Thermal sensitivity of endothelial cells on synthetic vascular graft material

Brinton, Mark R.; Tagge, Chad A.; Stewart, Russell J.; Cheung, Alfred K.; Shiu, Yan Ting; Christensen, Douglas A.

doi:10.3109/02656736.2011.638963

Cited by 20 publications

(16 citation statements)

References 33 publications

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“…It has been reported that exposure to heat stress caused apoptosis to occur in endothelial cells (Brinton et al 2012). Additionally, heat stress induced cell apoptosis by activating apoptosis-related genes, such as caspase and bax/bcl-2.…”

Section: Introductionmentioning

confidence: 99%

Down-regulation of miR-181a can reduce heat stress damage in PBMCs of Holstein cows

Chen

Shi

et al. 2016

In Vitro Cell.Dev.Biol.-Animal

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Heat stress can weaken the immune system and even increase livestock's susceptibility to disease. MicroRNA (miR) is short non-coding RNA that functions in post-transcriptional regulation of gene expression and some phenotypes. Our recent study found that miR-181a is highly expressed in the serum of heat-stressed Holstein cows, but the potential function of miR-181a is still not clarified. In this study, peripheral blood mononuclear cells (PBMCs), isolated from Holstein cows' peripheral blood, were used to investigate the effects of miR-181a inhibitor on heat stress damage. Our results showed that significant apoptosis and oxidative damage were induced by heat stress in PBMCs. However, with apoptosis, the levels of reactive oxygen species (ROS) and content of malondialdehyde (MDA) were reduced, while the content of glutathione (GSH) and the activity of superoxide dismutase (SOD) were increased even under heat stress conditions after transfecting miR-181a inhibitors to PBMCs. Meanwhile, mRNA expression of bax and caspase-3 was significantly decreased, but mRNA expression of bcl-2 was increased in transfected PBMCs. In conclusion, our results demonstrated that down-regulation of miR-181a can reduce heat stress damage in PBMCs of Holstein cows.

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Section: Introductionmentioning

confidence: 99%

Down-regulation of miR-181a can reduce heat stress damage in PBMCs of Holstein cows

Chen

Shi

et al. 2016

In Vitro Cell.Dev.Biol.-Animal

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“…Since HSPs are known to be protective [39–41], it is possible, albeit speculated, that the induction of HSPs may be also involved in the inhibitory effect of heat stress on apoptosis in LPS-stimulated PMECs. Interestingly, calpain has been suggested to target and cleave HSPs [42, 43].…”

Section: Discussionmentioning

confidence: 99%

Heat stress prevents lipopolysaccharide-induced apoptosis in pulmonary microvascular endothelial cells by blocking calpain/p38 MAPK signalling

et al. 2016

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Pulmonary microvascular endothelial cells (PMECs) injury including apoptosis plays an important role in the pathogenesis of acute lung injury during sepsis. Our recent study has demonstrated that calpain activation contributes to apoptosis in PMECs under septic conditions. This study investigated how calpain activation mediated apoptosis and whether heat stress regulated calpain activation in lipopolysaccharides (LPS)-stimulated PMECs. In cultured mouse primary PMECs, incubation with LPS (1 µg/ml, 24 h) increased active caspase-3 fragments and DNA fragmentation, indicative of apoptosis. These effects of LPS were abrogated by pre-treatment with heat stress (43 °C for 2 h). LPS also induced calpain activation and increased phosphorylation of p38 MAPK. Inhibition of calpain and p38 MAPK prevented apoptosis induced by LPS. Furthermore, inhibition of calpain blocked p38 MAPK phosphorylation in LPS-stimulated PMECs. Notably, heat stress decreased the protein levels of calpain-1/2 and calpain activities, and blocked p38 MAPK phosphorylation in response to LPS. Additionally, forced up-regulation of calpain-1 or calpain-2 sufficiently induced p38 MAPK phosphorylation and apoptosis in PMECs, both of which were inhibited by heat stress. In conclusion, heat stress prevents LPS-induced apoptosis in PMECs. This effect of heat stress is associated with down-regulation of calpain expression and activation, and subsequent blockage of p38 MAPK activation in response to LPS. Thus, blocking calpain/p38 MAPK pathway may be a novel mechanism underlying heat stress-mediated inhibition of apoptosis in LPS-stimulated endothelial cells.

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“…In these preliminary results, the levels of TNF-α, IL-1β and IL-6 varied with the recovery time following heat exposure, and were highest in the HS-6 group. Previous studies have suggested that intense heat stress may induce endothelial cell apoptosis, and that endothelial cells exhibit significant apoptosis during the acute-phase response to heat stress (28,29). A previous study by Gu et al (29) demonstrated that in vitro , the rate of apoptosis in human umbilical vein endothelial cells is associated with time after heat treatment, and apoptosis increased most markedly when human umbilical vein endothelial cells were treated at 43°C for 2 h, followed by replacement with fresh media and further incubation for 6 h. In the present study, the numbers of apoptotic aortic endothelial cells were highest in the HS-6 group.…”

Section: Discussionmentioning

confidence: 99%

Sodium tanshinone IIA sulfonate improves inflammation, aortic endothelial cell apoptosis, disseminated intravascular coagulation and multiple organ damage in a rat heat stroke model

Chen

Zhu

et al. 2017

Molecular Medicine Reports

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The aim of the present study was to investigate the effects of sodium tanshinone IIA sulfonate (STS) on inflammatory responses, aortic endothelial cell apoptosis, disseminated intravascular coagulation (DIC) and multiple organ damage in an animal model of classic heat stroke (CHS). The rats in the heat stroke (HS) and STS-treated heat stroke (STS-HS) groups were placed into a pre-warmed animal temperature controller (ATC) at 35°C. The moment at which the rectal temperature reached 43.5°C was considered as the time of onset of HS. In the HS groups, the rats were removed from the ATC and allowed to recover at 26°C for 0, 2, 6 or 12 h. In the STS-HS groups, the rats received femoral vein injections of 5–40 mg/kg STS immediately following the onset of HS and were subsequently placed at a temperature of 26°C to recover for 6 h. In the present study, the serum levels of tumor necrosis factor (TNF)-α, interleukin (IL)-1β and IL-6 were assessed using ELISA, and the numbers of apoptotic aortic endothelial cells were investigated using terminal deoxynucleotidyl transferase deoxyuridine triphosphate nick-end labeling combined with immunofluorescence. In the HS groups, the serum levels of TNF-α, IL-1β and IL-6, as well as the numbers of apoptotic aortic endothelial cells were increased compared with the normothermic control group. Additionally, the plasma prothrombin time, activated partial thromboplastin time and D-dimer level were significantly increased in the HS group compared with the normothermic control group following recovery for 6 h. By contrast, the platelet count was decreased in the HS group compared with the normothermic control group. The serum levels of creatinine, blood urea nitrogen, alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase and lactate dehydrogenase were increased and histopathological damage to multiple organs was observed in the HS group following recovery for 6 h. In the STS-HS groups, cytokine levels and apoptotic aortic endothelial cell numbers were reduced compared with the HS group after 6 h recovery. STS (40 mg/kg) treatment additionally improved the serum levels of organ injury indicators and plasma indicators of coagulopathy, and prevented histopathological damage to multiple organs. These findings demonstrated that STS treatment may ameliorate multiple organ damage by attenuating inflammatory responses, aortic endothelial cell apoptosis and DIC in CHS. These results suggested that STS may hold potential as an alternative therapeutic strategy for the treatment of patients with HS.

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Thermal sensitivity of endothelial cells on synthetic vascular graft material

Abstract: Cells grown on ePTFE were more susceptible to mild hyperthermia-induced death, compared to those on tissue culture dishes. Significant cell death on ePTFE mainly via apoptosis can be achieved by optimising temperature and duration of exposure.

Cited by 20 publications

References 33 publications

Down-regulation of miR-181a can reduce heat stress damage in PBMCs of Holstein cows

Down-regulation of miR-181a can reduce heat stress damage in PBMCs of Holstein cows

Heat stress prevents lipopolysaccharide-induced apoptosis in pulmonary microvascular endothelial cells by blocking calpain/p38 MAPK signalling

Sodium tanshinone IIA sulfonate improves inflammation, aortic endothelial cell apoptosis, disseminated intravascular coagulation and multiple organ damage in a rat heat stroke model

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