Contribution of caveolin-1 to ventricular nitric oxide in age-related adaptation to hypovolemic state

Arreche, Noelia; Sarati, Lorena Ivonne; Martínez, Carla; Fellet, Andrea L.; Balaszczuk, Ana M.

doi:10.1016/j.regpep.2012.08.002

Cited by 7 publications

(6 citation statements)

References 41 publications

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“…Furthermore, caveolin-1 is capable of attenuating the excitation of downstream protein molecules to reduce the release of eNOS, which weakens the negative feedback NO release by combining CSD microcell and eNOS ( 46 ). This increases the release of NO, leading to vasodilatation ( 2 ). Shen et al ( 28 ) demonstrated that the loss of caveolin-1 is associated with the generation of NO in the brain.…”

Section: Discussionmentioning

confidence: 99%

“…SAH can be divided into spontaneous and traumatic SAH ( 1 ). The annual incidence of spontaneous SAH is >10.5/100,000 individuals per year and, since the majority of spontaneous SAH cases are induced by aneurysm rupture, the annual incidence of aneurysm rupture-induced spontaneous SAH is 6–35.5/100,000 individuals per year ( 2 ). In recent years it has been demonstrated that the incidence of SAH is increasing ( 3 ).…”

Section: Introductionmentioning

confidence: 99%

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Alterations of caveolin-1 expression in a mouse model of delayed cerebral vasospasm following subarachnoid hemorrhage

Xiong

Wang

Ming

et al. 2016

Experimental and Therapeutic Medicine

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The aim of the present study was to evaluate the expression levels of caveolin-1 in the basilar artery following delayed cerebral vasospasm (DCVS) in a rat model of subarachnoid hemorrhage (SAH), in order to investigate the association between caveolin-1 and DCVS, and its potential as a treatment for DCVS of SAH. A total of 150 Sprague Dawley rats were randomly allocated into blank, saline and SAH groups. The SAH and saline groups were subdivided into days 3, 5, 7 and 14 following the establishment of the model. The murine model of SAH was established by double injection of autologous arterial blood into the cisterna magana and DCVS was detected using Bederson neurological severity scores. Hematoxylin and eosin (HE) staining was used to observe the inner perimeter of the basilar artery pipe and variations in the thickness of the basilar artery wall. Alterations in the levels of caveolin-1 protein in the basilar artery were measured using immunofluorescence and western blot analysis; whereas alterations in the mRNA expression levels of caveolin-1 were detected by reverse transcription-quantitative polymerase chain reaction. In the present study, 15 mice succumbed to SAH-induced DCVS in the day 3 (n=3), 5 (n=5) and 7 (n=2) groups. No mortality was observed in the blank control and saline groups during the process of observation in the SAH group, All mice in the SAH groups exhibited Bederson neurological severity scores ≥1; whereas no neurological impairment was detected in the blank and normal saline groups, demonstrating the success of the model. HE staining was used to assess vasospasm and the results demonstrated that the inner perimeter of the basal artery pipe decreased at day 3 in the SAH group; whereas values peaked in the day 7 group. The thickness of the basal artery wall significantly increased (P<0.05), as compared with the blank and saline groups, in which no significant alterations in the wall thickness and the inner perimeter of the basal artery pipe were detected. As detected by immunofluorescence and western blot analysis, the expression levels of caveolin-1 protein significantly decreased in the day 7 of SAH group, as compared with the blank and saline groups (P<0.01), in which no significant alterations were detected. Caveolin-1 mRNA expression levels significantly increased at the day 7 in the SAH group, as compared with the blank and the saline groups (P<0.01), as detected by RT-qPCR. Furthermore, significant differences were detected at day 14 in the SAH group, as compared with the blank and the saline groups (P>0.05), in which no significant alterations were detected. Therefore, the results of the present study demonstrated that caveolin-1 protein was downregulated in the basilar artery of a rat modeling SAH, which may be associated with DCVS. This suggested that caveolin-1 may be a potential target for the treatment of DCVS.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Alterations of caveolin-1 expression in a mouse model of delayed cerebral vasospasm following subarachnoid hemorrhage

Xiong

Wang

Ming

et al. 2016

Experimental and Therapeutic Medicine

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“…In the former, eNOS is linked with caveolin-3 and, to a lesser degree, caveolin-1, while, in endothelial cells, eNOS is associated only with caveolin-1 [85]. Arreche et al (2012) found increased NOS activity, decreased eNOS, and caveolin-1 protein levels, as well as increased iNOS activity in the ventricle of the middle-aged rats [86]. The dissociation of caveolin-1 from eNOS correlated with aging.…”

Section: Cardiovascular Aging and Nomentioning

confidence: 94%

An Overview of NO Signaling Pathways in Aging

et al. 2021

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Nitric Oxide (NO) is a potent signaling molecule involved in the regulation of various cellular mechanisms and pathways under normal and pathological conditions. NO production, its effects, and its efficacy, are extremely sensitive to aging-related changes in the cells. Herein, we review the mechanisms of NO signaling in the cardiovascular system, central nervous system (CNS), reproduction system, as well as its effects on skin, kidneys, thyroid, muscles, and on the immune system during aging. The aging-related decline in NO levels and bioavailability is also discussed in this review. The decreased NO production by endothelial nitric oxide synthase (eNOS) was revealed in the aged cardiovascular system. In the CNS, the decline of the neuronal (n)NOS production of NO was related to the impairment of memory, sleep, and cognition. NO played an important role in the aging of oocytes and aged-induced erectile dysfunction. Aging downregulated NO signaling pathways in endothelial cells resulting in skin, kidney, thyroid, and muscle disorders. Putative therapeutic agents (natural/synthetic) affecting NO signaling mechanisms in the aging process are discussed in the present study. In summary, all of the studies reviewed demonstrate that NO plays a crucial role in the cellular aging processes.

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“…Interestingly, a few studies suggest that changes in cav expression could alter cell function with aging [10]. We provided evidence using an experimental model of hypovolemic state that specific expression patterns of ventricular NOS isoforms, alterations for interaction, are involved in age-related adjustment to acute blood loss [11]. Considering that older adults are a high-risk population for hypovolemic state induced by a dehydration, we hypothesize that the NO pathways are involved in cardiac function regulation after long controlled water restriction, this response being different with aging.…”

Section: Introductionmentioning

confidence: 94%

Involvement of nitric oxide and caveolins in the age-associated functional and structural changes in a heart under osmotic stress

Arza

Netti

Perosi³

et al. 2015

Biomedicine & Pharmacotherapy

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Contribution of caveolin-1 to ventricular nitric oxide in age-related adaptation to hypovolemic state

Cited by 7 publications

References 41 publications

Alterations of caveolin-1 expression in a mouse model of delayed cerebral vasospasm following subarachnoid hemorrhage

Alterations of caveolin-1 expression in a mouse model of delayed cerebral vasospasm following subarachnoid hemorrhage

An Overview of NO Signaling Pathways in Aging

Involvement of nitric oxide and caveolins in the age-associated functional and structural changes in a heart under osmotic stress

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