کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8385809 | 1543698 | 2013 | 12 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Chlamydia trachomatis inhibits telomeric DNA damage signaling via transient hTERT upregulation
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کلمات کلیدی
p.i.PIDTRAPCTRPNAGCAqRT-PCRhTERT - htertMOI - MEPeptide nucleic acid - اسید نوکلئیک پپتیدelementary body - بدن ابتداییReticulate body - بدن تلطیف شدهpelvic inflammatory disease - بیماری التهابی لگنCell transformation - تحول سلولیTelomere - تلومرtelomere repeat amplification protocol - تلومر تکرار پروتکل تقویتTelomerase - تلومراز human telomerase reverse transcriptase - تلومراز انسانی معکوس transcriptaseApoptosis - خزان یاختهایpost infection - عفونت پستneoplastic - نئوپلاستیکquantitative real-time PCR - واکنش زنجیره ای پلیمراز واقعی در زمان واقعیmultiplicity of infection - چندین عفونتChlamydia trachomatis - کلامیدیا تراکوماتیس
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
بیوشیمی، ژنتیک و زیست شناسی مولکولی (عمومی)
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چکیده انگلیسی
Epidemiological data exist to support a positive association between Chlamydia trachomatis (Ctr) infection and gynecological cancers; however, putative cellular mechanisms for this association are lacking. Here, we identified Ctr-induced perturbations to host cell phenotypes in vitro that persisted after clearance of infection and could directly contribute to host cell transformation. In particular, human telomerase catalytic subunit (hTERT) mRNA expression and catalytic subunit activity were increased in acute infected late passage IMR90E1A cells. hTERT upregulation was accompanied by recruitment of ceramide, a known regulator of hTERT, to the chlamydial inclusion and was abrogated following doxycycline-mediated infection clearance. In cells cleared of Ctr infection, average telomere length was slightly increased and immunofluorescence staining of the DNA damage marker γH2A.X was reduced after clearance of infection compared with cells that had not been infected. Reduced p53 binding to the promoter of the cell cycle checkpoint regulator p21 was also detected in cells cleared of infection and p21 levels were reduced; moreover, this cell population exhibited increased resistance to etoposide-induced DNA damage. Thus, Ctr infection altered cell aging and survival pathways, which persisted after infection clearance. Cells that survive infection are likely to exhibit altered physiology, as evidenced by an increased resistance to DNA damage-induced apoptosis, which may support cellular transformation.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: International Journal of Medical Microbiology - Volume 303, Issue 8, December 2013, Pages 463-474
Journal: International Journal of Medical Microbiology - Volume 303, Issue 8, December 2013, Pages 463-474
نویسندگان
Inken Padberg, Sabrina JanÃen, Thomas F. Meyer,