Title : Mechanism for nicotine-induced up-regulation of Wnt signaling in human alveolar interstitial fibroblasts.

Pub. Date : 2011 Apr

PMID : 21133803






7 Functional Relationships(s)
Download
Sentence
Compound Name
Protein Name
Organism
1 Since the AIF versus MYF phenotype is determined by the expression of peroxisome proliferator-activated receptor gamma (PPARgamma) and Wingless/Int (Wnt) signaling, respectively, the authors hypothesized that nicotine-induced AIF-to-MYF transdifferentiation is characterized by the down-regulation of PPARgamma, and the up-regulation of the Wnt signaling pathway. Nicotine peroxisome proliferator activated receptor gamma Homo sapiens
2 Since the AIF versus MYF phenotype is determined by the expression of peroxisome proliferator-activated receptor gamma (PPARgamma) and Wingless/Int (Wnt) signaling, respectively, the authors hypothesized that nicotine-induced AIF-to-MYF transdifferentiation is characterized by the down-regulation of PPARgamma, and the up-regulation of the Wnt signaling pathway. Nicotine peroxisome proliferator activated receptor gamma Homo sapiens
3 Since the AIF versus MYF phenotype is determined by the expression of peroxisome proliferator-activated receptor gamma (PPARgamma) and Wingless/Int (Wnt) signaling, respectively, the authors hypothesized that nicotine-induced AIF-to-MYF transdifferentiation is characterized by the down-regulation of PPARgamma, and the up-regulation of the Wnt signaling pathway. Nicotine peroxisome proliferator activated receptor gamma Homo sapiens
4 Furthermore, activation of nicotinic acetylcholine receptor (nAChR)-alpha3 and -alpha7 and whether a PPARgamma agonist, rosiglitazone (RGZ), blocks nicotine-mediated Wnt activation were examined. Nicotine peroxisome proliferator activated receptor gamma Homo sapiens
5 Nicotine-mediated Wnt activation was almost completely blocked by pretreatment with either calphostin C or RGZ, indicating the central involvement of PKC activation and Wnt/PPARgamma interaction in nicotine-induced up-regulation of Wnt signaling, and hence AIF-to-MYF transdifferentiation, providing novel preventive/therapeutic targets for nicotine-induced lung injury. Nicotine peroxisome proliferator activated receptor gamma Homo sapiens
6 Nicotine-mediated Wnt activation was almost completely blocked by pretreatment with either calphostin C or RGZ, indicating the central involvement of PKC activation and Wnt/PPARgamma interaction in nicotine-induced up-regulation of Wnt signaling, and hence AIF-to-MYF transdifferentiation, providing novel preventive/therapeutic targets for nicotine-induced lung injury. Nicotine peroxisome proliferator activated receptor gamma Homo sapiens
7 Nicotine-mediated Wnt activation was almost completely blocked by pretreatment with either calphostin C or RGZ, indicating the central involvement of PKC activation and Wnt/PPARgamma interaction in nicotine-induced up-regulation of Wnt signaling, and hence AIF-to-MYF transdifferentiation, providing novel preventive/therapeutic targets for nicotine-induced lung injury. Nicotine peroxisome proliferator activated receptor gamma Homo sapiens