Biomedical subjects

Tae-Ho Hwang

Publications and source records attributed to Tae-Ho Hwang.

3 recordsLinked to original sources

PubMed2003

A single administration of adenoviral-mediated HGF cDNA permits survival of mice from acute hepatic failure.

Heptatocyte growth factor (HGF) having a variety of biological activity was suggested as a protective agent against acute toxic hepatic injury or a potentially therapeutic agent. For the efficient in vivo application of this factor, we employed adenoviral-mediated HGF gene delivery system. In this study, we constructed E1-deleted recombinant adenovirus carrying cDNA of human HGF (Ad.hHGF) and elucidated that HGF was efficiently expressed in the liver of C57/BL mice. A mouse model of acute hepatic failure was induced by high dose (1000mg/kg) of thioacetamide (TA) administration. Mice infected with Ad.hHGF showed a dramatic resistance to TA-induced acute hepatic injury. Serum ALT was increased transiently and then the level was normalized in Ad.hHGF-infected mice with TA administration. Furthermore, the survival rate was remarkably enhanced in the mice infected with Ad.hHGF. In the histological examination, massive hepatic necrosis induced by TA was almost completely protected by HGF produced by Ad.hHGF. Our results indicate that a single dose of HGF-encoding adenoviral vector maintained liver function and prevented the progression of liver necrosis in a mouse model of acute hepatic failure.

Adenoviridae↗

PubMed2002

Cbfa1-independent decrease in osteoblast proliferation, osteopenia, and persistent embryonic eye vascularization in mice deficient in Lrp5, a Wnt coreceptor.

The low-density lipoprotein receptor-related protein (Lrp)-5 functions as a Wnt coreceptor. Here we show that mice with a targeted disruption of Lrp5 develop a low bone mass phenotype. In vivo and in vitro analyses indicate that this phenotype becomes evident postnatally, and demonstrate that it is secondary to decreased osteoblast proliferation and function in a Cbfa1-independent manner. Lrp5 is expressed in osteoblasts and is required for optimal Wnt signaling in osteoblasts. In addition, Lrp5-deficient mice display persistent embryonic eye vascularization due to a failure of macrophage-induced endothelial cell apoptosis. These results implicate Wnt proteins in the postnatal control of vascular regression and bone formation, two functions affected in many diseases. Moreover, these features recapitulate human osteoporosis-pseudoglioma syndrome, caused by LRP5 inactivation.

Animals↗

PubMed2002

Ultrasonographic evidence of phenotypic instability during hepatocarcinogenesis in N-nitrosomorpholine-treated rats.

Carcinogen-induced hepatoma in immunocompetent animal models has shown a progress similar to the clinical course of human hepatoma. Ultrasonography (US) was used for consecutive evaluation of the phenotypic changes in Sprague-Dawley rats exposed for 8 weeks to N-nitrosomorpholine (NNM, 200 mg/L). Three distinctive US findings were ascites, coarseness (defined as small and heterogeneously widespread increased echogenecity), and nodularity (defined as a >0.6-cm-sized echogenic region and clearly showing a tumor-like mass). Abdominal ascites was observed in 5 of 26 rats at week 8 NNM posttreatment and the number of rats showing ascites gradually increased. Coarseness (22 of 26 rats) and nodularity (1 of 18) appeared at weeks 8 and 17 NNM posttreatment, respectively. The gross and histological findings indicated that coarseness and nodularity shown in US reflected fibrosis and hepatocellular carcinoma or cholangiofibroma, respectively. The computer-aided quantification of coarseness and nodularity showed that the regression-linked phenotypic instability was present in coarseness but not in nodularity. We conclude that the heterogeneity of preneoplasia in NNM-treated rats might be induced by phenotypic instability rather than random initiating events of preneoplastic lesion.

Animals↗