Role of MnSOD in propofol protection of human umbilical vein endothelial cells injured by heat stress

Wu, Fang; Dong, Xuesong; Zhang, H Q; Li, L; Xu, Qiong; Liu, Z F; Gu, Zhengtao; Su, Lei

doi:10.1007/s00540-015-2129-2

Cited by 7 publications

(8 citation statements)

References 44 publications

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“…Also in HUVECs, the protective effect of propofol against heat stress-induced cell injury is associated with the induction of manganese (Mn)SOD expression. 49 This more pronounced antioxidant effect of propofol seems to be dose and time dependent, because in both studies the dose (two- to three-fold higher) and time of incubation (six hours vs 30 minutes) were higher than in our study. A possible explanation of the partial antioxidant properties of propofol is its structural similarity to alfa-tocoferol, which increases SOD activity.…”

Section: Discussioncontrasting

confidence: 61%

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Angiotensin-converting enzyme inhibitors attenuate propofol-induced pro-oxidative and antifibrinolytic effect in human endothelial cells

Wojewódzka-Żelezniakowicz

Gromotowicz-Popławska

Kisiel

et al. 2017

J Renin Angiotensin Aldosterone Syst

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Introduction:The aim of this study was to investigate the effects of plasma and tissue angiotensin-converting enzyme inhibitors (ACE-Is) against propofol-induced endothelial dysfunction and to elucidate the involved mechanisms in vitro.Materials and methods:We examined the effects of propofol (50 μM), quinaprilat and enalaprilat (10−5 M) on fibrinolysis (t-PA, PAI-1, TAFI antigen levels), oxidative stress parameters (H2O2 and MDA antigen levels and SOD and NADPH oxidase mRNA levels) and nitric oxide bioavailability (NO2/NO3 concentration and NOS expression at the level of mRNA) in human umbilical vein endothelial cells (HUVECs).Results:We found that both ACE-Is promoted similar endothelial fibrinolytic properties and decreased oxidative stress in vitro. Propofol alone increased the release of antifibrinolytic and pro-oxidative factors from the endothelium and increased mRNA iNOS expression. We also found that the incubation of HUVECs in the presence of propofol following ACE-Is pre-incubation caused weakness of the antifibrinolytic and pro-oxidative potential of propofol and this effect was similar after both ACE-Is.Conclusions:This observation suggests that the studied ACE-Is exerted protective effects against endothelial cell dysfunction caused by propofol, independently of hemodynamics.

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Section: Discussioncontrasting

confidence: 61%

“…A possible explanation of the partial antioxidant properties of propofol is its structural similarity to alfa-tocoferol, which increases SOD activity. 49 …”

Section: Discussionmentioning

confidence: 99%

Angiotensin-converting enzyme inhibitors attenuate propofol-induced pro-oxidative and antifibrinolytic effect in human endothelial cells

Wojewódzka-Żelezniakowicz

Gromotowicz-Popławska

Kisiel

et al. 2017

J Renin Angiotensin Aldosterone Syst

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“…As upregulating MnSOD expression effectively reduces endothelial cell damage caused by oxidative stress 24 , we investigated whether mitochondrial ROS (O 2 −. ) accumulation due to HS was also involved in Pin1-induced p53 transcription-independent apoptotic activity by infecting p53 +/+ MAECs with MnSOD overexpression vector or control vector alone (control cells).…”

Section: Resultsmentioning

confidence: 99%

Ser46 phosphorylation of p53 is an essential event in prolyl-isomerase Pin1-mediated p53-independent apoptosis in response to heat stress

Zou

et al. 2019

Cell Death Dis

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Heat stroke has increased in frequency worldwide in recent years and continues to have a high morbidity and mortality. Identification of the mechanisms mediating heat stoke is important and necessary. Our preliminary study revealed heat stress (HS)-induced apoptosis of vascular endothelial cells was associated with reactive oxygen species (ROS)-induced p53 translocation into mitochondria. Previous studies have suggested the prolyl-isomerase Pin1 regulates p53 functioning through specific binding to p53 phosphorylation sites. Based on these studies, we presumed Pin1 is a key intermediate in regulation of mitochondrial p53 translocation through a HS-induced ROS-p53 transcription-independent apoptosis pathway. In this context, we revealed p53 had a crucial role in a HS-induced mitochondrial apoptotic pathway, where p53 protein rapidly translocated into mitochondria in endothelial cells both in vitro and in vivo. In particular, HS caused an increase in p53 phosphorylation at Ser46 that facilitated interactions with phosphorylation-dependent prolyl-isomerase Pin1, which has a key role in promoting HS-induced localization of p53 to mitochondria. Furthermore, we also found ROS production was a critical mediator in HS-induced Pin1/p53 signaling and was involved in regulating mitochondrial apoptosis pathway activation. Therefore, we have contributed to our profound understanding of the mechanism underlying HS-induced endothelial dysfunction in an effort to reduce the mortality and morbidity of heat stroke.

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“…LPS-induced overproduction of ROS, such as superoxide anion and hydrogen peroxide, can exacerbate tissue damage and inflammatory response [26]. Previous evidence has revealed that several antioxidant agents, such as vitamin D [27], propofol [28], and olmesartan [29], prevent ECs from injury induced by excessive oxidative stress. Thus, inhibition of oxidative stress may be one of the mechanisms to alleviate ALI.…”

Section: Discussionmentioning

confidence: 99%

Nicorandil Attenuates LPS-Induced Acute Lung Injury by Pulmonary Endothelial Cell Protection via NF-κB and MAPK Pathways

Shi

et al. 2019

Oxidative Medicine and Cellular Longevity

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Acute lung injury (ALI) is a devastating critical disease characterized by diffuse inflammation and endothelial dysfunction. Increasing evidence, including from our laboratory, has revealed that the opening of ATP-sensitive potassium (KATP) channels has promising anti-inflammation and endothelial protection activities in various disorders. However, the impacts of KATP channels on ALI remain obscure. In this study, we used nicorandil (Nico), a classic KATP channel opener, to investigate whether opening of KATP channels could alleviate ALI with an emphasis on human pulmonary artery endothelial cell (HPAEC) modulation. The results showed that Nico inhibited lipopolysaccharide- (LPS-) induced inflammatory response, protein accumulation, myeloperoxidase activity, and endothelial injury. In vitro, Nico reduced LPS-induced HPAEC apoptosis and the expression of cleaved-caspase-3, caspase-9, and CCAAT/enhancer-binding protein homologous protein (CHOP). Additionally, Nico inhibited inflammation by suppressing monocyte-endothelial adhesion and decreasing the expression of proinflammatory proteins. Moreover, Nico restored the expression and the distribution of adherens junction vascular endothelial- (VE-) cadherin. Further, Nico abolished the increase in intracellular reactive oxygen species (ROS) and the activation of NF-κB and mitogen-activated protein kinase (MAPK) in HPAECs. Glibenclamide (Gli), a nonselective KATP channel blocker, abrogated the effects of Nico, implying that opening of KATP channels contributes to the relief of ALI. Together, our findings indicated that Nico alleviated LPS-induced ALI by protecting ECs function via preventing apoptosis, suppressing endothelial inflammation and reducing oxidative stress, which may be attributed to the inhibition of NF-κB and MAPK signaling pathways.

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Role of MnSOD in propofol protection of human umbilical vein endothelial cells injured by heat stress

Abstract: Propofol protected the heat stress-injured cells, at least partly, through upregulating MnSOD expression, effectively reducing the direct or indirect cell damage caused by oxidative stress.

Cited by 7 publications

References 44 publications

Angiotensin-converting enzyme inhibitors attenuate propofol-induced pro-oxidative and antifibrinolytic effect in human endothelial cells

Angiotensin-converting enzyme inhibitors attenuate propofol-induced pro-oxidative and antifibrinolytic effect in human endothelial cells

Ser46 phosphorylation of p53 is an essential event in prolyl-isomerase Pin1-mediated p53-independent apoptosis in response to heat stress

Nicorandil Attenuates LPS-Induced Acute Lung Injury by Pulmonary Endothelial Cell Protection via NF-κB and MAPK Pathways

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