothermia in the intact organism. Thus, thyroid hromone or hormone derivatives have experimental promise as neuroprotective agents. |
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| id | doaj.art-1d5e84ab9275449d928f4d6e91769dda |
| institution | Directory Open Access Journal |
| issn | 1662-5099 |
| language | English |
| last_indexed | 2024-04-13T18:54:18Z |
| publishDate | 2011-10-01 |
| publisher | Frontiers Media S.A. |
| record_format | Article |
| series | Frontiers in Molecular Neuroscience |
| spelling | doaj.art-1d5e84ab9275449d928f4d6e91769dda2022-12-22T02:34:19ZengFrontiers Media S.A.Frontiers in Molecular Neuroscience1662-50992011-10-01410.3389/fnmol.2011.0002913931Molecular Basis for Certain Neuroprotective Effects of Thyroid HormonePaul eDavis0Paul eDavis1Hung-Yun eLin2Faith B Davis3Mary eLuidens4Shaker eMousa5James eCao6Min eZhou7Ordway STAlbany College of Pharmacy and Health SciencesOrdway STOrdway STAlbany Medical CollegeAlbany College of Pharmacy and Health SciencesAlbany Medical CollegeOhio State University College of MedicineThe pathophysiology of brain damage that is common to ischemia-reperfusion inury and brain trauma includes disordered neuronal and glial cell energetics, intracellular acidosis, calcium toxicity, extracellular excitotoxic glutamate accumulation and dysfunction of the cytoskeleton and endoplasmic reticulum. Thyroid hormone isoforms, 3, 5, 3'-triiodo-L-thyronine (T3) and L-thyroxine (T4), have nongenomic and genomic actions that are relevant to repair of certain features of the pathophysiology of brain damage. Thyroid hormone can nongenomically repair intracullar H+ accumulation by stimulation of the Na+/H+ exchanger and can support desirably low [Ca2+]i.c. by activation of plasma membrane Ca2+-ATPase. Thyroid hormone nongenomically stimulates astrocyte glutamate uptake, an action that protects both glial cells and neurons. The hormone supports the integrity of the cytoskeleton by its effect on actin. Several proteins linked to thyroid hormone action are also neuroprotective. For example, the hormone stimulates expression of the seladin-1 gene whose gene product is anti-apoptotic and is potentially protection in the setting of neurodegeneration. Transthyretin (TTR) is a serum transport protein for T4 that is important to blood-brain barrier transfer of the hormone and TTR has also been found to be neuroprotective in the setting of ischemia. Finally, the interesting thyronamine derivatives of T4 have been shown to protect against ischemic brain damage through their ability to induce hypothermia in the intact organism. Thus, thyroid hromone or hormone derivatives have experimental promise as neuroprotective agents.http://journal.frontiersin.org/Journal/10.3389/fnmol.2011.00029/fullischemia-reperfusion injuryThyroid hormoneCalcium ATPaseSeladin-1Sodium-proton ezxchangerThyronamines |
| spellingShingle | Paul eDavis Paul eDavis Hung-Yun eLin Faith B Davis Mary eLuidens Shaker eMousa James eCao Min eZhou Molecular Basis for Certain Neuroprotective Effects of Thyroid Hormone Frontiers in Molecular Neuroscience ischemia-reperfusion injury Thyroid hormone Calcium ATPase Seladin-1 Sodium-proton ezxchanger Thyronamines |
| title | Molecular Basis for Certain Neuroprotective Effects of Thyroid Hormone |
| title_full | Molecular Basis for Certain Neuroprotective Effects of Thyroid Hormone |
| title_fullStr | Molecular Basis for Certain Neuroprotective Effects of Thyroid Hormone |
| title_full_unstemmed | Molecular Basis for Certain Neuroprotective Effects of Thyroid Hormone |
| title_short | Molecular Basis for Certain Neuroprotective Effects of Thyroid Hormone |
| title_sort | molecular basis for certain neuroprotective effects of thyroid hormone |
| topic | ischemia-reperfusion injury Thyroid hormone Calcium ATPase Seladin-1 Sodium-proton ezxchanger Thyronamines |
| url | http://journal.frontiersin.org/Journal/10.3389/fnmol.2011.00029/full |
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