A Quantification of the Injury-Induced Changes in Central Aromatase, Oestrogenic Milieu and Steroid Receptor Expression in the Zebra Finch
| Autor: | Colin J. Saldanha, Lars H. Nelson, Carissa J. Mehos |
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| Rok vydání: | 2015 |
| Předmět: |
0301 basic medicine
Male medicine.medical_specialty Traumatic brain injury Endocrinology Diabetes and Metabolism Receptor expression Neuroprotection Article 03 medical and health sciences Cellular and Molecular Neuroscience 0302 clinical medicine Endocrinology Aromatase Internal medicine medicine Animals Receptor Zebra finch Neuroinflammation biology Estradiol Endocrine and Autonomic Systems medicine.disease Up-Regulation Androgen receptor 030104 developmental biology Receptors Estrogen Receptors Androgen Astrocytes Brain Injuries biology.protein Female Finches 030217 neurology & neurosurgery |
| Zdroj: | J Neuroendocrinol |
| ISSN: | 1365-2826 |
| Popis: | In songbirds and mammals, brain injury results in the upregulation of aromatase (estrogen synthase) expression in astroglia. The resulting, presumed synthesis of neural estradiol (E(2)) has neuroprotective effects including a decrease in neurodegeneration, neuroinflammation, and apoptosis. The development of therapeutic tools that exploit estrogenic neuroprotection in the treatment of neurotrauma require a precise quantification of the endogenous changes in neural aromatase and estradiol following brain injury. Surprisingly, the expected increase in neural estrogens following brain injury has not been demonstrated. Further, we are just beginning to unravel the mechanisms behind the protective effects of centrally synthesized estradiol. In the current study, levels of aromatase immunoprotein, neural estradiol, and steroid receptor mRNA were quantified in adult male and female zebra finches 48 hours following a unilateral penetrating brain injury. Both aromatase and estradiol were upregulated in the injured hemisphere of the brain compared to the uninjured hemisphere, demonstrating, for the first time, a robust increase in neural estradiol levels following injury. We did not detect an effect of injury on mRNA expression of the estrogen receptors (ER)-α, ER-β, or GPER-1, but observed a significant decrease in androgen receptor (AR) transcription in the injured lobe relative to the contralateral uninjured hemisphere. We conclude that mechanical damage causes a dramatic increase in local aromatization, and the resultant high levels of central estradiol are available to modulate steroid sensitive targets. Studies using alternate methods of receptor detection and/or time points may be necessary to understand the complete suite of mechanisms underlying the neuroprotective effects of induced estrogen synthesis in this animal model. |
| Databáze: | OpenAIRE |
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