| The rat model of progressive chronic renal faliure was built via 5/6 renalresection and then was verified by related pathological and biochemical assays.Immunohistochemistry (IHC) and RT-PCR showed that HO-1 protein fromliver, kidney, spleen and HO-1 mRNA from kidney, liver, spleen, stomach, lung,skeletal muscles, epididymis,testis, seminferoustuble, prostate,blood vessel, largeintestine,heart, blood cell of five chronic renal faliure rats were significantly higherthan of control rats, but there was no significant difference of the HO-1 mRNAexpression in intestine between the two groups. It suggested that HO-1 expression inmost tissues from chronic renal faliure rats was significantly increased. And showedthat TGF-βmRNA from kidney, liver, spleen, stomach, skeletal muscles,epididymis,testis, seminferoustuble, prostate, blood vessel, intestine,largeintestine,heart,blood cell of five chronic renal faliure rats were significantly higherthan in control rats, but there was no significant difference of the TGF-βmRNAexpression in lung between the two groups. It also suggested that TGF-βexpressionin most tissues from chronic renal faliure rats was significantly increased. The relatedanalysis showed that the related expression of HO-1 mRNA from kidney, spleen,stomach, lung, skeletal muscles, epididymis, intestine, large intestine, heart from both five chronic renal faliure rats and control rats were significantly lower than that ofTGF-βmRNA. The related expression of HO-1 mRNA from testis of five chronicrenal faliure rats was significantly higher than that of TGF-βmRNA, while therewas no significant difference between HO-1 and TGF-βmRNA in testis tissue ofcontrol rats.The related expression of HO-1 mRNA in seminferoustuble from bothfive chronic renal faliure rats and control rats were significantly higher than that ofTGF-βmRNA. The related expression of HO-1 mRNA in prostate from five chronicrenal faliure rats was significantly higher than that of TGF-βmRNA, while the relatedexpression of HO-1 mRNA in prostate from control rats was significantly lower thanthat of TGF-βmRNA. There were no significant difference between HO-1 andTGF-βmRNA in liver and blood cell from chronic renal faliure rats, but the relatedexpression of HO-1 mRNA from blood cell of control rats was significantly higherthan that of TGF-βmRNA,and the related expression of HO-1 mRNA in liver fromcontrol rats was significantly lower than that of TGF-βmRNA.The related expressionof HO-1 mRNA in blood vessel from five chronic renal faliure rats was significantlylower than that of TGF-βmRNA, but there were no significant difference betweenHO-1 mRNA and TGF-βmRNA in blood vessel from control rats. These resultssuggested that the expression relationship between HO-1mRNA and TGF-βmRNA insome tissues from chronic renal faliure rats had been changed, that is, the change ofrelated expression of HO-1mRNA and TGF-βmRNA in kidney, spleen, stomach,lung, skeletal muscles, epididymis, intestine, large intestine, heart, seminferoustublewere identical in two groups, but the change of related expression of HO-1mRNAand TGF-βmRNA in prostate is reverse in two groups. Although there was nosignificant difference of the related expression of HO-1mRNA and TGF-βmRNA intestis and blood vessel before chronic renal faliure, it was changed after chronic renalfailure.Oppsitely, although there was no significant difference the related expression of HO-1mRNA and TGF-βmRNA in liver and blood cell after chronic renal faliure,there was significant difference before chronic renal failure. It was postulated thatHO-1 might interacted with TGF-βunder specific temporal and spatial backgroundduring rat's chronic renal failure.AKR1C2 is one of tumor telated genes and it is closely related to tumorigenesis,such as, hepatocellular carcinoma, prostate cancer. To investigatethe expression of AKR1C2 gene in human renal carcinoma and its clinicalpathological significance. The expression of AKR1C2 gene was detected usingRT-PCR and Immunohistochemistry(IHC)and its relationship with patient's clinicalpathological characteristic was analysed among 30 cases of renal carcinoma tissuesand their adjacent noncancerous tissues. The RT-PCR results showed that theAKR1C2 mRNA expression was up-regulated in all 30 cases of renal carcinomatissue, and its expression was not detected in adjacent noncancerous tissues from 6out of 30 cases. Immunohistochemistry (IHC) showed that the AKR1C2 proteinexpression was up-regulated in all 30cases of kidney carcinoma tissue and itsexpression was not detected in adjacent noncancerous tissues from 13 out of 30 cases.The analysis of relationship between expression of AKR1C2 and clinical pathologicalcharacteristic among these patients was shown that the label index (LI)and theexpression index (EI) of AKR1C2 gene were positively related to the renalcarcinoma's Robson stage, tumor differentiation grade, the tumor pathological typeand metastasis. The results suggested that AKR1C2 gene was overexpression inhuman renal carcinoma tissue on the level of transcription and translation and it maybe helpful to the renal carcinogenesis and its development. In order to investigate therenalcarcinogenic effect of AKR1C2, we constructed 786-0 stable cell line transfectedwith pcDNA3.1/AKR1C2 or pcDNA3.1 via screening and using G418 for 4 weeks orso. The growth curve analysis showed the growth speed of 786-0 cells transfected with pcDNA3.1/AKR1C2 was much more rapid compared with 786-0 cellstransfected with pcDNA3.1 from the second days. It suggested that overexpression ofAKR1C2 could stimulate the growth and proliferation of 786-0 cells to a significantlygreater extent when compared with control cell. The soft-agar colony-formationassay showed that soft-agar colony-formation rate from 786-0 cells transfectedwith pcDNA3.1/AKR1 C2 and pcDNA3.1 AKR1C2 were 43.8％and19.2％,respectively. It revealed that 786-0 cell of overexpression AKR1C2 werestimulated to grow in soft agar compared with empty vector transfected control cells.It was postulated that AKR1C2 may promote 786-0 cells division and proliferation invitro by regulating and controling the cell cycle signal transduction pathway networkdirectly or indirectly. These results provide us a base to understand the AKR1C2functions during renalcarcinogenesis.
|
PDF Full Text Request