The following is a summary of “Estradiol and 3β-diol protect female cortical astrocytes by regulating connexin 43 Gap Junctions,” published in the December 2023 issue of Endocrinology by Kim et al.

Some research says estrogens can help protect neurons from damage like oxidative stress and keep their function. However, the most common way to think about this is that these steroids directly affect the neurons. But there was more and more proof that glial cells, like astrocytes, play a significant role in protecting cells. 

Researchers knew that the protein connexin 43 (Cx43), which is found in large amounts in astrocytes and is essential for cell-to-cell signaling, might be a target for estradiol (E2) and 3β-diol, which is an estrogenic product of DHT. Furthermore, they wanted to find out if either or both of these hormones lessen the damage caused by oxidative stress on cells by either lowering the production of Cx43 or blocking the opening and closing of the Cx43 channel. They studied how E2 and 3β-diol helped protect primary cortical astrocytes from iodoacetic acid (IAA), a mixed metabolic and oxidative stress.

On top of that, estrogen receptor blockers stopped these effects. However, E2 and 3β-diol did not change the levels of Cx43 mRNA in astrocytes. Instead, they stopped IAA from opening or letting Cx43 through at gap junctions. The results suggested that the astrocyte Cx43 gap junction may play a role in how estrogens protect cells in the brain, which has not been studied much. Because of the many diseases linked to Cx43 function or failure, learning more about the connection between gonadal steroids and Cx43 channels could help them figure out why some diseases affect men and women differently.

Source: sciencedirect.com/science/article/abs/pii/S030372072300196X