Nitric Oxide Modulates Muscle Progenitor Cells Migrating from the Somite Dermomyotome to Nascent Limb Buds in the Chick Embryo
Author: Tanya Velasco
Faculty Supervisor: Wilfred Denetclaw
Department: Biology
Nitric Oxide (NO) is a free radical, short-lived messenger gas molecule known to produce biological effects in chicken embryo myogenesis. In previous studies, it was demonstrated that NO promoted hepatocyte growth factor (HGF) during adult muscle regeneration, activating satellite cells for various processes. HGF also signals migratory muscle progenitor cells (MMPCs) migration in wing bud myogenesis. However, the signaling mechanism by HGF in wing bud muscle formation is not yet fully understood. We hypothesize that NO enables HGF to promote migration of MMPCs into wing buds. To monitor the migration of MMPCs into wing buds, we used Pax7 immunolabeling, confocal imaging, and image processing using FIJI software. To illustrate NO’s role in MMPC migration, we used a NOS inhibitor L-NAME 5mM-10mM (low) and 20mM-25mM (high) and NOS donor Deta-NONOate (5μM) in HH14-15 staged embryos for 24 hours. Our findings indicate that high L-NAME treatment resulted in decreased MMPC migration into wing buds. Low L-NAME concentrations did not significantly inhibit MMPC migration. At 5μM, DETA-NONOate-treated embryos showed reduced MMPC migration, possibly due to NO impeding MMPC epithelial-mesenchymal transition (EMT), a process enhancing migratory capacity under normal circumstances. In conclusion, our findings indicate NO signaling regulates MMPC migration to early-forming wing buds.