A new study in mice has identified FXR1, a protein in the same family as the one linked to Fragile X disease, as a potential target for the development of a new type of anti-hypertensive drug, according to the first study presented in the group The heart of America. Neurosurgery: From Genes to the 2022 Medical Session. The conference is being held on May 12-14, 2022, in Seattle and is the global exchange of new advances in new scientific discoveries developing in arteriosclerosis, thrombosis, cardiology, cardiovascular disease, vascular surgery blood and genomics of function.
Flexible X chromosome, or FXS, is a well-known cause of skeletal deformity leading to mutations on the X chromosome. The CDC estimates that FXS affects 1 in 7,000 men and 1 in 11,000 women born each year in the US. compared to girls.
FXS results in mutations to the FMR1 gene, which quantifies the amount of RNA binding protein RNA that is believed to play a role in enhancing the link between. nerve cells in the brain.
FXR1 belongs to one family of RNA-binding proteins such as FMRP and is a specific muscle. RNA-binding proteins help activate and kill cells and are essential for many cellular pathways.
“In my previous research on FXR1, I expect to see more notesTranslated, mRNA receptors interact with FXR1, “said Amanda St. Paul, lead author and Ph.D. candidate at the Lewis Katz School of Medicine at Temple University in Philadelphia.” so much to find out. FXR1 binds to many actin-binding proteins and other proteins in the cytoskeleton.
St. Paul and colleagues have developed a mouse model where FXR1 can be cleared into smooth muscle cells – the same combination. blood vessels in people. The rats were genetically modified so that the FXR1 gene could be erased by administering tamoxifen.
With the deletion of the FXR1 gene, the researchers noted that nerves smooth muscle cells they performed differently compared to that of rats with the active FXR1.
“We found that smooth muscle cells without FXR1 do not proliferate, do not stop, do not migrate, which are functions that rely on a functioning cytoskeleton. And these are all things that a smooth muscle cell should yi., “said St. Paul.
Killing FXR1 has an eye-opening effect: “When you remove FXR1 from smooth muscle in these mice, they also reduce diastolic blood pressure compared to mice,” says St. Paul.
Research has found that:
- Decreased FXR1 reduces the ability of blood cells to contract; same to you
- When FXR1 was deleted, the rats were reduced diastolic hypertension compared to control mice. This was measured using telemetry, an in-vivo measure of blood pressure.
According to St. Paul, these studies suggest that the activation of FXR1 in the smooth muscle tissue of the arteries, or the contracted pathway, may be an interesting way to promote hypertension. “Many drugs do not focus on the cytoskeleton. Since FXR1 is unique to the muscle, it gives us a unique purpose and a way to explore the future,” she said. “Millions of people have high blood pressure; finding new ways to improve high blood pressure is important. “
Future projects of St. Paul and colleagues will include research or FXR1 activities in it smooth muscle cells depends on its ability to interact with cytoskeletal proteins and if depleted FXR1 is effective in reducing blood pressure in mice with high blood pressure.
American Heart Association Neuroscience: From Genes to the 2022 Medical Session
American Heart Association
hintFragile X-related protein may be the new target for high blood pressure (2022, May 12) returned May 12, 2022 from https://medicalxpress.com/news/2022-05-protein- fragile-syndrome-blood-pressure .html
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Protein related to Fragile X syndrome may be a new target for blood pressure medicines Source link Protein related to Fragile X syndrome may be a new target for blood pressure medicines