Caveolin-1 and -3 dissociations from caveolae to cytosol in the heart during aging and after myocardial infarction in rat

Ratajczak, Philippe; Damy, Thibaud; Heymes, Christophe; Oliviéro, P.; Marotte, F.; Robidel, Estelle; Sercombe, Richard; Boczkowski, Jorge; Rappaport, L.; Samuel, Jane‐Lise

doi:10.1016/s0008-6363(02)00660-0

Cited by 117 publications

(95 citation statements)

References 33 publications

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“…In addition, caveolin-1 and -3 dissociation from caveolae occurs during aging, and NOS activity is negatively correlated with caveolin-1 levels in the cytosol. 27 To the extent that aging is associated with decreased caveolarassociated NOS, the effect of exogenous L-arginine could be additionally impaired. With arginase inhibition, L-arginine could restore responsiveness of cytosolic NOS and thus restore vasorelaxation.…”

Section: Discussionmentioning

confidence: 99%

Arginase Reciprocally Regulates Nitric Oxide Synthase Activity and Contributes to Endothelial Dysfunction in Aging Blood Vessels

et al. 2003

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Background-Although abnormal L-arginine NO signaling contributes to endothelial dysfunction in the aging cardiovascular system, the biochemical mechanisms remain controversial. L-arginine, the NO synthase (NOS) precursor, is also a substrate for arginase. We tested the hypotheses that arginase reciprocally regulates NOS by modulating L-arginine bioavailability and that arginase is upregulated in aging vasculature, contributing to depressed endothelial function. Methods and Results-Inhibition of arginase with (S)-(2-boronoethyl)-L-cysteine, HCl (BEC) produced vasodilation in aortic rings from young (Y) adult rats (maximum effect, 46.4Ϯ9.4% at 10 Ϫ5 mol/L, PϽ0.01). Similar vasorelaxation was elicited with the additional arginase inhibitors N-hydroxy-nor-L-arginine (nor-NOHA) and difluoromethylornithine (DFMO). This effect required intact endothelium and was prevented by 1H-oxadiazole quinoxalin-1-one (PϽ0.05 and PϽ0.001, respectively), a soluble guanylyl cyclase inhibitor. DFMO-elicited vasodilation was greater in old (O) compared with Y rat aortic rings (60Ϯ6% versus 39Ϯ6%, PϽ0.05). In addition, BEC restored depressed L-arginine (10 Ϫ4 mol/L)-dependent vasorelaxant responses in O rings to those of Y. Arginase activity and expression were increased in O rings, whereas NOS activity and cyclic GMP levels were decreased. BEC and DFMO suppressed arginase activity and restored NOS activity and cyclic GMP levels in O vessels to those of Y.Conclusions-These findings demonstrate that arginase modulates NOS activity, likely by regulating intracellular L-arginine availability. Arginase upregulation contributes to endothelial dysfunction of aging and may therefore be a therapeutic target.

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Section: Discussionmentioning

confidence: 99%

Arginase Reciprocally Regulates Nitric Oxide Synthase Activity and Contributes to Endothelial Dysfunction in Aging Blood Vessels

et al. 2003

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“…This roughly corresponds to the patterns seen in staining of the NMJs, because NMJ staining for caveolin-3 in neonates is considerably less intense than in adults (unpublished observations). Ratajczak et al (2003) reported some dissociation of caveolin-3 from sarcolemmal caveolae in aging cardiac muscle.…”

Section: Discussionmentioning

confidence: 99%

Concentration of Caveolin-3 at the Neuromuscular Junction in Young and Old Rat Skeletal Muscle Fibers

Carlson

Dedkov

et al. 2003

J Histochem Cytochem.

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S U M M A R YCaveolin-3, a muscle-specific member of the caveolin family, is strongly localized to the neuromuscular junction (NMJ) in adult rat muscle fibers, where it co-localizes with ␣ -bungarotoxin staining. In 24-month-old rats, less distinct staining corresponds with the normal aging changes in the NMJ. After denervation, the pattern and intensity of staining begin to break up as early as 3 days, and by 10 days little staining remains. The functional implications of this concentration of caveolin-3 at the NMJ remain obscure, but it is possible that its absence could account for some of the phenotypic characteristics of individuals with caveolin-3 mutations.

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“…Further work is warranted in unravelling the roles of caveolae and caveolin-3 in control of cardiomyocyte EGFR signalling. Importantly, significant reductions in myocardial caveolin-3 expression/localisation with ageing (Kawabe et al, 2001;Ratajczak et al, 2003;Peart et al, 2007), infarction (Ratajczak et al, 2003), and disease (Piech et al, 2003;Penumathsa et al, 2008;Crossman et al, 2011;Sharma et al, 2011;Lei et al, 2013) have the potential to dysregulate myocardial EGFR signalling.…”

Section: Cell Membrane Localisation -Membrane Rafts Caveolae and Cavmentioning

confidence: 99%

Transactivation of the epidermal growth factor receptor in responses to myocardial stress and cardioprotection

Reichelt

O’Brien

Thomas

et al. 2017

The International Journal of Biochemistry & Cell Biology

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Caveolin-1 and -3 dissociations from caveolae to cytosol in the heart during aging and after myocardial infarction in rat

Abstract: We demonstrate that dissociation of caveolin from caveolae is associated with aging and heart failure, the process being related to the decreased NOS activity.

Cited by 117 publications

References 33 publications

Arginase Reciprocally Regulates Nitric Oxide Synthase Activity and Contributes to Endothelial Dysfunction in Aging Blood Vessels

Arginase Reciprocally Regulates Nitric Oxide Synthase Activity and Contributes to Endothelial Dysfunction in Aging Blood Vessels

Concentration of Caveolin-3 at the Neuromuscular Junction in Young and Old Rat Skeletal Muscle Fibers

Transactivation of the epidermal growth factor receptor in responses to myocardial stress and cardioprotection

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