Akt/eNOS signaling pathway mediates inhibition of endothelial progenitor cells by palmitate-induced ceramide

Fu, Mao; Li, Zhihong; Tan, Tao; Guo, Wenbing; Xie, Nanzi; Liu, Qing; Zhu, Hua; Xie, Xiaoyun; Han, Lei

doi:10.1152/ajpheart.00503.2014

Cited by 13 publications

(11 citation statements)

References 30 publications

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“…eNOS has been suggested to play a key role in the bioactivation of early endothelial progenitor cells [12]. In our previous study, we also demonstrated that the eNOS inhibitor significantly decreased the infiltration of endothelial progenitor cells in transplanted lung tissue by interfering with eNOS expression [14].…”

Section: Discussionmentioning

confidence: 59%

“…Previous studies have shown that NO produced by eNOS controls vascular remodelling and angiogenesis. The AKT/eNOS pathway has been suggested to play a pivotal role in bioactivation of endothelial progenitor cells, such as their mobilization, differentiation, homing and angiogenic properties [12,13]. Moreover, in our previous study, we found that eNOS inhibitor (L-NIO) decreases the recruitment of endothelial progenitor cells in transplanted lung [14].…”

Section: Introductionmentioning

confidence: 77%

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Endothelial colony-forming cells reduced the lung injury induced by cardiopulmonary bypass in rats

et al. 2020

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Background: Cardiopulmonary bypass (CPB) results in severe lung injury via inflammation and endothelial injury. The aim of this study was to evaluate the effect of endothelial colony-forming cells (ECFCs) on lung injury in rats subjected to CPB. Methods: Thirty-two rats were randomized into the sham, CPB, CPB/ECFC and CPB/ECFC/L-NIO groups. The rats in the sham group received anaesthesia, and the rats in the other groups received CPB. The rats also received PBS, ECFCs and L-NIO-pre-treated ECFCs. After 24 h of CPB, pulmonary capillary permeability, including the PaO 2 /FiO 2 ratio, protein levels in bronchoalveolar lavage fluid (BALF) and lung tissue wet/dry weight were evaluated. The cell numbers and cytokines in BALF and peripheral blood were tested. Endothelial injury, lung histological injury and apoptosis were assessed. The oxidative stress response and apoptosis-related proteins were analysed. Results: After CPB, all the data deteriorated compared with those obtained in the S group (sham vs CPB vs CPB/ ECFC vs CPB/ECFC/L-NIO: histological score 1.62 ± 0.51 vs 5.37 ± 0.91 vs 3.37 ± 0.89 vs 4.37 ± 0.74; PaO 2 /FiO 2 389 ± 12 vs 233 ± 36 vs 338 ± 28 vs 287 ± 30; wet/dry weight 3.11 ± 0.32 vs 6.71 ± 0.73 vs 4.66 ± 0.55 vs 5.52 ± 0.57; protein levels in BALF: 134 ± 22 vs 442 ± 99 vs 225 ± 41 vs 337 ± 53, all P < 0.05). Compared to the CPB treatment, ECFCs significantly improved pulmonary capillary permeability and PaO 2 /FiO 2. Similarly, ECFCs also decreased the inflammatory cell number and pro-inflammatory factors in BALF and peripheral blood, as well as the oxidative stress response in the lung tissue. ECFCs reduced the lung histological injury score and apoptosis and regulated apoptosis-related proteins in the lung tissue. Compared with the CPB/ECFC group, all the indicators were partly reversed by the L-NIO. Conclusions: ECFCs significantly reduced lung injury induced by inflammation after CPB.

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Section: Discussionmentioning

confidence: 59%

Section: Introductionmentioning

confidence: 77%

Endothelial colony-forming cells reduced the lung injury induced by cardiopulmonary bypass in rats

et al. 2020

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“…In this study, we established a rat CPB model to observe the effect of ECFCs on CPB-related lung injury. Moreover, the eNOS plays a pivotal role in bioactivation of early endothelial progenitor cells [12], and we also found that eNOS inhibitor (L-NIO) decreased the recruitment of endothelial progenitor cells in transplanted lung [13]. We postulated that eNOS also plays a pivotal role in the bioactivation of ECFCs.…”

Section: Introductionmentioning

confidence: 54%

“…After CPB, apoptosis also played a pivotal role in lung injury [42]. Both inflammatory factors (TNF-α) and reactive oxygen species induced by lung ischaemia lead to cell apoptosis [43] eNOS has been suggested to play a key role in the bioactivation of early endothelial progenitor cells [12]. In our previous study, we also demonstrated that the eNOS inhibitor significantly decreased the infiltration of endothelial progenitor cells in transplanted lung tissue by interfering with eNOS expression [13].…”

Section: Discussionmentioning

confidence: 86%

Endothelial colony-forming cells reduced the lung injury induced by cardiopulmonary bypass in rats

Sun

Zhao

Tai

et al. 2020

Preprint

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Background: Cardiopulmonary bypass (CPB) results in severe lung injury via inflammation and endothelial injury. The aim of this study was to evaluate the effect of endothelial colony-forming cells (ECFCs) on lung injury in rats subjected to CPB. Methods: Thirty-two rats were randomized into the sham, CPB, CPB/ECFC and CPB/ECFC/L-NIO groups. The rats in the sham group received anaesthesia, and the rats in the other groups received CPB. The rats also received PBS, ECFCs and L-NIO-pretreated ECFCs. After 24 hours of CPB, pulmonary capillary permeability, including the PaO 2 /FiO 2 ratio, protein levels in bronchoalveolar lavage fluid (BALF) and lung tissue wet/dry weight, was evaluated. The cell numbers and cytokines in BALF and peripheral blood were tested. Endothelial injury, lung histological injury and apoptosis were assessed. The oxidative stress response and apoptosis-related proteins were analysed. Results: After CPB, all the data deteriorated compared with those obtained in the S group (sham vs CPB vs CPB/ECFC vs CPB/ECFC/L-NIO: histological score: 1.62±0.51 vs 5.37±0.91 vs 3.37±0.89 vs 4.37±0.74; PaO 2 /FiO 2 : 389±12 vs 233±36 vs 338±28 vs 287±30; wet/dry weight: 3.11±0.32 vs 6.71±0.73 vs 4.66±0.55 vs 5.52±0.57; protein levels: 134±22 vs 442±99 vs 225±41 vs 337±53, all P<0.05). Compared to the CPB treatment, ECFCs significantly improved pulmonary capillary permeability and PaO 2 /FiO 2 . Similarly, ECFCs also decreased the inflammatory cell number and pro-inflammatory factors in BALF and peripheral blood, as well as the oxidative stress response in the lung tissue. ECFCs reduced the lung histological injury score and apoptosis and regulated apoptosis-related proteins in the lung tissue. Compared with CPB/ECFC group, all the indicators were partly reversed by the L-NIO. Conclusions: ECFCs significantly reduced lung injury induced by inflammation after CPB.

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“…Ceramide accumulation inhibits EPCs proliferation, migration, and tube formation via its inhibition of Akt/eNOS pathway [151].…”

Section: Ceramide and Sphingolipidsmentioning

confidence: 99%

Insights into the molecular mechanisms of diabetes-induced endothelial dysfunction: focus on oxidative stress and endothelial progenitor cells

et al. 2015

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Diabetes mellitus is a heterogeneous, multifactorial, chronic disease characterized by hyperglycemia owing to insulin insufficiency and insulin resistance (IR). Recent epidemiological studies showed that the diabetes epidemic affects 382 million people worldwide in 2013, and this figure is expected to be 600 million people by 2035. Diabetes is associated with microvascular and macrovascular complications resulting in accelerated endothelial dysfunction (ED), atherosclerosis, and cardiovascular disease (CVD). Unfortunately, the complex pathophysiology of diabetic cardiovascular damage is not fully understood. Therefore, there is a clear need to better understand the molecular pathophysiology of ED in diabetes, and consequently, better treatment options and novel efficacious therapies could be identified. In the light of recent extensive research, we re-investigate the association between diabetes-associated metabolic disturbances (IR, subclinical inflammation, dyslipidemia, hyperglycemia, dysregulated production of adipokines, defective incretin and gut hormones production/action, and oxidative stress) and ED, focusing on oxidative stress and endothelial progenitor cells (EPCs). In addition, we re-emphasize that oxidative stress is the final common pathway that transduces signals from other conditions-either directly or indirectly-leading to ED and CVD.

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Akt/eNOS signaling pathway mediates inhibition of endothelial progenitor cells by palmitate-induced ceramide

Cited by 13 publications

References 30 publications

Endothelial colony-forming cells reduced the lung injury induced by cardiopulmonary bypass in rats

Endothelial colony-forming cells reduced the lung injury induced by cardiopulmonary bypass in rats

Endothelial colony-forming cells reduced the lung injury induced by cardiopulmonary bypass in rats

Insights into the molecular mechanisms of diabetes-induced endothelial dysfunction: focus on oxidative stress and endothelial progenitor cells

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