Objective: To investigate all trans retinoid Acid (ATRA) inhibition of cell growth in human retinoblastoma Y79 cells, and its mechanism. Methods: Antiproliferation effects of ATRA on Y79 cells were determined by 3 H thymidine incorporation. Cell cycle analysis was performed by flow cytometry. JNK phosphorylation was analyzed by Western blot analysis. Results: After 36 h treatment with 10 -6 mol?L -1 ATRA, 3 H thymidine incorporation decreased to 40%, under the same condition, Y79 cells were arrested in G 0 /G 1 and Sub G 1 peak appeared. Curcumin, JNK blocker, blocked the growth inhibition by ATRA. JNK was phosphorylated in 10 to 20 min. Conclusion: JNK phosphorylating mediated ATRA inhibition of apoptosis in Y79 cells. These results suggested that ATRA might have clinical application for treatment of retinoblastoma.

AIM:To investigate the effect of rosiglitazone on the expression of aquaporin-1 (AQP1), vascular endothelial growth factor-A ( VEGF-A ) and cyclooxygenase-2 ( COX-2 ) in human peritoneal microvascular endothelial cells.METHODS: Cultured peritoneal microvascular endothelial cells were divided into 4 groups.The morphological changes of the cells were observed under inverted microscope .The protein expression of AQP1, VEGF-A and COX-2 in hu-man peritoneal microvascular endothelial cells was determined by Western blotting .The mRNA expression of AQP1, VEGF-A and COX-2 in the cells was measured by real-time PCR.RESULTS:Rosiglitazone stimulated the proliferation of the cells.Rosiglitazone up-regulated the expression of AQP1, and down-regulated the expression of VEGF-2 and COX-2 at mRNA and protein levels in the cells .The PPAR-γantagonist GW9662 partly inhibited the up-regulation of AQP1 expres-sion by rosiglitazone (P<0.05), but had no obvious effect on the expression of VEGF-A and COX-2 (P>0.05).CON-CLUSION:Rosiglitazone up-regulates the expression of AQP 1 and down-regulates the expression of VEGF-A and COX-2 in human peritoneal microvascular endothelial cells , thus promoting water transportation and attenuating peritoneal fibrosis during peritoneal dialysis .

Objective: To investigate the effects and underlying mechanisms of aspirin on endoplasmic reticulum stress in podocytes induced by hyperlipemia. Methods: Cultured podocytes were divided into four groups: control group, aspirin (100 μg/ml) group, oxidized low density lipoprotein (ox-LDL, 100 μg/ml) group, aspirin+ox-LDL group. The expression of protein kinase R-1ike endoplasmic reticulum kinase (PERK), eukaryotic translation initiation factor 2α (eIF2α), activating transcription factor-4 (ATF4) and CAAT/enhancer binding protein homologous protein (CHOP) at 6 h, 12 h, 24 h, 48 h were evaluated by real-time PCR. The related proteins of p-PERK and p-eIF2α at 24 h and ATF4 at 12 h were evaluated by Western blotting, respectively. Results: The expressions of PERK, eIF2α peaked at 24 h, while ATF4 and CHOP peaked at 12 h in ox-LDL group and aspirin+ox-LDL group. Compared with control group, the expressions of PERK, eIF2α, ATF4 and CHOP were significantly higher in ox-LDL group at each times (all P<0.05). Compared with ox-LDL group, the expressions of the above indicators were significantly lower in aspirin+ox-LDL group at each times (all P<0.05). At 24 h, compared with control group, the expressions of p-PERK and p-eIF2α were significantly higher in ox-LDL group (both P<0.05). Compared with ox-LDL group, the expressions of p-PERK and p-eIF2α were significantly lower in aspirin+ox-LDL group (both P<0.05). At 12 h, the expression of ATF4 protein in each group was similar to that of mRNA. There were no significant difference in the expressions of all indicators between aspirin group and control group. Conclusions Hyperlipidemia may cause endoplasmic reticulum stress in podocytes by inducing phosphorylation of PERK and eIF2α, activating ATF4 transcription and inducing high expression of CHOP. Aspirin may partially block the PERK pathway, which may have protective effects for podocytes.