My recent results indicate a decrease in the expression of beta-catenin in rat cardiomyocytes in response to a specific drug and in-silico model of binding energies between the said drug and LRP5/6 is extremely high (over 1000 kcal/mol). My question is, is it still possible to have an inhibition of the canonical Wnt/B-catenin pathway despite this non-permissive binding energy?
hi Pola Sobiecka
There is a possibility. The Wnt pathway has a dual role in cardiomyocyte development & differentiation. In the early heart developmental stage, the Wnt pathway remains activated while in the late mature stage, Wnt pathways get inhibited. This modulation is regulated by Wnt ligands, receptors, and antagonists. Now, LRP5/6 is a co-receptor, if possible we look for the role of death complex components such as DKK, GSK3b, and well as antagonists sFRPs, u may get better.
If the wnt antagonist level appears to increase & death components are found to be stable then because of that b-catenin might have degraded so the result came down. Also, u can check the phospho-b-catenin and Frizzled receptor levels.
Do your rat cardiomyocytes is H9C2 cells?
Regards
Saurabh
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