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Articles by Y Jia
Total Records ( 4 ) for Y Jia
  K Matsumoto , J Huang , N Viswakarma , L Bai , Y Jia , Y. T Zhu , G Yang , J Borensztajn , M.S Rao , Y. J Zhu and J. K. Reddy
 

Nuclear receptor coactivator [peroxisome proliferator-activated receptor-binding protein (PBP)/mediator subunit 1 (MED1)] is a critical component of the mediator transcription complex. Disruption of this gene in the mouse results in embryonic lethality. Using the PBP/MED1 liver conditional null (PBP/MED1Liv) mice, we reported that PBP/MED1 is essential for liver regeneration and the peroxisome proliferator-activated receptor ligand Wy-14,643-induced receptor-mediated hepatocarcinogenesis. We now examined the role of PBP/MED1 in genotoxic chemical carcinogen diethylnitrosamine (DEN)-induced and phenobarbital-promoted hepatocarcinogenesis. The carcinogenic process was initiated by a single intraperitoneal injection of DEN at 14 days of age and initiated cells were promoted with phenobarbital (PB) (0.05%) in drinking water. PBP/MED1Liv mice, killed at 1, 4 and 12 weeks, revealed a striking proliferative response of few residual PBP/MED1-positive hepatocytes that escaped Cre-mediated deletion of PBP/MED1 gene. No proliferative expansion of PBP/MED1 null hepatocytes was noted in the PBP/MED1Liv mouse livers. Multiple hepatocellular carcinomas (HCCs) developed in the DEN-initiated PBP/MED1fl/fl and PBP/MED1Liv mice, 1 year after the PB promotion. Of interest is that all HCC developing in PBP/MED1Liv mice were PBP/MED1 positive. None of the tumors was PBP/MED1 negative implying that hepatocytes deficient in PBP/MED1 are not susceptible to neoplastic conversion. HCC that developed in PBP/MED1Liv mouse livers were transplantable in athymic nude mice and these maintained PBP/MED1fl/fl genotype. PBP/MED1fl/fl HCC cell line derived from these tumors expressed PBP/MED1 and deletion of PBP/MED1fl/fl allele by adeno-Cre injection into tumors caused necrosis of tumor cells. These results indicate that PBP/MED1 is essential for the development of HCC in the mouse.

  Y Zhang , Y Jia , R Zheng , Y Guo , Y Wang , H Guo , M Fei and S. Sun
  BACKGROUND:

The liver is frequently subject to insult because of viral infection, alcohol abuse, or toxic chemical exposure. Extensive research has been conducted to identify blood markers that can better discern liver damage, but little progress has been achieved in clinical practice. Recently, circulating microRNAs (miRNAs) have been reported as potential biomarkers for the noninvasive diagnosis of cancer. In this study, we investigated whether plasma miRNAs have diagnostic utility in identifying liver disease.

METHODS:

The study was divided into 2 phases: marker selection by real-time quantitative PCR analysis of a small set of plasma samples, and marker validation with a large set of plasma samples from 83 patients with chronic hepatitis B viral infections, 15 patients with skeletal muscle disease, and 40 healthy controls. Two mouse model systems, d-galactosamine- and alcohol-induced liver injury, were also developed to evaluate whether differences in miRNA concentration were associated with various liver diseases.

RESULTS:

Among the miRNA candidates identified, miR-122 presented a disease severity–dependent change in plasma concentration in the patients and animal models. Compared with an increase in aminotransferase activity in the blood, the change in miR-122 concentration appeared earlier. Furthermore, this change was more specific for liver injury than for other organ damage and was more reliable, because the change was correlated with liver histologic stage.

CONCLUSIONS:

Our findings suggest that circulating miR-122 has potential as a novel, predictive, and reliable blood marker for viral-, alcohol-, and chemical-induced liver injury.

  Z. G Xu , L. N Miao , Y. C Cui , Y Jia , H Yuan and M. Wu
 

Background. Angiotensin II type 1 receptor (AT1) plays an important role in the development of diabetic nephropathy (DN). However, the roles played by 12-lipoxygenase (12-LO) in the AT1 expression in glomerular cells exposed to high glucose (HG) and diabetic glomeruli remain unclear. Our objective in the present study was to investigate the role of 12-LO in the AT1 expression in glomerular cells and glomeruli under diabetic conditions.

Methods. Mesangial cells (MCs), podocytes and glomeruli isolated from rats were used in this study. The rats fed a high fat diet received low-dose streptozotocin to make type 2 diabetes. The 12-LO product 12(S)-hydroxyeicosatetraenoic acid [12(S)-HETE] was infused to rats by osmotic mini-pump. Morphometric measurement for glomerular volume, competitive reverse transcription polymerase chain reaction for mRNA expression, western blot and immunohistochemistry for protein expression were performed, respectively.

Results. Both the 12(S)-HETE and HG increased AT1 protein expression in MCs and podocytes. Furthermore, the levels of the AT1 were significantly higher in glomeruli derived from 12(S)-HETE-treated rats compared with control rats. In addition, HG-induced AT1 expression was significantly reduced by the 12-LO inhibitor cinnamyl-3,4-dihydroxy--cynanocinnamate (CDC). Compared with the non-diabetic controls, DN rats showed significant glomerular hypertrophy and albuminuria. This was associated with significant increases in AT1 protein expression. These abnormalities were prevented by treatment of the CDC.

Conclusions. These results indicate that AT1 expression is enhanced, at least in part, by 12-LO in the type 2 diabetic glomeruli, and 12-LO inhibition can ameliorate DN progression through downregulation of AT1 expression.

  J Jia , C Wang , Z Shi , J Zhao , Y Jia , Z Zhao Hui , X Li , Z Chen and P. Zhu
 

Objective. To explore the therapeutic potential of CD147/HAb18 mAb in the treatment of RA in severe combined immunodeficiency (SCID) mice engrafted with human cartilage and rheumatoid synovium tissue (SCID-HuRAg).

Methods. SCID-HuRAg mice were treated separately with CD147/HAb18 mAb, anti-TNF- mAb or a combination of both. The mice in control group were treated with anti-Japanese encephalitis virus mAb. The volume of engrafts was measured and the number of inflammatory cells and cartilage erosion score were examined. Expression of MMP-2, -3 and -9 was determined by immunohistochemistry. Human inflammatory cytokine levels in mouse sera were assessed using cytometric bead array kit.

Results. The volume of engrafts decreased significantly in SCID-HuRAg mice treated separately with anti-CD147 mAb or anti-TNF- mAb, and in the mice treated with anti-CD147 mAb plus anti-TNF- mAb (P < 0.05). Significant reduction was observed in cartilage erosion score in anti-CD147 treatment group and combined treatment group (P < 0.05). Immunohistochemical analysis showed that expression of MMP-2, -3 and -9 was lower in the anti-CD147 treatment group and combined treatment group than in the control mAb group (P < 0.05). Moreover, the level of TNF-, IL-6 and -8 in CD147 mAb group showed a significant decrease compared with that of the control mAb group (P < 0.05).

Conclusions. CD147/HAb18 mAb can reduce cartilage erosion and synovitis by inhibition of the MMPs and reduction of inflammatory cytokines in SCID-HuRAg mice, which suggests that CD147/HAb18 mAb is a promising treatment option for RA patients.

 
 
 
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