Increased Intestinal Permeability: Implications for Thoracoabdominal Aneurysm Repair

Cohen, Jon R.; Sardari, Frederic; Paul, Jose; Parikh, Sandip; Sarfati, Isaac; Danna, Debra; Grella, Louis; Dorfman, B.; Wise, Leslie

doi:10.1007/bf02006998

Cited by 35 publications

(13 citation statements)

References 8 publications

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“…with mice placed on normal chow diet, a trend of increased NE mRNA expression was seen at 6 weeks, and a significant elevation in aortic NE mRNA expression level was found in all other groups (8,12, and 24 weeks) ( Figure 1A). Circulating NE activity ( Figure 1B) was observed to be elevated in mice fed an HFD from 6 weeks and significantly increased in all other groups tested (8,12, and 24 weeks). Following HFD, both plasma NE activity and aortic NE expression levels were further increased and peaked in mice fed an HFD for 12 weeks ( Figure 1A and 1B).…”

Section: Discussionmentioning

confidence: 94%

“…6 Apart from neutrophils, freshly isolated monocytes, macrophages, and endothelial cells also express NE, 7 while its expression in vascular smooth muscle cells (SMCs) remains controversial. 7,8 As a result of its capacity to efficiently degrade a broad range of ECM proteins and modulate the activity of many inflammatory cytokines and apolipoproteins, NE has been implicated in the pathogenesis of a variety of destructive and inflammatory diseases, 1 most notably chronic and acute lung diseases such as chronic obstructive pulmonary disease, cystic fibrosis, acute lung injury, and acute respiratory distress syndrome. 2 However, unlike the intensive investigation into the functional involvements of NE in lung diseases, the significance of NE in cardiovascular diseases has received less attention.…”

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confidence: 99%

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Genetic and Pharmacologic Inhibition of the Neutrophil Elastase Inhibits Experimental Atherosclerosis

Wen

Chen

et al. 2018

JAHA

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BackgroundTo investigate whether neutrophil elastase (NE) plays a causal role in atherosclerosis, and the molecular mechanisms involved.Methods and Results NE genetic–deficient mice (Apolipoprotein E−/−/NE −/− mice), bone marrow transplantation, and a specific NE inhibitor (GW311616A) were employed in this study to establish the causal role of NE in atherosclerosis. Aortic expression of NE mRNA and plasma NE activity was significantly increased in high‐fat diet (HFD)–fed wild‐type (WT) (Apolipoprotein E−/−) mice but, as expected, not in NE‐deficient mice. Selective NE knockout markedly reduced HFD‐induced atherosclerosis and significantly increased indicators of atherosclerotic plaque stability. While plasma lipid profiles were not affected by NE deficiency, decreased levels of circulating proinflammatory cytokines and inflammatory monocytes (Ly6Chi/CD11b+) were observed in NE‐deficient mice fed with an HFD for 12 weeks as compared with WT. Bone marrow reconstitution of WT mice with NE −/− bone marrow cells significantly reduced HFD‐induced atherosclerosis, while bone marrow reconstitution of NE −/− mice with WT bone marrow cells restored the pathological features of atherosclerotic plaques induced by HFD in NE‐deficient mice. In line with these findings, pharmacological inhibition of NE in WT mice through oral administration of NE inhibitor GW311616A also significantly reduced atherosclerosis. Mechanistically, we demonstrated that NE promotes foam cell formation by increasing ATP‐binding cassette transporter ABCA1 protein degradation and inhibiting macrophage cholesterol efflux.ConclusionsWe outlined a pathogenic role for NE in foam cell formation and atherosclerosis development. Consequently, inhibition of NE may represent a potential therapeutic approach to treating cardiovascular disease.

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Section: Discussionmentioning

confidence: 94%

mentioning

confidence: 99%

Genetic and Pharmacologic Inhibition of the Neutrophil Elastase Inhibits Experimental Atherosclerosis

Wen

Chen

et al. 2018

JAHA

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“…Many gut IR models have been described in the literature, but very few used supraceliac clamping. Several dog (13)(14)(15)(16), rabbit (17), or mouse (18,19) models have been reported. To the best of our knowledge, no rat model of supraceliac aortic clamping has been described until now.…”

Section: Discussionmentioning

confidence: 98%

d-Lactate is not a reliable marker of gut ischemia–reperfusion in a rat model of supraceliac aortic clamping*

Collange

Tamion

Chanel

et al. 2006

Critical Care Medicine

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“…However, intestinal ischemia and reperfusion injury may play another key role in influencing patient outcome in this type of operation [3]. It is well known that increasing intestinal permeability caused by longer visceral ischemia is implicated in the genesis of coagulopathic bleeding [4]. Furthermore, this condition may modulate elevated serum levels of proinflammatory cytokines that leads to remote organ injury (i.e.…”

Section: Introductionmentioning

confidence: 99%

Assessment of hepatosplanchnic pathophysiology during thoracoabdominal aortic aneurysm repair using visceral perfusion and shunt☆

Kunihara

Shiiya

Wakasa

et al. 2009

European Journal of Cardio-Thoracic Surgery

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Increased Intestinal Permeability: Implications for Thoracoabdominal Aneurysm Repair

Cited by 35 publications

References 8 publications

Genetic and Pharmacologic Inhibition of the Neutrophil Elastase Inhibits Experimental Atherosclerosis

Genetic and Pharmacologic Inhibition of the Neutrophil Elastase Inhibits Experimental Atherosclerosis

d-Lactate is not a reliable marker of gut ischemia–reperfusion in a rat model of supraceliac aortic clamping*

Assessment of hepatosplanchnic pathophysiology during thoracoabdominal aortic aneurysm repair using visceral perfusion and shunt☆

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