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1.
Biomedical and Environmental Sciences ; (12): 792-801, 2017.
Article in English | WPRIM | ID: wpr-311346

ABSTRACT

<p><b>OBJECTIVE</b>This study aimed to investigate the susceptibility of mice with streptozotocin(STZ)-induced diabetes mellitus (TIDM) to the uptake of pentavalent inorganic arsenic (iAsV) and the possible molecular mechanism.</p><p><b>METHODS</b>TIDM was induced in mice by STZ. TIDM and normal mice were treated with 15.0 mg/kg Na2HAsO4·12H2O by intragastric administration. Then, the concentrations of arsenic in various tissues were measured by atomic fluorescence spectrometry. The gene expression levels of Pit1 and Pit2 were quantified by real-time RT-PCR, and their protein levels were detected by Western blotting in mouse heart, kidney, and liver tissues.</p><p><b>RESULTS</b>The concentrations of arsenic in STZ-induced TIDM mouse tissues were higher at 2 h after intragastric administration of Na2HAsO4·12H2O. Compared with the levels in normal mice, PIT1 and PIT2, which play a role in the uptake of iAsV, were upregulated in the livers and hearts of TIDM mice. PIT1 but not PIT2 was higher in TIDM mouse kidneys. The upregulation of Pit1 and Pit2 expression could be reversed by insulin treatment.</p><p><b>CONCLUSION</b>The increased uptake of iAsV in TIDM mouse tissues may be associated with increased PIT1 and/or PIT2 expression.</p>


Subject(s)
Animals , Male , Mice , Arsenic , Pharmacokinetics , Diabetes Mellitus, Experimental , Metabolism , Environmental Pollutants , Pharmacokinetics , Gene Expression Regulation , Physiology , Mice, Inbred ICR , Sodium-Phosphate Cotransporter Proteins, Type III , Genetics , Metabolism , Transcription Factor Pit-1 , Genetics , Metabolism
2.
Chinese Journal of Plastic Surgery ; (6): 48-50, 2007.
Article in Chinese | WPRIM | ID: wpr-297099

ABSTRACT

<p><b>OBJECTIVE</b>We have studied 4 generations 12 patients in a family which has blepharophimosis-ptosis-epicanthus-inversus syndrome (BPES) for the gene, FOXL2, the group also have 12 normal members in this family and other 80 normal individuals for contrast.</p><p><b>METHODS</b>The FOXL2 gene was amplified by polymerase chain reaction and then analyzed by direct genomic sequencing.</p><p><b>RESULTS</b>A 892C > T at nucleotides in FOXL2 was found in the twelve affected patients. No mutations was found in any of the health members in the family.</p><p><b>CONCLUSIONS</b>FOXL2 may be a important pathogenesis for the disease in this Chinese family.</p>


Subject(s)
Adolescent , Adult , Aged , Aged, 80 and over , Child , Child, Preschool , Female , Humans , Male , Middle Aged , Young Adult , Asian People , Genetics , Blepharophimosis , Ethnology , Genetics , Forkhead Box Protein L2 , Forkhead Transcription Factors , Genetics , Genotype , Mutation , Pedigree , Phenotype , Sequence Analysis, DNA , Syndrome
3.
Chinese Journal of Plastic Surgery ; (6): 147-150, 2007.
Article in Chinese | WPRIM | ID: wpr-297072

ABSTRACT

<p><b>OBJECTIVE</b>To construct eukaryotic expression vector of the truncated septin2 and investigate the influence on the cultured mouse epidermal cell and fibroblast in vitro exerted by the transgenic expression product.</p><p><b>METHODS</b>The short splicing fragment was obtained by amplifying the reverse transcription product of the fetal mouse skin mRNA with PCR. Then its recombinant expression vector pcDNA3.1 (-)/septin2s was constructed and used to transfect the mouse epidermal cell and fibroblast cultured in vitro. The expression of the foreign gene was detected with RT-PCR and the changes of cell proliferation were observed and analysed.</p><p><b>RESULTS</b>RT-PCR results indicated that pcDNA3.1/septin2 was expressed in the cultured mouse epidermal cells and fibroblasts in vitro. We found that the epidermal cells accelerated their reproduction, but the fibroblasts had no obvious changes.</p><p><b>CONCLUSION</b>We successfully constructed eukaryotic expressive vectors of pcDNA3.1/ septin2s and transfected it into mouse epidermal cells and fibroblasts in vitro. The results settle a basis for showing effect of septin2s on fetal mouse skin.</p>


Subject(s)
Animals , Mice , Cell Line , Cytoskeletal Proteins , Genetics , DNA, Recombinant , Epithelial Cells , Cell Biology , Fibroblasts , Cell Biology , GTP-Binding Proteins , Genetics , Genetic Vectors , Mice, Inbred BALB C , Septins , Skin , Cell Biology , Transfection
4.
Chinese Journal of Plastic Surgery ; (6): 58-61, 2005.
Article in Chinese | WPRIM | ID: wpr-255103

ABSTRACT

<p><b>OBJECTIVE</b>To construct eukaryotic expression vector of ribosomal protein sl5(RPs15) gene and study its effect on mouse skin fibroblasts in vitro.</p><p><b>METHODS</b>The RPs15 cDNA encoding region of fetal mouse skin was amplified by reverse transcription-polymerase chain reaction (RT-PCR) method and cloned into eukaryotic expression vector pcDNA3.1(-). The recombinant plasmid was transfected into adult mouse skin fibroblasts by FuGENE6 transfection reagents. Then the expression of RPs15 gene, was detected and its biological effect on fibroblasts was measured.</p><p><b>RESULTS</b>The DNA sequencing result of pcDNA3.1/RPs15 was identical with the reported. The RPs15 gene was expressed in transfected fibroblasts. The growth density of fibroblasts decreased with the conformation changing accordingly.</p><p><b>CONCLUSIONS</b>The eukaryotic expression vector pcDNA3.1/RPs15 is successively constructed and can be expressed in mouse skin fibroblasts. The results set up a basis for further study of the effect of RPs15 gene on skin fibroblasts.</p>


Subject(s)
Animals , Mice , Cells, Cultured , DNA Repair , DNA, Complementary , Genetics , Epithelial Cells , Metabolism , Fibroblasts , Metabolism , Genetic Vectors , Nuclear Proteins , Genetics , Plasmids , Ribosomal Proteins , Skin , Cell Biology , Transfection
5.
Chinese Journal of Medical Genetics ; (6): 372-375, 2005.
Article in English | WPRIM | ID: wpr-280048

ABSTRACT

<p><b>OBJECTIVE</b>To screen mutations in the forkhead transcriptional factor 2 gene (FOXL2) in six Chinese families with blepharophimosis, ptosis, and epicanthus inversus syndrome(BPES).</p><p><b>METHODS</b>PCR amplification and direct sequencing of the FOXL2 coding region in genomic DNA were performed in affected patients and 80 healthy controls. BLAST analysis of the sequence was made on Internet.</p><p><b>RESULTS</b>A novel 951-953(delC) was found in the two affected patients of a Chinese family with BPES. No mutations were found in the healthy controls. The 951-953(delC) may cause a frameshift mutation after codon 238 that exists downstream of the forkhead domain, resulting in the production of truncated proteins.</p><p><b>CONCLUSION</b>These findings indicated that the 951-953(delC) deletion mutation in the two patients resulted in truncated proteins and hence led to their BPES. To the authors' knowledge, the 951-953(delC) in FOXL2 has not been previously reported.</p>


Subject(s)
Female , Humans , Male , Amino Acid Sequence , Base Sequence , Blepharophimosis , Genetics , Blepharoptosis , Genetics , China , Eyelid Diseases , Genetics , Family Health , Forkhead Box Protein L2 , Forkhead Transcription Factors , Genetics , Molecular Sequence Data , Mutation , Pedigree , Sequence Alignment
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