ABSTRACT
Immortal bovine mammary epithelial cell lines are useful for providing an efficient indicator for transgene expression and for the technological improvement of genetic modification. The preparation of hTERT (human telomerase reverse transcriptase)-mediated immortalized MECs (mammary epithelial cells) requires a down-regulation of p16(INK4a). Here, we report the establishment of two immortal bovine MEC lines by expression of hTERT gene alone under serum-containing culture conditions. This two cell lines maintain the general characteristics of MECs and have been stably passed more than 200 generations accompanying telomere extension, and were identified as non-malignant transformation. Investigation on transcriptional profile showed a similar down-regulation in both p16(INK4a) and p53. By comparing with non-immortal hTERT-positive MECs, we speculated that there are some spontaneous p16(INK4a)-reduced cells under normal culture conditions and the immortalization required for a co-ordinate repression of p53 and p16(INK4a) signalling pathways. Interestingly, two immortal cell lines showed a significant distinction in proliferation rate, implying that other mechanisms might be involved in proliferation control.
Subject(s)
Cell Line, Transformed , Epithelial Cells/metabolism , Telomerase/genetics , Animals , Cattle , Cell Proliferation , Cyclin-Dependent Kinase Inhibitor p16/genetics , Cyclin-Dependent Kinase Inhibitor p16/metabolism , Down-Regulation , Epithelial Cells/cytology , Female , Humans , Mammary Glands, Animal/cytology , Signal Transduction , Telomerase/metabolism , Tumor Suppressor Protein p53/genetics , Tumor Suppressor Protein p53/metabolismABSTRACT
OBJECTIVE: To investigate the relationship of angiotensin I-converting enzyme (ACE) gene polymorphism to diabetic retinopathy and diabetes myocardial infarction. METHODS: ACE insertion/deletion(I/D) polymorphism was determined by PCR. RESULTS: No evidence showed that ACE gene was associated with diabetic retinopathy. By comparison of the type 2 diabetes patients with myocardial infarction versus those without-myocardial infarction, it was found that the frequencies of homozygote DD (41.2% versus 33.2%) and of allele D (64.7% versus 55.0%) increased remarkably; the difference was statistically significant (P<0.05). CONCLUSION: Allele D(RR=1.50) and genotype DD(RR=1.33) seemed to be a genetic risk factor for type 2 diabetes myocardial infarction.
Subject(s)
Diabetes Mellitus, Type 2/complications , Diabetic Retinopathy/genetics , Myocardial Infarction/genetics , Peptidyl-Dipeptidase A/genetics , Polymorphism, Genetic , Adult , Aged , Diabetic Retinopathy/etiology , Female , Humans , Male , Middle Aged , Myocardial Infarction/etiology , Risk FactorsABSTRACT
To study the association of genes polymorphisms in glutathione S-transferase M1 and T1 with asthma bronchial. The distribute frequency of allele(+) and allele(o) between GSTM1 and GSTT1 of 60 patients asthma bronchial and 60 control groups in Tangshan was studied with PCR. The result shown GSTM1 deficiency allele(0/0) frequency of asthma bronchial was 81.2%, which showed significantly higher(chi(2)=32.46, P<0.001; wchi(2)=28.75,P<0.001) than the control groups; GSTT1 was similar to GSTM1. But GSTT1 zero allele(0/0) frequency of asthma bronchial were 71.7%, which were significantly higher (chi(2)=26.72, P<0.001; wchi(2)=35.75, P<0.001) than the control groups(11.7%). Zero allele of GSTM1 and GSTT1 were showed the most features in the asthma bronchial. Associated significantly in the genes polymorphisms of GSTM1 and GSTT1 with asthma bronchial, their genes mutation may be the genetic risk factor of asthma bronchial.
