The Effects of Estrogen on Intracellular Calcium Release and Amyloid Beta 1-42-induced Cytokine Expression in Human Microglia

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Nattinee Jantaratnotai
Yupin Sanvarinda


Microglia act as the macrophages of the brain. They can secrete proinflammatory

molecules that could exacerbate neuronal injury in many models such as ischemia, oxidative

stress, and neurodegenerative diseases. Estrogen is known to be neuroprotective in these

models. In the present study, amyloid beta peptides (Aβ), the main component of amyloid

plaques found in the brains of Alzheimer's patients was used as a stimulator of microglia.

There is massive evidence that Aβ cause a number of cytotoxic events that finally lead to

neuronal apoptosis and reactive gliosis which seem to be reversed by preadministration of

estrogen. The roles of estrogen and Aβ upon glial activation are not as well studied as in

neurons. For microglia, estrogen treatment can decrease NO, superoxide, and TNF-α

production, thus attenuating the inflammatory responses induced by LPS or Aβ. However,

these studies were usually done in murine microglia. The roles of estrogen upon human

microglia have never been explored before. We would like to see if estrogen differentially

regulate microglia from human compared to murine. By employing human microglia, it

should better reflect the response to estrogen in real patients. Cytokine expression was

examined to determine the degree of microglial activation. Also, the potential molecular

mechanism by which estrogen exerts upon microglia was detected using spectrofluorometry

to see if estrogen can regulate the intracellular calcium in microglia.

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2003 Annual Meeting Abstracts/Lectures