RGD Reference Report - Nicotine-induced retardation of chondrogenesis through down-regulation of IGF-1 signaling pathway to inhibit matrix synthesis of growth plate chondrocytes in fetal rats.

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Nicotine-induced retardation of chondrogenesis through down-regulation of IGF-1 signaling pathway to inhibit matrix synthesis of growth plate chondrocytes in fetal rats.
Authors:	Deng, Y Cao, H Cu, F Xu, D Lei, Y Tan, Y Magdalou, J Wang, H Chen, L
Citation:	Deng Y, etal., Toxicol Appl Pharmacol. 2013 May 15;269(1):25-33. doi: 10.1016/j.taap.2013.02.008. Epub 2013 Feb 27.
RGD ID:	10045858
Pubmed:	PMID:23454400 (View Abstract at PubMed)
DOI:	DOI:10.1016/j.taap.2013.02.008 (Journal Full-text)
Previous studies have confirmed that maternal tobacco smoking causes intrauterine growth retardation (IUGR) and skeletal growth retardation. Among a multitude of chemicals associated with cigarette smoking, nicotine is one of the leading candidates for causing low birth weights. However, the possible mechanism of delayed chondrogenesis by prenatal nicotine exposure remains unclear. We investigated the effects of nicotine on fetal growth plate chondrocytes in vivo and in vitro. Rats were given 2.0 mg/kg.d of nicotine subcutaneously from gestational days 11 to 20. Prenatal nicotine exposure increased the levels of fetal blood corticosterone and resulted in fetal skeletal growth retardation. Moreover, nicotine exposure induced the inhibition of matrix synthesis and down-regulation of insulin-like growth factor 1 (IGF-1) signaling in fetal growth plates. The effects of nicotine on growth plates were studied in vitro by exposing fetal growth plate chondrocytes to 0, 1, 10, or 100 muM of nicotine for 10 days. Nicotine inhibited matrix synthesis and down-regulated IGF-1 signaling in chondrocytes in a concentration-dependent manner. These results suggest that prenatal nicotine exposure induces delayed chondrogenesis and that the mechanism may involve the down-regulation of IGF-1 signaling and the inhibition of matrix synthesis by growth plate chondrocytes. The present study aids in the characterization of delayed chondrogenesis caused by prenatal nicotine exposure, which might suggest a candidate mechanism for intrauterine origins of osteoporosis and osteoarthritis.

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Object Symbol	Species	Term	Qualifier	Evidence	With	Notes	Source	Original Reference(s)
Igf1	Rat	cellular response to nicotine		IEP			RGD
Igf1	Rat	response to nicotine		IEP			RGD
Igf1r	Rat	response to nicotine		IEP			RGD

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Genes (Rattus norvegicus)

Igf1 (insulin-like growth factor 1)

Igf1r (insulin-like growth factor 1 receptor)

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Nicotine-induced retardation of chondrogenesis through down-regulation of IGF-1 signaling pathway to inhibit matrix synthesis of growth plate chondrocytes in fetal rats.