ArticleAmerican journal of physiology. Heart and circulatory physiology2010
Inhibition of telomerase activity alters tight junction protein expression and induces transendothelial migration of HIV-1-infected cells.
Article in American journal of physiology. Heart and circulatory physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 21 citations in OpenAlex.
- Disruption of blood-brain barrier: effects of HIV Tat on brain microvascular endothelial cells and tight junction proteins.Journal of neurovirology · 2023Review
- Delay of endothelial cell senescence protects cerebral barrier against age-related dysfunction: role of senolytics and senomorphics.Tissue barriers · 2023Article
- Dynamic Crosstalk between Vascular Smooth Muscle Cells and the Aged Extracellular Matrix.International journal of molecular sciences · 2021Review
- Rosiglitazone suppresses HIV-1 Tat-induced vascular inflammation via Akt signaling.Molecular and cellular biochemistry · 2015Article
- Blood-brain barrier dysfunction developed during normal aging is associated with inflammation and loss of tight junctions but not with leukocyte recruitment.Immunity & ageing : I & A · 2015Article
- IL-17A induces MIP-1α expression in primary astrocytes via Src/MAPK/PI3K/NF-kB pathways: implications for multiple sclerosis.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2014Article
- PPAR agonist-mediated protection against HIV Tat-induced cerebrovascular toxicity is enhanced in MMP-9-deficient mice.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2014Article
- Aging and HIV/AIDS: pathogenetic role of therapeutic side effects.Laboratory investigation; a journal of technical methods and pathology · 2014Review
- Hypoxia induces connexin 43 dysregulation by modulating matrix metalloproteinases via MAPK signaling.Molecular and cellular biochemistry · 2013Article
- The hCMEC/D3 cell line as a model of the human blood brain barrier.Fluids and barriers of the CNS · 2013Article
- HIV-1 induces telomerase activity in monocyte-derived macrophages, possibly safeguarding one of its reservoirs.Journal of virology · 2012Article
- Endothelial cell senescence is associated with disrupted cell-cell junctions and increased monolayer permeability.Vascular cell · 2012Article
- Rodent models of HAND and drug abuse: exogenous administration of viral protein(s) and cocaine.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2012Review
- PPARα and PPARγ protect against HIV-1-induced MMP-9 overexpression via caveolae-associated ERK and Akt signaling.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2011Article
- Cocaine hijacks σ1 receptor to initiate induction of activated leukocyte cell adhesion molecule: implication for increased monocyte adhesion and migration in the CNS.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2011Article
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9 authors at 2 institutions in 1 country.
Funding
Abstract
Telomerase, via its catalytic component telomerase reverse transcriptase (TERT), extends telomeres of eukaryotic chromosomes. The importance of this reaction is related to the fact that telomere shortening is a rate-limiting mechanism for human life span that induces cell senescence and contributes to the development of age-related pathologies. The aim of the present study was to evaluate whether the modulation of telomerase activity can influence human immunodeficiency virus type 1 (HIV-1)-mediated dysfunction of human brain endothelial cells (hCMEC/D3 cells) and transendothelial migration of HIV-1-infected cells. Telomerase activity was modulated in hCMEC/D3 cells via small interfering RNA-targeting human TERT (hTERT) or by using a specific pharmacological inhibitor of telomerase, TAG-6. The inhibition of hTERT resulted in the upregulation of HIV-1-induced overexpression of intercellular adhesion molecule-1 via the nuclear factor-kappaB-regulated mechanism and induced the transendothelial migration of HIV-1-infected monocytic U937 cells. In addition, the blocking of hTERT activity potentiated a HIV-induced downregulation of the expression of tight junction proteins. These results were confirmed in TERT-deficient mice injected with HIV-1-specific protein Tat into the cerebral vasculature. Further studies revealed that the upregulation of matrix metalloproteinase-9 is the underlying mechanisms of disruption of tight junction proteins in hCMEC/D3 cells with inhibited TERT and exposed to HIV-1. These results indicate that the senescence of brain endothelial cells may predispose to the HIV-induced upregulation of inflammatory mediators and the disruption of the barrier function at the level of the brain endothelium.
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