The article was published on Cell Metabolism in January 2019. The authors Mikihito Hayashi et al. (Tokyo Medical and Dental University, Tokyo, Japan) find that the osteoprotective protein semaphorin 3A (Sema3A), which acts on osteocytes to promote their survival and maintain bone homeostasis.
Background & Aims & Conclusions
Osteocyte survival is key to bone homeostasis and is perturbed in menopause and aging. Sema3A, a secreted protein that is a member of semaphorin family proteins, increased bone mass by suppressing osteoclastic bone resorption and promoting bone formation.
In this article, the researchers evaluated the role of Sema3A in estrogen action and bone aging. The result shows that estrogen suppressed the Sema3a-targeting miRNAs miR-497 and miR-195, thereby enhancing Sema3A expression. Sema3A acts on its receptor on osteocytes to promote their survival and maintain bone homeostasis.
In ovariectomized mice, Sema3A deficiency led to a severe osteoporotic phenotype marked by fewer osteocytes, which is caused by specificity loss of Sema3A or its receptor component neuropilin-1 (Nrp1) in osteocyte.
An activator of soluble guanylate cyclase-cGMP signaling mimicked Sema3A action and ameliorated bone loss after ovariectomy. In humans, serum levels of Sema3A decreased with age or after menopause.
These results collectively suggest that Sema3A expressed in osteocytes is a key regulator of bone homeostasis. Sema3A may be targeted to promote osteocyte survival as a treatment for metabolic bone disease.
Part II: The Brief Introduction of Our Product
The level of Sema 3A in mouse and human were detected by mouse Semaphorin-3A (SEMA3A) ELISA kit (CSB-EL020980MO) and human Semaphorin 3A (Sema 3A) ELISA Kit (CSB-E15913h) respectively. The results are as follows:
