Effects of HIV‐1 gp120 and tat on endothelial cell sensescence and senescence‐associated microRNAs
AuthorHijmans, Jamie G.
Levy, Ma'ayan V.
Brewster, Lillian M.
Bammert, Tyler D.
Greiner, Jared J.
DeSouza, Christopher A.
AffiliationUniv Arizona, Dept Med, Div Infect Dis, Tucson, AZ USA
MetadataShow full item record
CitationPhysiol Rep, 6 (6), 2018, e13647, https://doi.org/10.14814/phy2.13647
Rights© 2018 The Authors. Physiological Reports published by Wiley Periodicals, Inc. on behalf of The Physiological Society and the American Physiological Society. This is an open access article under the terms of the Creative Commons Attribution License.
Collection InformationThis item from the UA Faculty Publications collection is made available by the University of Arizona with support from the University of Arizona Libraries. If you have questions, please contact us at firstname.lastname@example.org.
AbstractThe aim of this study was to determine, in vitro, the effects of X4 and R5 HIV-1 gp120 and Tat on: (1) endothelial cell senescence and (2) endothelial cell microRNA (miR) expression. Endothelial cells were treated with media without and with: R5 gp120 (100 ng/mL), X4 gp120 (100 ng/mL), or Tat (500 ng/mL) for 24 h and stained for senescence-associated beta-galactosidase (SA-beta-gal). Cell expression of miR-34a, miR-217, and miR-146a was determined by RT-PCR. X4 and R5 gp120 and Tat significantly increased (similar to 100%) cellular senescence versus control. X4 gp120 significantly increased cell expression of miR-34a (1.60 +/- 0.04 fold) and miR-217 (1.52 +/- 0.18), but not miR-146a (1.25 +/- 0.32). R5 gp120 significantly increased miR-34a (1.23 +/- 0.07) and decreased miR-146a (0.56 +/- 0.07). Tat significantly increased miR-34a (1.49 +/- 0.16) and decreased miR-146a (0.55 +/- 0.23). R5 and Tat had no effect on miR- 217 (1.05 +/- 0.13 and 1.06 +/- 0.24; respectively). HIV-1 gp120 (X4 and R5) and Tat promote endothelial cell senescence and dysregulation of senescence-associated miRs.
NoteOpen access journal.
VersionFinal published version
SponsorsNational Institutes of Health (NIH) [HL131458]
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