大鼠部分肝切除前后热激处理对过氧化物酶基因表达的影响

用过氧化物酶原位复性电泳（SDS－POD－PAGE）技术分析了部分肝切除（partial hepatectomy,PH)、部分肝切除后再热激（partial hepatectomy following heat shock,PH-HS)和先热激再部分肝切除（heat shock following partial hepatectomy,HS-PH)后肝再生期间过氧化物酶（POD）基因表达差异,结果表明,PH中表达的POD基因种类（7个）＞PH－HS（5个）＞HS－PH（3个）;三个模型的POD总活性为：HS－PH＞PH－HS。根据实验结果推测,POD在肝再生和肝损伤恢复中起一定作用。     

Identification and characterization of 177 unreported genes associated with liver regeneration

The mammalian liver has a very strong regeneration capacity after partial hepatectomy (PH). To further learn the genes participating in the liver regeneration (LR), 551 cDNAs selected from subtracted cDNA libraries of the regenerating rat liver were screened by microarray, and their expression profiles were studied by cluster and generalization analyses. Among them, 177 genes were identified unreported and up-or down-regulated more than twofold at one or more time points after PH, of which 62 genes were down-regulated to less than 0.5; 99 genes were up-regulated to 2-10 folds, and 16 genes were either up- or down-regulated at different time points during LR. By using BLAST and GENSCAN, these genes were located on responsible chromosomes with 131 genes on the long arms of the chromosomes. The cluster and generalization analyses showed that the gene expression profiles are similar in 2 and 4, 12 and 16, 96 and 144 h respectively after PH, suggesting that the actions of the genes expressed in the same profiles are similar, and those expressed in different profiles have less similarity. However, the types,characteristics and functions of the 177 genes remain to be further studied.     

Identifcation and Characterization of 177 Unreported Genes Associated with Liver Regeneration

The mammalian liver has a very strong regeneration capacity after partial hepa- tectomy (PH). To further learn the genes participating in the liver regeneration (LR), 551 cDNAs selected from subtracted cDNA libraries of the regenerating rat liver were screened by microarray, and their expression pro?les were studied by cluster and generalization analyses. Among them, 177 genes were identi?ed unre- ported and up- or down-regulated more than twofold at one or more time points after PH, of wh…     

Hepcidin plays a negative role in liver regeneration

Hepcidin is a key regulator of iron metabolism. The expres- sion of hepcidin is significantly induced by iron overload, inflammation, and infection of pathogens. Recent studies have indicated that the expression of hepcidin in the liver is also regulated during liver regeneration. However, the mechanism of the regulation of hepcidin expression and its role in liver regeneration remain unclear. In this study, we found that the hepatocyte growth factor inhibited hepcidin expression in the liver during the late stage of liver regener- ation. Meanwhile, we investigated the effect of hepcidin on liver regeneration. Mice overexpressing hepcidin-1 exhib- ited impaired hepatic regeneration after partial hepatect- omy, as determined by immunohistochemieal staining of the proliferation cell nuclear antigen. Our results demon- strated a negative role of hepcidin in modulating liver re- generation, and suggested that a sustained high iron level by the down-regulation of hepcidin at the late stage of liver regeneration is required for hepatocyte proliferation.     

Expression of the Tribolium castaneum （Coleoptera： Tenebrionidae） hsp83 gene and its relation to oogenesis during ovarian maturation

Heat shock proteins (HSP) can protect organisms and cells from thermal damage. In this study, we cloned the full length cDNA encoding the HSP83 protein (the homologue of HSP90) of Tribolium castaneum (red flour beetle). The isolated cDNA contains the full coding sequence, a partial 5′ untranslated region of 55 bp and the complete 3′ untranslated region. We found the hsp83 gene is located on chromosome 5 of the T. castaneum genome. The predicted HSP83 protein sequence has a high similarity (on average 86.77%) with that of other insect species. The expression of the hsp83 gene in the whole body and in the ovary could be induced with heat stress (40°C for 1 h) in newly hatched (within 3 h post emergence) and mature (10 days post emergence) beetles. Under normal conditions, the hsp83 expression in the ovary is about 3-fold higher than in the whole body at both stages. No significant difference in hsp83 expression was observed between the two ovarian developmental stages regardless if the beetles were treated with heat shock or not. The expression of the HSP83 protein in the whole body could also be induced with heat stress in newly hatched and mature beetles. However, in the ovary, HSP83 was only expressed in the follicle cells of mature beetles and not in newly hatched beetles, regardless if the beetles were treated with heat shock or not. Furthermore, the females were not able to produce mature oocytes after knock-down of the hsp83 expression by injecting dsRNA. These results suggest that the HSP83 protein is involved in protection against heat stress and could be involved in oogenesis during ovarian maturation of T. castaneum.     

Cloning and characterization of a mouse liver-specific gene mfrep-1, up-regulated in liver regeneration

Human fibrinogen-related protein-1/liver fibrinogen-related protein-1 (HFREP-l/LFIRE-1), a liver-specific protein, is a member of fibrinogen superfamily that exerts various biological activities. However, the function of HFREP-l/LFIRE-1 in liver remains unknown. Here we isolated its mouse ortholog gene-mouse fibrinogen-related protein-1 (mfrep-1), which encoded 314 amino acids, exhibiting 80.4% similarity to HFREP-l/LFIRE-1. Northern blot analysis revealed that 1.2-kb mfrep-1 mRNA was detected selectively in mouse liver. To explore the function of MFREP-1, we examined the levels of mfrep-1 mRNA during regeneration after 70% partial hepatectomy (PHx) in mice, mfrep-1 mRNA increased in the regenerating liver and reached the first shoulder peak at 2-4 h after PHx. Cycloheximide pretreatment could suppress the induction of mfrep-1, indicating the up-regulation of this gene need de novo protein synthesis. Its mRNA continued to elevate at 6 h thereafter and reached the second peak at 24 h. The enhanced express     

Large scale of identification of differentially expressed genes in the regenerating rat liver after SISPH

After partial hepatectomy (PH), the remnant paren-chyma can completely recover lost liver mass and function in about one week[1,2]. Although adult hepa-tocytes are normally quiescent, they are readily primed to pass from G0 to G1 phase within 2―6 h after PH. The first peak of DNA synthesis appears 24 h after PH, while cell division peaks at 36 h. The liver cells then enter a second cell cycle, and redifferentiation and reconstruction of structure and function[3―6] take place. A great nu…     

Human augmenter of liver regeneration: molecular cloning, biological activity and roles in liver regeneration

The complete amino acid sequence of human augmenter of liver regeneration (hALR) was reported by deduction from nucleotide sequence of its complementary DNA . The cDNA for hALR was isolated by screening a human fetal liver cDNA library and the sequencing of this insert revealed an open reading frame encoding a protein with 125aa and highly homologous (87% ) with rat ALR encoding sequence. The recombinant hALR expressed from its cDNA in transient expression experiments in cos-7 cells could stimulate DNA synthesis of HTC hepatoma cell in the dose-dependent and heat-resistant way. Northern blot analysis with rat ALR cDNA as probe confirmed that ALR mRNA was expressed in the normal rat liver at low level and that dramatically increased in the regenerating liver after partial hepatectomied rat. This size of hALR mRNA is 1.4 kb long and expressed in human fetal liver, kidney and testis. These findings indicated that liver itself may be the resource of ALR and suggested that ALR seems to be an im-portant parac     

Induction of Antioxidant and Heat Shock Protein Responses During Torpor in the Gray Mouse Lemur,Microcebus murinus

A natural tolerance of various environmental stresses is typically supported by various cytoprotective mechanisms that protect macromolecules and promote extended viability. Among these are antioxidant defenses that help to limit damage from reactive oxygen species and chaperones that help to minimize protein misfolding or unfolding under stress conditions. To understand the molecular mechanisms that act to protect cells during primate torpor, the present study characterizes antioxidant and heat shock protein(HSP) responses in various organs of control(aroused)and torpid gray mouse lemurs, Microcebus murinus. Protein expression of HSP70 and HSP90 a was elevated to 1.26 and 1.49 fold, respectively, in brown adipose tissue during torpor as compared with control animals, whereas HSP60 in liver of torpid animals was 1.15 fold of that in control(P 0.05). Among antioxidant enzymes, protein levels of thioredoxin 1 were elevated to 2.19 fold in white adipose tissue during torpor, whereas Cu–Zn superoxide dismutase 1 levels rose to 1.1 fold in skeletal muscle(P 0.05). Additionally, total antioxidant capacity was increased to 1.6 fold in liver during torpor(P 0.05), while remaining unchanged in the five other tissues. Overall, our data suggest that antioxidant and HSP responses are modified in a tissue-specific manner during daily torpor in gray mouse lemurs. Furthermore, our data also show that cytoprotective strategies employed during primate torpor are distinct from the strategies in rodent hibernation as reported in previous studies.