Key result
C-ANP4-23 and NPR-C peptide fragments 1, 2, and 3 inhibited AngII-, ET-1-, and AVP-stimulated protein synthesis in A10 vascular smooth muscle cells in a concentration-dependent manner.
Why the study?
Does NPR-C activation inhibit vasoactive peptide-induced hypertrophy in vascular smooth muscle cells?
Does NPR-C activation inhibit vasoactive peptide-induced hypertrophy in vascular smooth muscle cells?
NPR-C activation and its intracellular peptide fragments inhibit vasoactive peptide-induced protein synthesis in vascular smooth muscle cells via Gqalpha/MAP kinase/PI3K/AKT pathways.
No takes yet. Share an insight, caveat, or question.
May support NPR-C as a target to limit VSMC hypertrophy; hypothesis-generating and requires in vivo validation before any clinical consideration.
Li et al. (2006) studied Vascular hypertrophy (in vitro model). C-ANP4-23 and NPR-C peptides (peptides 1, 2, 3) vs. Control peptides (X, Y, Z) or basal conditions was evaluated on Protein synthesis (3H-leucine incorporation). C-ANP4-23 and NPR-C peptide fragments 1, 2, and 3 inhibited AngII-, ET-1-, and AVP-stimulated protein synthesis in A10 vascular smooth muscle cells in a concentration-dependent manner.
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