Key result
C-type natriuretic peptide (10^-6 M) increased longitudinal growth of embryonic mouse tibiae by 42% compared to control, an anabolic effect that was blocked by p38 MAP kinase inhibition.
Why the study?
Does C-type natriuretic peptide regulate endochondral bone growth through p38 MAP kinase pathways in tibia organ cultures?
Population
Tibia organ culture system and micro-dissected tibiae
Comparison
C-type natriuretic peptide with or without… vs null
Design
Preclinical
Authors
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Extends CNP anabolic effects to p38 MAP kinase in mouse tibiae; clinical translation for skeletal diseases remains untested.
Does C-type natriuretic peptide regulate endochondral bone growth through p38 MAP kinase pathways in tibia organ cultures?
Effect estimate: 42% increase
p-value: p=<0.05
CNP regulates endochondral bone growth via p38 MAP kinase-dependent pathways, identifying novel target genes and mechanisms with implications for skeletal diseases.
Agoston et al. (2007) studied Endochondral bone growth. C-type natriuretic peptide (CNP) vs. Vehicle (BSA) was evaluated on Longitudinal growth of tibiae (42% increase, p=<0.05). C-type natriuretic peptide (10^-6 M) increased longitudinal growth of embryonic mouse tibiae by 42% compared to control, an anabolic effect that was blocked by p38 MAP kinase inhibition.
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