2018
DOI: 10.14814/phy2.13647
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Effects of HIV-1 gp120 and tat on endothelial cell sensescence and senescence-associated microRNAs

Abstract: The 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 β‐galactosidase (SA‐β‐gal). Cell expression of miR‐34a, miR‐217, and miR‐146a was determined by RT‐PCR. X4 and R5 gp120 and Tat significantly increased (~100%) ce… Show more

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Cited by 21 publications
(23 citation statements)
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“…Thus, expression of HIV Tat in endothelial cells or in transgenic mice upregulates the expression of the microRNA miR-34a [ 32 ], a molecule that targets sirtuin 1 (SIRT1), leading to the induction of senescence [ 33 , 34 ]. Together with Tat and Nef, other HIV proteins can also increase the expression of this senescence-associated microRNA and contribute to the induction of cell senescence, as revealed after the expression of the gp120 protein from X4 and R5 HIV-1 strains in endothelial cells [ 35 ]. Analysis of senescence markers such as p16 INK4a , p53 or SA-beta-gal activity revealed that expression of Tat and Nef proteins from the simian immunodeficiency virus (SIV) in adipose tissue and human adipose stem cells also results in the induction of senescence [ 36 ].…”
Section: Virus and Senescencementioning
confidence: 99%
“…Thus, expression of HIV Tat in endothelial cells or in transgenic mice upregulates the expression of the microRNA miR-34a [ 32 ], a molecule that targets sirtuin 1 (SIRT1), leading to the induction of senescence [ 33 , 34 ]. Together with Tat and Nef, other HIV proteins can also increase the expression of this senescence-associated microRNA and contribute to the induction of cell senescence, as revealed after the expression of the gp120 protein from X4 and R5 HIV-1 strains in endothelial cells [ 35 ]. Analysis of senescence markers such as p16 INK4a , p53 or SA-beta-gal activity revealed that expression of Tat and Nef proteins from the simian immunodeficiency virus (SIV) in adipose tissue and human adipose stem cells also results in the induction of senescence [ 36 ].…”
Section: Virus and Senescencementioning
confidence: 99%
“…ET-1 mediates the reduction of vascular nitric oxide production by ECs, leading to the smooth muscle proliferation and migration, which in turn leads to arterial vasoconstriction (80), whereas EMAPII is released in response to stress such as hypoxia, mechanical strain and apoptosis (81) and acts as a pro-apoptotic factor. In addition, a recent study has shown that HIV gp120 (X4 and R5) promotes EC senescence and impairs the regulation of senescence-associated microRNAs (82). Senescent ECs develop a dysfunctional phenotype acquiring pro-inflammatory, pro-oxidant, vasoconstrictor, and prothrombotic properties (83).…”
Section: Hiv Encoded Proteins and Endothelial Dysfunctionmentioning
confidence: 99%
“…A recent report indicates that HIV Tat along with morphine induces autophagy in pulmonary ECs, suggesting a role for Tat in HIV-related pulmonary arterial hypertension in the presence of opioids (107). In addition, Tat also promotes EC senescence and dysregulation of senescence-associated microRNAs (82).…”
Section: Hiv Encoded Proteins and Endothelial Dysfunctionmentioning
confidence: 99%
“…Since the BBB plays an essential role in neurological health by preventing unwanted compounds from entering the CNS, dysfunction associated with endothelial cell senescence is a likely contributor to HAND. Endothelial cells have previously been demonstrated to undergo premature senescence in response to external stressors such as TNFα, H 2 O 2 and even HIV gp120 (Hijmans et al, 2018; Khan et al, 2017; Rojas et al, 2017). We therefore hypothesize that the antiretroviral reverse transcriptase inhibitors tenofovir (TDF) and emtricitabine (FTC) constitute an HIV-associated stressor that prematurely may induce senescence in human umbilical vein endothelial cells (HUVECs) and alter their functional physiology.…”
Section: Introductionmentioning
confidence: 99%