National Institute of Health (NIH) funded researchers are gaining a better understanding of some of the workings of the uterus. Throughout a woman’s menstrual cycle, hormone levels are continually changing in the uterus. At the start of the cycle, the hormone estrogen gradually increases and encourages the thickening of the endometrium (or uterine lining). Once the ovary releases an egg, levels of the hormone progesterone begin to increase. Progesterone counteracts the estrogen in relation to the endometrium, preventing the lining from getting too thick in the case of egg fertilization. If the uterine lining is too thick, a fertilized egg will have difficulty implanting itself.
What researchers have recently discovered is the role of a protein called Hand2 in the whole process. It was previously recognized that Hand2 increases along with the levels of progesterone following the release of an egg. However, it is now understood that Hand2 acts as a sort of switch to turn off the estrogen from stimulating the endometrium. At least, that is how the protein works in the mice who were studied. Now plans are underway to continue the study in women to determine the effects on the human uterus.
The effects of this study could be helpful in terms of finding female infertility treatment and possibly in endometriosis treatment as well. Failure to produce Hand2 within the uterus could be a cause for infertility and, it is speculated, a cause for endometriosis, as the result of a lack of Hand2 is a thickened uterine lining. Obviously it is too early to tell what the findings will reveal, but the speculated findings could open up the door to exciting research and possible treatments in regards to female reproductive health.
No comments:
Post a Comment