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2016 ; 118
(5
): 856-66
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Critical Role for Telomerase in the Mechanism of Flow-Mediated Dilation in the
Human Microcirculation
#MMPMID26699654
Beyer AM
; Freed JK
; Durand MJ
; Riedel M
; Ait-Aissa K
; Green P
; Hockenberry JC
; Morgan RG
; Donato AJ
; Peleg R
; Gasparri M
; Rokkas CK
; Santos JH
; Priel E
; Gutterman DD
Circ Res
2016[Mar]; 118
(5
): 856-66
PMID26699654
show ga
RATIONALE: Telomerase is a nuclear regulator of telomere elongation with recent
reports suggesting a role in regulation of mitochondrial reactive oxygen species.
Flow-mediated dilation in patients with cardiovascular disease is dependent on
the formation of reactive oxygen species. OBJECTIVE: We examined the hypothesis
that telomerase activity modulates microvascular flow-mediated dilation, and loss
of telomerase activity contributes to the change of mediator from nitric oxide to
mitochondrial hydrogen peroxide in patients with coronary artery disease (CAD).
METHODS AND RESULTS: Human coronary and adipose arterioles were isolated for
videomicroscopy. Flow-mediated dilation was measured in vessels pretreated with
the telomerase inhibitor BIBR-1532 or vehicle. Statistical differences between
groups were determined using a 2-way analysis of variance repeated measure (n?4;
P<0.05). L-NAME (N(?)-nitro-L-arginine methyl ester; nitric oxide synthase
inhibitor) abolished flow-mediated dilation in arterioles from subjects without
CAD, whereas polyethylene glycol-catalase (PEG-catalase; hydrogen peroxide
scavenger) had no effect. After exposure to BIBR-1532, arterioles from non-CAD
subjects maintained the magnitude of dilation but changed the mediator from
nitric oxide to mitochondrial hydrogen peroxide (% max diameter at 100 cm H2O:
vehicle 74.6±4.1, L-NAME 37.0±2.0*, PEG-catalase 82.1±2.8; BIBR-1532 69.9±4.0,
L-NAME 84.7±2.2, PEG-catalase 36.5±6.9*). Conversely, treatment of microvessels
from CAD patients with the telomerase activator AGS 499 converted the
PEG-catalase-inhibitable dilation to one mediated by nitric oxide (% max diameter
at 100 cm H2O: adipose, AGS 499 78.5±3.9; L-NAME 10.9±17.5*; PEG-catalase
79.2±4.9). Endothelial-independent dilation was not altered with either
treatment. CONCLUSIONS: We have identified a novel role for telomerase in
re-establishing a physiological mechanism of vasodilation in arterioles from
subjects with CAD. These findings suggest a new target for reducing the oxidative
milieu in the microvasculature of patients with CAD.
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