Amazing stuff!
Notice the Yale University still sprads DEI and woke ideology! What is a pregnant parent? This "parent" was almost certainly a woman! Very disturbing and disparaging of mothers!
What does the first name Pericles of the current Dean of Yale U Pericles Lewis mean if anything? Pericles, the great Greek statesman, is probably wildly spinning in his grave given this ideology and indoctrination espoused by Yale U!
"... in a new study, ... researchers ... show that the placenta doesn’t produce serotonin but instead regulates its delivery to the embryo and fetus. They found that serotonin comes from the pregnant parent [???], with the placenta acting as a “serotonin shield” that controls how much reaches the embryo and fetus. ...
how a parent’s [???] serotonin levels might affect the development of their baby’s body and brain, the researchers say. ...
Often called a “happiness hormone,” serotonin regulates mood, so it’s often associated with the brain. In reality, less than 5% of serotonin is made in the brain, with 95% of it made in the gut. But serotonin does more than just regulate mood. It’s also a growth hormone. In the gut, it gets taken up by platelets and is delivered to parts of the body that need to grow, including in wound healing. ...
During pregnancy, serotonin also helps with growth: It travels into the placenta through a special protein known as the serotonin transporter (SERT) where it plays a critical role in the development of the embryo and fetus. ...
For the new study, researchers sought to better understand these relationships by using a pure source of placenta cells, unlike in previous studies that looked at either whole animals or isolated mouse placentas. To do so, they first purified human cytotrophoblasts, which are the stem cells that make all the cells of the placenta. They then added serotonin to those cells to see where it would go and discovered it concentrated in the nucleus. Next, they used a selective serotonin reuptake inhibitor (SSRI) that blocked SERT — the antidepressant escitalopram, commonly known by the brand name Lexapro — to show that the normal growth, function, and differentiation of these cells was completely blocked.
They also used another inhibitor called cystamine to block serotonylation, or the process by which serotonin is added to proteins like histone 3, which turns genes “on” and “off.” Again, that completely blocked the normal growth of the cells.
Blocking either SERT or serotonylation led to significant changes in gene expression of RNAs in the cytotrophoblasts, they found.
Some genes — including ones involved in making, moving, and growing cells — became downregulated, or less active, when serotonin couldn’t enter the cell. Other genes — including ones that help cells stay alive and protect them — became upregulated, or more active. According to the researchers, these findings show that serotonin is critical for the growth of the cytotrophoblasts, the placenta, and by extension, the fetus. ...
For example, ... this explains why taking SSRIs — which decrease the levels of serotonin into the placenta — leads to smaller babies, and why, conversely, increased levels of serotonin may lead to bigger babies, with bigger brains, who may be at increased risk for developmental disabilities like autism. ..."
From the abstract *unfortunately, a very technical abstract):
"Serotonin (5-hydroxytryptamine; 5-HT) is transported into the human placenta through the serotonin transporter (SERT/SLC6A4) on the surface of the syncytiotrophoblast. During this transit, a significant amount of 5-HT becomes concentrated in the cytotrophoblast nucleus.
We used immunochemistry, inhibitors of SERT and transglutaminase 2, and RNA sequencing to elucidate the mechanism and consequences of this nuclear localization.
Exogenous 5-HT recapitulated the uptake of 5-HT into the trophoblasts and its preferential concentration in cytotrophoblast nuclei we observed in the intact placenta. Cystamine eliminated the staining of the nuclei in placental explants by exogenous 5-HT, suggesting that serotonylation mediated this phenomenon. This was confirmed by Western blots and immunoprecipitation that identified histone 3, and specifically the 5th glutamine residue in histone 3, as a site of serotonylation. Inhibiting SERT with escitalopram or transglutaminase 2 with cystamine blocked cytotrophoblast differentiation in vitro and led to marked changes in RNA expression. Of the 38 524 mRNAs identified in these trophoblasts, cystamine changed the expression of 1986 and escitalopram significantly altered 374. Both treatments altered the expression of 155 mRNAs either positively or negatively. The downregulated genes were involved with cell proliferation, morphogenesis, motility, and growth, whereas genes that were upregulated controlled cell survival and protection pathways.
These findings suggest that maternal 5-HT promotes placental, embryonic/fetal, and organismal development through histone serotonylation and consequent alterations in gene expression. They raise the possibility that alterations in 5-HT flux in the placenta affect placental and fetal growth, as well as organismal somatic, neurologic developmental, and pathological trajectories."
Role of Serotonin on Gene Expression and Physiology in Human Cytotrophoblasts and Placenta (open access)
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