Estrogen Formation and Inactivation Following TBI: What we Know and Where we Could go.

Kelli A Duncan

doi:10.3389/fendo.2020.00345

Abstract

Traumatic brain injury (TBI) is responsible for various neuronal and cognitive deficits as well as psychosocial dysfunction. Characterized by damage inducing neuroinflammation, this response can cause an acute secondary injury that leads to widespread neurodegeneration and loss of neurological function. Estrogens decrease injury induced neuroinflammation and increase cell survival and neuroprotection and thus are a potential target for use following TBI. While much is known about the role of estrogens as a neuroprotective agent following TBI, less is known regarding their formation and inactivation following damage to the brain. Specifically, very little is known surrounding the majority of enzymes responsible for the production of estrogens. These estrogen metabolizing enzymes (EME) include aromatase, steroid sulfatase (STS), estrogen sulfotransferase (EST/SULT1E1), and some forms of 17β-hydroxysteroid dehydrogenase (HSD17B) and are involved in both the initial conversion and interconversion of estrogens from precursors. This article will review and offer new prospective and ideas on the expression of EMEs following TBI.

Highlights

Traumatic brain injury (TBI) is a leading cause of human death and morbidity worldwide
Very little is known about the expression of SULT1E1 following TBI, there is some data on the role of estradiol-sulfate (E2-SO4) in rodent models
Like STS, we did not see a significant increase or decrease in expression of SULT1E1 following TBI (Figures 2C,D), the expression was far more variable than that of STS

Summary

Introduction

Traumatic brain injury (TBI) is a leading cause of human death and morbidity worldwide. In addition to these effects on cell/neuronal survival, estrogens can regulate neuroinflammation following injury. Estrogen synthesis following TBI reduces the concentration of pro-inflammatory cytokines and decreases the secondary wave of degeneration observed following damage to the brain [30, 48,49,50].

Results

Conclusion