N-acetylcysteine stimulates osteoblastic differentiation of mouse calvarial cells.
J Cell Biochem. 2008 Mar 1;103(4):1246-55
Authors: Jun JH, Lee SH, Kwak HB, Lee ZH, Seo SB, Woo KM, Ryoo HM, Kim GS, Baek JH
Estrogen deficiency causes osteoporosis via increased generation of reactive oxygen species (ROS), and thus, antioxidants may prove to be the effective therapeutic candidates. We examined the effects of the antioxidant N-acetylcysteine (NAC) on osteoblastic differentiation in mouse calvarial cells. NAC (10-30 mM) enhanced alkaline phosphatase activity, mRNA expression of osteoblast differentiation-associated genes and mineralized nodule formation. It also increased expression of bone morphogenetic proteins-2, -4, and -7. The osteogenic activity of NAC was partially reduced by inhibition of glutathione synthesis. Since caffeic acid phenethyl ester did not stimulate osteoblast differentiation, it is unlikely that ROS scavenging activity of NAC is sufficient for osteogenic activity. We observed that NAC suppressed small GTPase RhoA activity and activation of RhoA by Pasteurella multocida toxin suppressed the osteogenic activity of NAC. These results suggest that NAC might exert its osteogenic activity via increased glutathione synthesis and inhibition of RhoA activation.
PMID: 17979115 [PubMed - indexed for MEDLINE]
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PubMed: BMP-7
NCBI: db=PubMed; Term=BMP-7
