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Gastric peroxisome proliferator activator receptor-γ expression and cytoprotective actions of its ligands against ischemia-reperfusion injury in rats.

Naito Y, Takagi T, Katada K, Tomatsuri N, Mizushima K, Handa O, Kokura S, Yagi N, Ichikawa H, Yoshikawa T - J Clin Biochem Nutr (2011)

Bottom Line: The gastric expression of tumor necrosis factor-α and cytokine-induced neutrophil chemoattractant-1 increased significantly in rats treated ischemia-reperfusion, and these increases were significantly inhibited by treatment with pioglitazone.The network including calnexin, endoplasmic reticulum stress protein, heat shock proteins, and proteasome genes was induced by pioglitazone treatment.In conclusion, activation of gastric epithelial PPAR-γ receptor by its ligands may represent a novel therapeutic approach for gastric inflammation via up-regulation of heat shock proteins and endoplasmic reticulum-related proteins.

View Article: PubMed Central - PubMed

Affiliation: Department of Molecular Gastroenterology and Hepatology, Kyoto Prefectural University of Medicine, Kamigyo-ku, Kyoto 602-8566, Japan.

ABSTRACT
The beneficial effects by peroxisome proliferator-activated receptor-γ (PPAR-γ) on gastric injury induced by ischemia-reperfusion have been confirmed, however, the precise mechanism of its cytoprotection is not elucidated thoroughly. The aim of the present study was to determine the gastric localization of PPAR-γ expression in the rat gastric mucosa, and to clarify the mechanism of its cytoprotective properties. The gastric expression of PPAR-γ was confirmed by RT-PCR and western blot, and localized on gastric epithelial cells. The protective effect of PPAR-γ ligands, pioglitazone or 15-deoxy-Δ(12,14)-prostaglandin J(2), on gastric ischemia-reperfusion injury was reversed by the co-administration with PPAR-γ antagonist. The gastric expression of tumor necrosis factor-α and cytokine-induced neutrophil chemoattractant-1 increased significantly in rats treated ischemia-reperfusion, and these increases were significantly inhibited by treatment with pioglitazone. Among the 1,032 probes, 18 probes were up-regulated at least 1.5-fold, 17 were down-regulated at least 1.5-fold by pioglitazone. The network including calnexin, endoplasmic reticulum stress protein, heat shock proteins, and proteasome genes was induced by pioglitazone treatment. In conclusion, activation of gastric epithelial PPAR-γ receptor by its ligands may represent a novel therapeutic approach for gastric inflammation via up-regulation of heat shock proteins and endoplasmic reticulum-related proteins.

No MeSH data available.


Related in: MedlinePlus

Quantitative real-time PCR for genes up-regulated by pioglitazone treatment. cDNA was prepared from gastric mucosa, and PCR was performed using an ABI 7300. The bars show levels of expression of each gene normalized to that of β-actin.
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Figure 5: Quantitative real-time PCR for genes up-regulated by pioglitazone treatment. cDNA was prepared from gastric mucosa, and PCR was performed using an ABI 7300. The bars show levels of expression of each gene normalized to that of β-actin.

Mentions: To confirm the data derived from GeneChip analysis, we further validated the expression of some genes by real-time quantitative PCR. As shown in Fig. 5, real time PCR study showed that the expression of CANX, ERP70, HSPCA, and PSMB4, but not HSPA5, was significantly increased by the treatment with pioglitazone.


Gastric peroxisome proliferator activator receptor-γ expression and cytoprotective actions of its ligands against ischemia-reperfusion injury in rats.

Naito Y, Takagi T, Katada K, Tomatsuri N, Mizushima K, Handa O, Kokura S, Yagi N, Ichikawa H, Yoshikawa T - J Clin Biochem Nutr (2011)

Quantitative real-time PCR for genes up-regulated by pioglitazone treatment. cDNA was prepared from gastric mucosa, and PCR was performed using an ABI 7300. The bars show levels of expression of each gene normalized to that of β-actin.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC3045692&req=5

Figure 5: Quantitative real-time PCR for genes up-regulated by pioglitazone treatment. cDNA was prepared from gastric mucosa, and PCR was performed using an ABI 7300. The bars show levels of expression of each gene normalized to that of β-actin.
Mentions: To confirm the data derived from GeneChip analysis, we further validated the expression of some genes by real-time quantitative PCR. As shown in Fig. 5, real time PCR study showed that the expression of CANX, ERP70, HSPCA, and PSMB4, but not HSPA5, was significantly increased by the treatment with pioglitazone.

Bottom Line: The gastric expression of tumor necrosis factor-α and cytokine-induced neutrophil chemoattractant-1 increased significantly in rats treated ischemia-reperfusion, and these increases were significantly inhibited by treatment with pioglitazone.The network including calnexin, endoplasmic reticulum stress protein, heat shock proteins, and proteasome genes was induced by pioglitazone treatment.In conclusion, activation of gastric epithelial PPAR-γ receptor by its ligands may represent a novel therapeutic approach for gastric inflammation via up-regulation of heat shock proteins and endoplasmic reticulum-related proteins.

View Article: PubMed Central - PubMed

Affiliation: Department of Molecular Gastroenterology and Hepatology, Kyoto Prefectural University of Medicine, Kamigyo-ku, Kyoto 602-8566, Japan.

ABSTRACT
The beneficial effects by peroxisome proliferator-activated receptor-γ (PPAR-γ) on gastric injury induced by ischemia-reperfusion have been confirmed, however, the precise mechanism of its cytoprotection is not elucidated thoroughly. The aim of the present study was to determine the gastric localization of PPAR-γ expression in the rat gastric mucosa, and to clarify the mechanism of its cytoprotective properties. The gastric expression of PPAR-γ was confirmed by RT-PCR and western blot, and localized on gastric epithelial cells. The protective effect of PPAR-γ ligands, pioglitazone or 15-deoxy-Δ(12,14)-prostaglandin J(2), on gastric ischemia-reperfusion injury was reversed by the co-administration with PPAR-γ antagonist. The gastric expression of tumor necrosis factor-α and cytokine-induced neutrophil chemoattractant-1 increased significantly in rats treated ischemia-reperfusion, and these increases were significantly inhibited by treatment with pioglitazone. Among the 1,032 probes, 18 probes were up-regulated at least 1.5-fold, 17 were down-regulated at least 1.5-fold by pioglitazone. The network including calnexin, endoplasmic reticulum stress protein, heat shock proteins, and proteasome genes was induced by pioglitazone treatment. In conclusion, activation of gastric epithelial PPAR-γ receptor by its ligands may represent a novel therapeutic approach for gastric inflammation via up-regulation of heat shock proteins and endoplasmic reticulum-related proteins.

No MeSH data available.


Related in: MedlinePlus