Palmitic and Linoleic Acids Impair Endothelial Progenitor Cells by Inhibition of Akt/eNOS Pathway

Guo, Wenbing; Yang, Qidong; Liu, Yunhai; Xie, Xiaoyun; Wang-Miao,; Niu, Ruichao

doi:10.1016/j.arcmed.2008.02.001

Cited by 28 publications

(28 citation statements)

References 28 publications

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“…We have previously demonstrated that palmitic and linoleic acids may impair eNOS phosphorylation at the Ser1177 site resulting in reduced NO production, which contributes to the dysfunction of EPCs [34]. The present study demonstrated that UTI significantly increased eNOS phosphorylation and bioavailable NO without affecting total eNOS.…”

Section: Guo Et Al: Urinary Trypsin Inhibitor Repairs Lung Injurysupporting

confidence: 60%

Urinary Trypsin Inhibitor Attenuates Acute Lung Injury by Improving Endothelial Progenitor Cells Functions

Guo

Xie

et al. 2015

Cell Physiol Biochem

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Background: Urinary Trypsin Inhibitor (UTI) is involved in various aspects of tissue repair, regeneration and development. However, the potential role of UTI in protection against acute lung injury (ALI) remains largely unknown. In the present study, we demonstrated that UTI treatment could ameliorate ALI induced by oleic acid (OA) treatment in rabbit model. Methods: Intravenous application of UTI (10000 U/kg/d) significantly improved the pathologies associated with OA-induced ALI. The lungs were stained with hematoxylin and eosin to scored the lung injury. Peripheral blood mononuclear cells were isolated by density gradient centrifugation with Ficoll-Plaque Plus. The proliferation and ability of tube structure formation of EPCs were observed and the level of phosphorylated Akt protein expression and eNOS protein expression were assayed. Results: Consistent with pathological scores, UTI treatment significantly reduced wet/dry ratio of OA injured lungs. A quantification of capillary density revealed that UTI treatment led to about 2 fold increase over uninjured control and about 1.5 fold increase over PBS treatment. The capacity for tube formation of EPCs on ECM gel was significantly reduced in the ALI group and recovered with UTI treatment. Quantification of western blot bands was summarized and showed that UTI treatment activates Akt/eNOS signaling. NO production could contribute to the improvement of EPCs function by UTI treatment. Conclusions: UTI-induced phosphorylation/activation of eNOS and Akt, increases the intracellular level of NO, thereby improving tube formation and proliferation function of EPCs. EPCs function is crucial for re-endothelialization after denuding injuries of arteries.

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Section: Guo Et Al: Urinary Trypsin Inhibitor Repairs Lung Injurysupporting

confidence: 60%

Urinary Trypsin Inhibitor Attenuates Acute Lung Injury by Improving Endothelial Progenitor Cells Functions

Guo

Xie

et al. 2015

Cell Physiol Biochem

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“…Based on this fact, our findings coincide with the uncoupling mechanism of eNOS in atherosclerotic endothelial dysfunction reported by (Yang and Ming, 2006). Unexpectedly, atherogenic rats supplemented with pumpkin seeds showed a significant decrease in serum NO concentrations as it dropped by 41% from 24.52 to 14.58 µmol / L (p<0.001), a rational explanation could be that pumpkin seeds consist of palmitic acid and linoleic acid at a concentration of 38.6 and 92.0 mg / g dry weight respectively (Glew et al ., 2006 ), and these fatty acids are capable to inducing 9(1):131-137 http://dx.doi.org/10.4314/ajtcam.v9i1.18 136 dephosphorylation and/or inactivation of eNOS on Ser1177 leading to a decrease of the enzyme functional activity and thereafter reducing the level of NO (Guo et al ., 2008).…”

Section: Discussionmentioning

confidence: 99%

The Effect of Pumpkin (<i>Cucurbita pepo</i> L) Seeds and L-Arginine Supplementation on Serum Lipid Concentrations in Atherogenic Rats

Abuelgassim

AL-showayman²

2011

Afr. J. Trad. Compl. Alt. Med.

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The present study aimed to examine the effect of pumpkin (Cucurbita pepo L.) seeds supplementation on androgenic diet-induced atherosclerosis. Rat were divided into two main groups , normal control and atherogenic control rats , each group composed of three subgroups one of them supplemented with 2% arginine in drinking water and the other supplemented with pumpkin seeds in diet at a concentration equivalent to 2% arginine. Supplementation continued for 37 days. Atherogenic rats supplemented with pumpkin seeds showed a significant decrease (p<0.001) in their serum concentrations of total cholesterol and LDL -C as they dropped from 4.89 mmol / L to 2.55 mmol /L and from 3.33 mmol / L to 0.70 mmol / L respectively. Serum concentrations of HDL-C were also significantly elevated in the same group. Although, atherogenic rats supplemented with 2% arginine showed significant increase in serum concentration of HDL-C, no significant changes were observed in their serum concentrations of total cholesterol and LDL-C. Our results showed that treatment of atherogenic rats with pumpkin seeds significantly decreased serum concentrations of TC and LDL-C. Our findings suggest that pumpkin seeds supplementation has a protective effect against atherogenic rats and this protective effect was not attributed to the high arginine concentrations in pumpkin seeds.

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“…Palmitic and linoleic acids inhibit EPCs adhesion, migration, proliferation, and vasculogenesis capabilities of EPCs in a dose-dependent manner via inhibition of eNOS. However, only palmitic acid is shown to inhibit Akt phosphorylation [161]. Moreover, palmitic acid effect is shown to be mediated via its binding to peroxisome proliferator activated receptor (PPARc) and subsequent inhibition of STAT5A expression.…”

Section: Non-esterified Fatty Acids (Nefa)mentioning

confidence: 97%

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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Palmitic and Linoleic Acids Impair Endothelial Progenitor Cells by Inhibition of Akt/eNOS Pathway

Cited by 28 publications

References 28 publications

Urinary Trypsin Inhibitor Attenuates Acute Lung Injury by Improving Endothelial Progenitor Cells Functions

Urinary Trypsin Inhibitor Attenuates Acute Lung Injury by Improving Endothelial Progenitor Cells Functions

The Effect of Pumpkin (<i>Cucurbita pepo</i> L) Seeds and L-Arginine Supplementation on Serum Lipid Concentrations in Atherogenic Rats

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

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