Estrogen may protect against depression after heart attack

image credit: universityhealthnews.com

Estrogen may protect against heart failure-related depression by preventing the production of inflammation-causing chemicals in the brain. The study is published ahead of print in the American Journal of Physiology -- Heart and Circulatory Physiology.

Research suggests that people with heart failure -- including those who survive heart attacks -- are two to three times more likely to suffer from depression than the general population. The reason for heart failure-related depression is thought to be increased inflammation in the brain. Previous studies have also found that post-menopausal women with heart disease have a greater risk of depression than younger women and men of all ages.

New findings link estrogen and T cell immune response to autoimmune inflammation

thediabeticjourney.com

Women are more prone to the development of autoimmune diseases. The female hormone estrogen is likely to affect the immune system. A team of scientists from Turku Center for Biotechnology and University of Georgia reported new findings related to the involvement of estrogen hormone receptor in autoimmune diseases.

The incidence of autoimmune diseases such as MS, RA, and SLE is higher in women than in men. The estrogen hormone secreted in women may contribute to the pathogenesis of these diseases.

A research team led by Docent Zhi Chen from Turku Center for Biotechnology of the University of Turku has collaborated with researchers from the University of Georgia, United States to address the long-standing issue of hormonal effect on autoimmune diseases.

Estrogen hormone shows its action on cells mostly through estrogen receptor alpha (ERα). Researchers from Turku generated mice with ERα protein specifically deleted in T cells.

"The eureka moment of our research is that in a mouse model of human inflammatory bowel disease, transfer of naive T helper cells from ERα deficient mice did not succumb to colitis, unlike transfer from their counterparts," Docent Zhi Chen tells.

"Furthermore, using cutting-edge technique RNA sequencing approach combined with in vitro and in vivo experiments, we discovered that ERα regulates multiple aspects of T cell function, including T cell activation, proliferation and survival," Chen adds.

Regulatory T cells are group of T cells that help in preventing autoimmune diseases. The researchers found that ERα influences the function and differentiation of regulatory T cells.

Source: sciencedaily.com

Estrogen discovery could shed new light on fertility problems

via fineartamerica.com

"Estrogen produced in the brain is necessary for ovulation in monkeys, according to researchers at the University of Wisconsin-Madison who have upended the traditional understanding of the hormonal cascade that leads to release of an egg from the ovaries.

Their findings, published Dec. 11 in the journal Proceedings of the National Academy of Science, may reveal the cause of some undiagnosed infertility problems and point the way to new methods of birth control.

For decades, scientists have known that a group of neurons in a part of the brain called the hypothalamus and cells in the pituitary gland control the menstrual cycle. The brain stimulates the pituitary to make hormones that, early in the menstrual cycle, spur the ovaries to produce estrogens -- predominantly a type of estrogen called estradiol.

Estradiol builds in the bloodstream until it reaches a concentration that causes a surge of the hypothalamic and pituitary hormones, including one called luteinizing hormone, which in turn trigger an ovary to release an egg.

"It's a feedback loop, and scientists have thought for some time that it was all to do with the estrogen from the ovaries," says Ei Terasawa, professor of pediatrics at the UW-Madison School of Medicine and Public Health and senior scientist at the Wisconsin National Primate Research Center. "Then, in 2013, we discovered the hypothalamus was releasing estradiol like the ovaries, and we were so surprised. We knew it had to be important..."

Learn more:

https://www.sciencedaily.com/releases/2017/12/171212124725.htm

Do women with migraine have higher estrogen levels?

via time.com

"Researchers have long known that sex hormones such as estrogen play a role in migraine. But there's been little research on how that works. Do women with migraine have higher estrogen levels in general? Higher levels at the peak of the monthly cycle?

Research published in the June 1, 2016, online issue of Neurology®, the medical journal of the American Academy of Neurology, shows that, for women with a history of migraine, estrogen levels may drop more rapidly in the days just before menstruation than they do for women who do not have migraine history. For other hormone patterns, there were no differences between women with migraine and women who did not have migraine.

The study also showed that the women with a migraine history had a faster rate of estrogen decline regardless of whether they had a migraine during that cycle.

"These results suggest that a 'two-hit' process may link estrogen withdrawal to menstrual migraine. More rapid estrogen decline may make women vulnerable to common triggers for migraine attacks such as stress, lack of sleep, foods and wine," said study author Jelena Pavlovi?, MD, PhD, of Albert Einstein College of Medicine/Montefiore Medical Center in Bronx, NY, and a member of the American Academy of Neurology..."

Learn More:

https://www.sciencedaily.com/releases/2016/06/160601163522.htm

Tamoxifen resistance linked to high estrogen levels in utero

"An animal study suggests that resistance to tamoxifen therapy in some estrogen receptor positive breast cancers may originate from in utero exposure to endocrine disrupting chemicals. The study provides a new path forward in human research as about half of the breast cancers treated with this common cancer therapy do not respond well, say researchers at the Georgetown Lombardi Comprehensive Cancer Center, who led the multi-institutional research.

The study, published in the Journal of the National Cancer Institute (JNCI), identified four genes that are linked to tamoxifen resistance and poor prognosis of breast cancer, by comparing results obtained in a new animal model, in human breast cancer cells grown in culture, and in publically available datasets collected from thousands of estrogen receptor positive breast cancer patients treated with tamoxifen.

"Higher estrogen levels in utero have been known to increase risk of estrogen positive breast cancer in laboratory animals -- and humans -- but it wasn't known until this study that these elevated levels may also be responsible for tamoxifen resistance," says the study's co-lead author, Leena Hilakivi-Clarke, PhD, a professor of oncology at Georgetown Lombardi..."

Learn more:

https://www.sciencedaily.com/releases/2016/09/160908131224.htm

Estrogen protects women against the flu, study finds

via micro.magent.fsu.edu

"The female sex hormone estrogen has anti-viral effects against the influenza A virus, commonly known as the flu, a new study in American Journal of Physiology -- Lung Cellular and Molecular Physiology reports.

A virus infects and causes sickness by entering a cell and making copies of itself inside the host cell. When released from infected cells, the virus can spread through the body and between people. How much a virus has replicated determines its severity. Less replication of the virus means the infected person may experience less disease or is less likely to spread the disease to someone else, says Sabra Klein, PhD, of Johns Hopkins University and lead investigator of the study.

To examine how estrogen affected the flu virus's ability to replicate, the research team gathered nasal cells -- the cell type that the flu virus primarily infects -- from male and female donors. The researchers exposed the cell cultures to the virus, estrogen, the environmental estrogen bisphenol A and selective estrogen receptor modulators (SERM), which are compounds that act like estrogen that are used for hormone therapy..."

Learn more:

https://www.sciencedaily.com/releases/2016/01/160112093424.htm