Influence of Elevated Levels of C‐Reactive Protein on Circulating Endothelial Progenitor Cell Function

Fasing, Kevin; Nissan, Benjamin J.; Greiner, Jared J.; Stauffer, Brian L.; DeSouza, Christopher A.

doi:10.1111/cts.12137

Cited by 6 publications

(3 citation statements)

References 30 publications

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“…CRP is a protein produced by the liver as a response to acute inflammation and regulated in response to interleukin‐6 (IL‐6) or interleukin‐1β (IL‐1β) in hepatocytes [25]. Recent reports have revealed that an increased CRP level as part of the inflammatory response leads to endothelial dysfunction by reducing endothelial nitric oxide synthase and downregulating angiogenesis and has an inverse correlation with the functions of endothelial progenitor cells that participate in vascularization and secretion of angiogenic growth factors [26, 27]. Jun JH reported that CRP might regulate abnormal vessel formation in liver cirrhosis [28].…”

Section: Discussionmentioning

confidence: 99%

Massage of the Hepatoduodenal Ligament Recovers Portal Vein Flow Immediately After the Pringle Maneuver in Hepatectomy

et al. 2020

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Background The Pringle maneuver is often used in liver surgery to minimize bleeding during liver transection. Many authors have demonstrated that intermittent use of the Pringle maneuver is safe and effective when performed appropriately. However, some studies have reported that the Pringle maneuver is a significant risk factor for portal vein thrombosis. In this study, we evaluated the effectiveness of portal vein flow after the Pringle maneuver and the impact that massaging the hepatoduodenal ligament after the Pringle maneuver has on portal vein flow. Materials and Methods Patients treated with the Pringle maneuver for hepatectomies performed to treat hepatic disease at our hospital between August 2014 and March 2019 were included in the study (N = 101). We divided these patients into two groups, a massage group and nonmassage group. We measured portal vein blood flow with ultrasonography before and after clamping of the hepatoduodenal ligament. We also evaluated laboratory data after the hepatectomy. Results Portal vein flow was significantly lower after the Pringle maneuver than before clamping of the hepatoduodenal ligament. The portal vein flow after the Pringle maneuver was improved following massage of the hepatoduodenal ligament. After hepatectomy, serum prothrombin time was significantly higher and serum C-reactive protein was significantly lower in the massage group than in the nonmassage group. Conclusion Massaging the hepatoduodenal ligament after the Pringle maneuver is recommended in order to quickly recover portal vein flow during hepatectomy and to improve coagulability.

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Section: Discussionmentioning

confidence: 99%

Massage of the Hepatoduodenal Ligament Recovers Portal Vein Flow Immediately After the Pringle Maneuver in Hepatectomy

et al. 2020

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“…Recently, it has been reported that increased CRP levels as part of the inflammatory response lead to endothelial dysfunction by reducing endothelial nitric oxide synthase and down-regulating angiogenesis as well as by an inverse correlation with functions of endothelial progenitor cells that participate in vascularization and secrete angiogenic growth factors [ 17 , 18 ]. Also, Enjoji et al reported that CRP and VEGF showed a positive correlation in acute cholangitis patients, but in chronic PBC patients, the correlation was not significant [ 19 ].…”

Section: Discussionmentioning

confidence: 99%

Decreased C-reactive protein induces abnormal vascular structure in a rat model of liver dysfunction induced by bile duct ligation

et al. 2016

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Background/AimsChronic liver disease leads to liver fibrosis, and although the liver does have a certain regenerative capacity, this disease is associated with dysfunction of the liver vessels. C-reactive protein (CRP) is produced in the liver and circulated from there for metabolism. CRP was recently shown to inhibit angiogenesis by inducing endothelial cell dysfunction. The objective of this study was to determine the effect of CRP levels on angiogenesis in a rat model of liver dysfunction induced by bile duct ligation (BDL).MethodsThe diameter of the hepatic vein was analyzed in rat liver tissues using hematoxylin and eosin (H&E) staining. The expression levels of angiogenic factors, albumin, and CRP were analyzed by real-time PCR and Western blotting. A tube formation assay was performed to confirm the effect of CRP on angiogenesis in human umbilical vein endothelial cells (HUVECs) treated with lithocholic acid (LCA) and siRNA-CRP.ResultsThe diameter of the hepatic portal vein increased significantly with the progression of cirrhosis. The expression levels of angiogenic factors were increased in the cirrhotic liver. In contrast, the expression levels of albumin and CRP were significantly lower in the liver tissue obtained from the BDL rat model than in the normal liver. The CRP level was correlated with the expression of albumin in hepatocytes treated with LCA and siRNA-CRP. Tube formation was significantly decreased in HUVECs when they were treated with LCA or a combination of LCA and siRNA-CRP.ConclusionCRP seems to be involved in the abnormal formation of vessels in hepatic disease, and so it could be a useful diagnostic marker for hepatic disease.

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“…Furthermore, the culprit was shown to be the increase in mitochondrial ROS generation that was aggravated by CRP effect in modulating the expression of the anti-oxidant enzymes glutathione peroxidase and Mn superoxide dismutase (MnSOD) [76]. However, recent work by Fasing et al showed no association between CRP plasma level and circulating EPCs [77].…”

Section: C-reactive Protein (Crp)mentioning

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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Influence of Elevated Levels of C‐Reactive Protein on Circulating Endothelial Progenitor Cell Function

Cited by 6 publications

References 30 publications

Massage of the Hepatoduodenal Ligament Recovers Portal Vein Flow Immediately After the Pringle Maneuver in Hepatectomy

Massage of the Hepatoduodenal Ligament Recovers Portal Vein Flow Immediately After the Pringle Maneuver in Hepatectomy

Decreased C-reactive protein induces abnormal vascular structure in a rat model of liver dysfunction induced by bile duct ligation

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

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