Estrogen and Its Receptors

“Estrogens” are a family of molecules that play a role in the development and maintenance of female characteristics and sexual reproduction. They are a type of steroid molecule with a carbon atom skeleton consisting of four rings.

Estrogens exert their effects on target tissues by binding to Estrogen Receptors, which are protein molecules found inside the cells that are the targets for estrogen actions. These receptors have a specific site where estrogens or similar molecules can bind. Only cells that contain Estrogen Receptors are affected by estrogens circulating in the bloodstream. The analogy can be made to turning on an electrical switch connected to a light. When the switch is turned on, the light goes on. Similarly, when the cell responds to certain substances, specific activities are activated. When estrogen binds to the estrogen receptor, this complex sends a message to the cell to create a new cell.

Estrogen Receptors are normally found in the cell’s nucleus along with DNA molecules. In the absence of estrogen, Estrogen Receptors are inactive and have no influence on DNA, which contains the cell’s genes. However, when estrogen enters a cell and reaches the nucleus, it binds to its receptor, causing the shape of the receptor to change. This estrogen-receptor complex then binds to specific DNA sites called estrogen response elements, which are located near genes that are controlled by estrogen. Once attached to the estrogen response elements in DNA, this complex binds to coactivator proteins, activating nearby genes. The activated genes produce messenger RNA molecules, which guide the synthesis of specific proteins. These proteins can influence cell behavior in various ways depending on the type of cell involved.

For example, in liver cells, estrogen promotes the production of proteins that affect cholesterol levels in the blood. Cholesterol is not soluble in blood and needs to bind to special cholesterol-carrying proteins called lipoproteins to be transported through the body. The liver produces low-density lipoproteins (LDL) and high-density lipoproteins (HDL). LDL cholesterol is considered the “bad” form because it tends to deposit cholesterol directly onto the inner walls of arteries, leading to plaque formation and potential heart disease. In contrast, HDL is considered the “good” form because it inhibits plaque formation and carries cholesterol away from the arteries back to the liver.

The overall effect of estrogens on liver cells is to increase HDL cholesterol levels and decrease LDL cholesterol levels, thus helping to lower the risk of heart disease.

In some target tissues, estrogen’s primary effect is to stimulate cell growth and division, a process called cell proliferation. For example, in breast tissue, estrogen triggers the proliferation of cells lining the milk glands, preparing the breast for milk production in case of pregnancy. Estrogen also promotes the proliferation of cells in the endometrium, the inner lining of the uterus, preparing the uterus for possible embryo implantation. During a normal menstrual cycle, estrogen levels drop significantly at the end of each cycle if pregnancy does not occur. As a result, the endometrium disintegrates and is shed from the uterus and vagina in a process called menstruation.

Paradoxically, estrogen can have both beneficial and harmful effects. The benefits include programming the breast and uterus for sexual reproduction, safeguarding the heart by controlling cholesterol production, and preserving bone strength. However, estrogen’s ability to promote cell proliferation in the breast and uterus can increase the risk of developing breast or uterine cancer.

Given estrogen’s potential to promote cancer development, substances that block estrogen’s action may be helpful in preventing or treating these types of cancer. Antiestrogens work by binding to estrogen receptors, preventing estrogen from binding to these receptors and activating genes for growth-promoting proteins. Some compounds that block estrogen’s action in certain tissues can also mimic estrogen’s action in other.

Written by Nature Pure Labs SW, Inc. founder and scientist Leonid Markman.

References

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  2. Setchell, K.D. Phytoestrogens. Am. J. Clin. Nutr. 1998, 68, 1333S-1346S.
  3. Adlercreutz,H. , Mazur, W. Phyto-oestrogens and western diseases. Ann. Med. 1997, 29, 95-120.

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