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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

(a) Immunohistochemical staining for PPAR-γ in stomach tissue of rats. (b–e) Nuclear localization of PPAR-γ in RGM-1 cells (b, ×50, c, ×200, e, negative control) and MKN45 cells (d, ×200). (f) Western blot detection of PPAR-γ protein in homogenates of gastric mucosal tissues before and after ischemia-reperfusion (I-R). (g) Expression of PPAR-γ mRNA in the gastric mucosa determined by RT-PCR. 1, sham-operation, 2, ischemia-reperfusion, 3, ischemia-reperfusion + pioglitazone (10 mg/kg), 4, sham + pioglitazone.
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Figure 1: (a) Immunohistochemical staining for PPAR-γ in stomach tissue of rats. (b–e) Nuclear localization of PPAR-γ in RGM-1 cells (b, ×50, c, ×200, e, negative control) and MKN45 cells (d, ×200). (f) Western blot detection of PPAR-γ protein in homogenates of gastric mucosal tissues before and after ischemia-reperfusion (I-R). (g) Expression of PPAR-γ mRNA in the gastric mucosa determined by RT-PCR. 1, sham-operation, 2, ischemia-reperfusion, 3, ischemia-reperfusion + pioglitazone (10 mg/kg), 4, sham + pioglitazone.

Mentions: To identify the localization of PPAR-γ within stomach, we performed immunohistochemical analysis of PPAR-γ protein. As shown inFig. 1a, the expression of PPAR-γ was observed in mucosal epithelial cells and parietal cells. Using cultured rat gastric mucosal cells (RGM-1), the nuclear-dominant localization of PPAR-γ was confirmed (Fig. 1 b and c), although the levels of PPAR-γ expression in normal gastric mucosal cells was much lower than those of gastric cancer cells. Western blotting also showed the clear expression of PPAR-γ in the rat gastric mucosa (Fig. 1f), and its levels were not changed by I-R but slightly increased by the treatment with pioglitazone. RT-PCR also demonstrated the PPAR-γ mRNA expression in the gastric mucosa (Fig. 1g). The expression levels were slightly decreased after I-R.


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)

(a) Immunohistochemical staining for PPAR-γ in stomach tissue of rats. (b–e) Nuclear localization of PPAR-γ in RGM-1 cells (b, ×50, c, ×200, e, negative control) and MKN45 cells (d, ×200). (f) Western blot detection of PPAR-γ protein in homogenates of gastric mucosal tissues before and after ischemia-reperfusion (I-R). (g) Expression of PPAR-γ mRNA in the gastric mucosa determined by RT-PCR. 1, sham-operation, 2, ischemia-reperfusion, 3, ischemia-reperfusion + pioglitazone (10 mg/kg), 4, sham + pioglitazone.
© Copyright Policy - open-access
Related In: Results  -  Collection

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Figure 1: (a) Immunohistochemical staining for PPAR-γ in stomach tissue of rats. (b–e) Nuclear localization of PPAR-γ in RGM-1 cells (b, ×50, c, ×200, e, negative control) and MKN45 cells (d, ×200). (f) Western blot detection of PPAR-γ protein in homogenates of gastric mucosal tissues before and after ischemia-reperfusion (I-R). (g) Expression of PPAR-γ mRNA in the gastric mucosa determined by RT-PCR. 1, sham-operation, 2, ischemia-reperfusion, 3, ischemia-reperfusion + pioglitazone (10 mg/kg), 4, sham + pioglitazone.
Mentions: To identify the localization of PPAR-γ within stomach, we performed immunohistochemical analysis of PPAR-γ protein. As shown inFig. 1a, the expression of PPAR-γ was observed in mucosal epithelial cells and parietal cells. Using cultured rat gastric mucosal cells (RGM-1), the nuclear-dominant localization of PPAR-γ was confirmed (Fig. 1 b and c), although the levels of PPAR-γ expression in normal gastric mucosal cells was much lower than those of gastric cancer cells. Western blotting also showed the clear expression of PPAR-γ in the rat gastric mucosa (Fig. 1f), and its levels were not changed by I-R but slightly increased by the treatment with pioglitazone. RT-PCR also demonstrated the PPAR-γ mRNA expression in the gastric mucosa (Fig. 1g). The expression levels were slightly decreased after I-R.

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