Hypertonicity Induces Injury to Cultured Human Endothelium: Attenuation by Glutamine

Parolari, Alessandro; Sala, Roberto; Antona, Carlo; Bussolati, Ovidio; Alamanni, Francesco; Mezzadri, Paola; DallˈAsta, Valeria; Gazzola, Gian C.; Biglioli, Paolo

doi:10.1016/s0003-4975(97)00998-3

Cited by 27 publications

(16 citation statements)

References 22 publications

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“…Cell volume affects the most basic processes of cell function, and hence exerts an important role in the onset, severity, and outcome of myocardial infarction. Earlier studies (Parolari et al 1997) indicated that glutamine administration can avert the severe osmolar changes associated with possible cell death.…”

Section: Discussionmentioning

confidence: 99%

Antioxidant defence of L-glutamine on mitochondrial function in experimentally induced myocardial infarction in rats

Anandan¹,

Kumar²,

Ganesan³

et al. 2013

Egypt. J. Bio.

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Myocardial infarction is a major public health concern and the leading cause of death all over the world. A better understanding of the processes involved in myocardial infarction has stimulated the search for biomolecules, which could limit the myocardial injury. We determined the protective activity of L-glutamine on mitochondrial function in isoprenalineinduced myocardial infarction in rats, an animal model of myocardial infarction in man. Oral pre-treatment with glutamine significantly inhibited the isoprenaline-induced changes in the levels of troponin T and homocysteine in the plasma. It conserved the activities of tricarboxylic acid cycle enzymes (isocitrate dehydrogenase, α-ketoglutarate dehydrogenase, succinate dehydrogenase, malate dehydrogenase) and respiratory marker enzyme (NADH dehydrogenase) and the level of myocardial ATP content at levels comparable to that of normal controls. It also attenuated isoprenaline-induced oxidative stress in rat mitochondria and preserved the antioxidant defence system at near normal. The results indicate that the cardioprotective effect of glutamine can be correlated directly with its ability to activate the energy status and antioxidant defence system.

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Section: Discussionmentioning

confidence: 99%

Antioxidant defence of L-glutamine on mitochondrial function in experimentally induced myocardial infarction in rats

Anandan¹,

Kumar²,

Ganesan³

et al. 2013

Egypt. J. Bio.

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“…There is more interventricular interdependence and the pediatric heart is more rate dependent for cardiac output than the adult. Due to the presence of shunt lesions there might be diastolic steal of blood during cardiopulmonary bypass which further affects myocardial perfusion and protection [18][19][20][21][22][23][24][25][26][27][28][29][30].…”

Section: Functional and Physiological Differencesmentioning

confidence: 99%

“…A proposed explanation ofthis difference is that, the mechanisms responsible for ischemic preconditioning may already be active in the immature heart [20,[21][22][23][24][25][26][27][28][29][30][31][32][33][34].…”

Section: Ischemic Preconditioningmentioning

confidence: 99%

“…Amino acids aspartate and glutamate enter the tri carboxylic acid cycle and have been shown to be promising substrates [29]. Glutamate has been found to have a protective effect on endothelial injury caused by hyperosmolar cardioplegia solutions [30]. There is evidence that addition of adenosine to cardioplegia solutions, or its administration during reperfusion results in better recovery of ATP levels and contributes to overall improved function during the post ischemic recovery period [31][32][33].…”

Section: Cardioplegiamentioning

confidence: 99%

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Myocardial Protection in Neonates and Infants: What have we Learnt? Where do we Go?

SachinTalwar¹

2015

J Heart Circ

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Myocardial protection in neonates and infants during heart surgery is still a matter of considerable debate. Multiple centers around the world have devised their own methods. Despite multiple claims of superiority of one method over another, there is no firm evidence in favor of one method over another and considerable research work is required in this field. This review summarizes the past, present and future of myocardial protection in children.

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“…이러한 측면에서 in vitro 조건에서 혈 청(serum) 공급의 차단은 내피세포의 apoptosis를 촉진하는 환경을 제공해 줄 수 있다 [3,17,25,27]. 또한 에너지 대사 측면에서 글루타민의 공급제한 역시 내피세포의 apoptosis를 유도하는 인자로서 작용 [24]할 수 있으나, 그에 대한 구체적인 기전은 알려진 바 없다.…”

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Effects of Glutamine Deprivation and Serum Starvation on the Growth of Human Umbilical Vein Endothelial Cells

정진우¹,

이혜현²,

박철³

et al. 2013

Journal of Life Science

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Glutamine and serum are essential for cell survival and proliferation in vitro, yet the signaling pathways that sense glutamine and serum levels in endothelial cells remain uninvestigated. In this study, we examined the effects of glutamine deprivation and serum starvation on the fate of endothelial cells using a human umbilical vein endothelial cell (HUVEC) model. Our data indicated that glutamine deprivation and serum starvation trigger a progressive reduction in cell viability through apoptosis induction in HUVECs as determined by DAPI staining and flow cytometry analysis. Although the apoptotic effects were more predominant in the glutamine deprivation condition, both apoptotic actions were associated with an increase in the Bax/Bcl-2 (or Bcl-xL) ratio, down-regulation of the inhibitor of apoptosis protein (IAP) family proteins, activation of caspase activities, and concomitant degradation of poly (ADP-ribose) polymerases. Moreover, down-regulation of the expression of Bid or up-regulation of truncated Bid (tBid) were observed in cells grown under the same conditions, indicating that glutamine deprivation and serum starvation induce the apoptosis of HUVECs through a signaling cascade involving death-receptor-mediated extrinsic pathways, as well as mitochondria-mediated intrinsic caspase pathways. However, apoptosis was not induced in cells grown in glutamine-and serum-free media when compared with cells exposed to glutamine deprivation or serum starvation alone. Taken together, our data indicate that glutamine deprivation and serum starvation suppress cell viability without apoptosis induction in HUVECs.Key words : HUVECs, glutamine deprivation, serum starvation, apoptosis *Corresponding author *Tel：+82-51-850-7413, Fax：+82-51-853-4036 *E-mail : choiyh@deu.ac.kr This is an Open-Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

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Hypertonicity Induces Injury to Cultured Human Endothelium: Attenuation by Glutamine

Cited by 27 publications

References 22 publications

Antioxidant defence of L-glutamine on mitochondrial function in experimentally induced myocardial infarction in rats

Antioxidant defence of L-glutamine on mitochondrial function in experimentally induced myocardial infarction in rats

Myocardial Protection in Neonates and Infants: What have we Learnt? Where do we Go?

Effects of Glutamine Deprivation and Serum Starvation on the Growth of Human Umbilical Vein Endothelial Cells

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