دورية أكاديمية

Increased in vitro glial fibrillary acidic protein expression, telomerase activity, and telomere length after productive human immunodeficiency virus-1 infection in murine astrocytes.

التفاصيل البيبلوغرافية
العنوان: Increased in vitro glial fibrillary acidic protein expression, telomerase activity, and telomere length after productive human immunodeficiency virus-1 infection in murine astrocytes.
المؤلفون: Ojeda D; Instituto de Investigaciones Biomédicas en Retrovirus y Sida, Universidad de Buenos Aires-CONICET, Buenos Aires, Argentina., López-Costa JJ, Sede M, López EM, Berria MI, Quarleri J
المصدر: Journal of neuroscience research [J Neurosci Res] 2014 Feb; Vol. 92 (2), pp. 267-74. Date of Electronic Publication: 2013 Nov 19.
نوع المنشور: Journal Article; Research Support, Non-U.S. Gov't
اللغة: English
بيانات الدورية: Publisher: Wiley Interscience Country of Publication: United States NLM ID: 7600111 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1097-4547 (Electronic) Linking ISSN: 03604012 NLM ISO Abbreviation: J Neurosci Res Subsets: MEDLINE
أسماء مطبوعة: Publication: New York, NY : Wiley Interscience
Original Publication: New York, Liss.
مواضيع طبية MeSH: Astrocytes/*metabolism , Astrocytes/*virology , Glial Fibrillary Acidic Protein/*biosynthesis , Telomerase/*metabolism , Telomere/*pathology, AIDS Dementia Complex ; Animals ; Astrocytes/pathology ; Cells, Cultured ; Disease Models, Animal ; HIV-1 ; Mice ; Mice, Inbred BALB C ; Reverse Transcriptase Polymerase Chain Reaction ; Telomere/metabolism
مستخلص: Although HIV-associated neurocognitive disorders (HAND) result from injury and loss of neurons, productive infection routinely takes place in cells of macrophage lineage. In such a complex context, astrocytosis induced by local chemokines/cytokines is one of the hallmarks of HIV neuropathology. Whether this sustained astrocyte activation is able to alter telomere-aging process is unknown. We hypothesized that interaction of HIV with astrocytes may impact astrocyte telomerase activity (TA) and telomere length in a scenario of astrocytic activation measured by expression of glial fibrillary acidic protein (GFAP). To test this hypothesis, cultured murine astrocytes were challenged with pseudotyped HIV/vesicular stomatitis virus (HIV/VSV) to circumvent the absence of viral receptors; and GFAP, telomerase activity, and telomere length were quantified. As an early and transient event after HIV infection, both TA activity and telomere length were significantly augmented (P < 0.001). Later, a strong negative correlation (-0.8616, P < 0.0001) between virus production and telomerase activity was demonstrated. Once HIV production had reached a peak (7 dpi), the TA decreased, showing levels similar to those of noninfected cells. In contrast, the astrocyte became activated, exhibiting significantly increased levels of GFAP expression directly related to the level of HIV/VSV replication (P < 0.0001). Our results suggest that HIV-infected astrocytes exhibit early disturbance in their cellular functions, such as telomerase activity and telomere length, that may attenuate cell proliferation and enhance the astrocyte dysregulation, contributing to HIV neuropathogenesis. Understanding the mechanisms involved in HIV-mediated persistence by altering the telomere-related aging processes could aid in the development of therapeutic modalities for neurological complications of HIV infection.
(Copyright © 2013 Wiley Periodicals, Inc.)
فهرسة مساهمة: Keywords: GFAP; HIV-1; astrocytes; telomerase; telomere length
المشرفين على المادة: 0 (Glial Fibrillary Acidic Protein)
EC 2.7.7.49 (Telomerase)
تواريخ الأحداث: Date Created: 20131121 Date Completed: 20140818 Latest Revision: 20131211
رمز التحديث: 20221213
DOI: 10.1002/jnr.23294
PMID: 24254728
قاعدة البيانات: MEDLINE
الوصف
تدمد:1097-4547
DOI:10.1002/jnr.23294