Role of superoxide in hemorrhagic shock-induced P-selectin expression

Fm, Akgür; Mf, Brown; Gb, Zibari; Jc, McDonald; Cj, Epstein; Cr, Ross; Granger, D. N.

doi:10.1152/ajpheart.2000.279.2.h791

Cited by 72 publications

(55 citation statements)

References 30 publications

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“…Body temperature was monitored and maintained at 37°C. After 3 h, mice were resuscitated with the shed blood plus a volume of lactated Ringer solution corresponding to 50% of the shed blood volume, which was infused with a syringe pump over 30 min (3,4). Adequacy of resuscitation was determined by the restoration of blood pressure.…”

Section: Methodsmentioning

confidence: 99%

Lipopolysaccharide-binding protein modulates hepatic damage and the inflammatory response after hemorrhagic shock and resuscitation

Lehnert¹,

Uehara²,

Bradford³

et al. 2006

American Journal of Physiology-Gastrointestinal and Liver Physi

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Lipopolysaccharide-binding protein modulates hepatic damage and the inflammatory response after hemorrhagic shock and resuscitation. Am J Physiol Gastrointest Liver Physiol 291: G456 -G463, 2006. First published May 18, 2006 doi:10.1152/ajpgi.00480.2005.-Hemorrhagic shock and resuscitation cause endotoxemia and hepatocellular damage. Because lipopolysaccharide-binding protein (LBP) enhances cellular responses to endotoxin, our aim was to determine whether LBP contributes to hemorrhage/resuscitation-induced injury by comparing LBP knockout and wild-type mice. Under pentobarbital anaesthesia, wild-type and LBP-deficient mice were hemorrhaged to 30 mmHg for 3 h and then resuscitated with shed blood plus half the volume of lactated Ringer solution. Serum alanine aminotransferase (ALT) necrosis, neutrophil infiltration, and 4-hydroxynonenal by histology/ cytochemistry and stress kinase activation by immunoblot analysis were then determined. ALT in wild-type mice was 2,461 Ϯ 383 and 1,418 Ϯ 194 IU/l (means Ϯ SE), respectively, at 2 and 6 h after resuscitation versus sham ALT of 102 Ϯ 6 IU/l. In LBP-deficient mice, ALT was blunted at both time points to 1,108 Ϯ 340 and 619 Ϯ 171 IU/l (P Ͻ 0.05). Liver necrosis after 6 h was also attenuated from 3.5 Ϯ 0.8% in wild-type mice to 1.3 Ϯ 0.5% in LBP-deficient mice (P Ͻ 0.05). After hemorrhage/resuscitation, neutrophil infiltration increased 71% more in wild-type than LBP knockout mice. Similarly, hepatic 4-hydroxynonenal staining, indicative of lipid peroxidation, decreased from 33.8 Ϯ 4.5% in wild-type mice to 11.6 Ϯ 1.9% in knockout mice (P Ͻ 0.05).

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Section: Methodsmentioning

confidence: 99%

Lipopolysaccharide-binding protein modulates hepatic damage and the inflammatory response after hemorrhagic shock and resuscitation

Lehnert¹,

Uehara²,

Bradford³

et al. 2006

American Journal of Physiology-Gastrointestinal and Liver Physi

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“…37,38 Similarly, mice that are genetically deficient in critical protein subunits (eg, p47 phox ) of NAD(P)H oxidase or transgenic mice that overexpress SOD exhibit attenuated leukocyte adhesion responses in models of oxidative stress. 39 Studies demonstrating that treatment of otherwise normal animals with inhibitors of NOS 40 and endothelial NOS-knockout mice 41 exhibit increased leukocyte adhesion support the view that a critical determinant of whether the vasculature assumes a proinflammatory or an antiinflammatory (and therefore, a prothrombogenic or an antithrombogenic) phenotype is the balance between ROS and NO.…”

Section: Oxidative Stressmentioning

confidence: 99%

Modulation of the Inflammatory Response in Cardiovascular Disease

2004

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Abstract-There is a growing body of evidence that inflammation might play an important role in the initiation and progression of cardiovascular diseases (CVDs). The designation of CVD as a chronic inflammatory process is further supported by evidence that the risk factors for CVD cause endothelial cells throughout the vascular tree to assume an inflammatory phenotype. These activated endothelial cells characteristically exhibit oxidative stress and increased adhesiveness for circulating leukocytes. Although initial efforts to define the mechanisms underlying the inflammatory phenotype in diseased endothelial cells have focused on the linkage between oxidative stress and adhesion molecule activation/expression, recent work has implicated a variety of additional factors that can modulate the magnitude and/or nature of the inflammatory responses in CVD. Platelets, angiotensin II, and the CD40/CD40 ligand signaling system are gaining recognition as contributors to the pathogenesis of CVD. These factors appear to converge with known pathways that link oxidative stress with adhesion molecule expression and help to explain the apparent integration of coagulation with inflammation in CVD. These factors also hold the promise of offering multiple sites for therapeutic intervention in CVD. Key Words: oxidative stress Ⅲ integrins Ⅲ angiotensin II Ⅲ adhesion molecules I nflammation is gaining widespread attention for its role in the initiation and progression of cardiovascular disease (CVD). Epidemiological studies have revealed strong associations between biochemical markers of systemic inflammation and both the presence of and future risk for symptomatic CVD. Animal experimentation as well as clinical studies has provided convincing evidence that the known risk factors for CVD (hypertension, diabetes, hypercholesterolemia, and smoking) can elicit both an inflammatory and a prothrombogenic phenotype in the vascular system. The phenotypic changes are more pronounced in endothelial cells and can include oxidative stress, increased expression of endothelial cell adhesion molecules (CAMs), activation of cell signaling pathways (eg, the CD40/CD40 ligand [CD40L] dyad), and the consequent adhesion and activation of leukocytes and platelets. In the microcirculation, the inflammatory manifestations of CVD are more readily visible in postcapillary venules. There is growing evidence, however, that the endothelium-dependent arteriolar dysfunction often associated with CVD is also linked to the systemic inflammatory response. [1][2][3][4] Because the expression of adhesion glycoproteins by activated endothelial cells is a rate-determining step in the recruitment of inflammatory cells, much attention has been devoted to the role of endothelial CAMs in CVD. This attention has produced considerable evidence for the: (1) altered endothelial CAM expression in animal models of CVD 2,5 ; (2) use of circulating levels of soluble endothelial CAMs (eg, soluble intercellular adhesion molecule-1 [sICAM-1]) as a marker for the severity of inflammati...

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“…[5][6][7] It is also becoming apparent that ROS may regulate the neutrophil lifespan, modify the extracellular matrix through which the neutrophils migrate, and modulate the function of other cells participating in the inflammatory response. [8][9][10][11][12] Given the potential for self-damage, a key feature of the inflammatory response is to confine ROS generation in time and space to areas where it is required. One way in which this is thought to occur is through a form of signal integration in which prior exposure to local proinflammatory factors is necessary for maximal activation by subsequent oxidase-triggering signals.…”

mentioning

confidence: 99%

Sequential activation of class IB and class IA PI3K is important for the primed respiratory burst of human but not murine neutrophils

Condliffe

Davidson

Anderson

et al. 2005

Blood

269

275

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It is well established that preexposure of human neutrophils to proinflammatory cytokines markedly augments the production of reactive oxygen species (ROS) to subsequent stimuli. This priming event is thought to be critical for localizing ROS to the vicinity of the inflammation, maximizing their role in the resolution of the inflammation, and minimizing the damage to surrounding tissue. We have used a new generation of isoform-selective phosphoinositide 3-kinase (PI3K) inhibitors to show that ROS production under these circumstances is regulated by temporal control of class I PI3K activity. Stimulation of tumor necrosis factor-␣ (TNF-␣)-primed human neutrophils with N-formylmethionyl-leucyl-phenylalanine (fMLP) results in biphasic activation of PI3K; the first phase is largely dependent on PI3K␥, and the second phase is largely dependent on PI3K␦. The second phase of PI3K activation requires the first phase; it is this second phase that is augmented by TNF-␣ priming and that regulates parallel activation of ROS production. Surprisingly, although TNF-␣-primed mouse bone marrow-derived neutrophils exhibit superficially similar patterns of PI3K activation and ROS production in response to fMLP, these responses are substantially lower and largely dependent on PI3K␥ alone. These results start to define which PI3K isoforms are responsible for modulating neutrophil responsiveness to infection and inflammation. IntroductionNeutrophils are critical components of the immune system and have a vital role in combating bacterial and fungal infections. 1 A key weapon in the neutrophil armory is the so-called "respiratory burst," the generation of reactive oxygen species (ROS) by a multicomponent oxidase complex. 2,3 Patients with chronic granulomatous disease (CGD) caused by defective expression of active oxidase components experience recurrent, life-threatening infections. 4 The role of ROS in fighting infections is complex. ROS are involved in the killing process directly through the damaging actions of oxygen radicals and their halogenated derivatives and indirectly through the activation of phagosomal proteases. [5][6][7] It is also becoming apparent that ROS may regulate the neutrophil lifespan, modify the extracellular matrix through which the neutrophils migrate, and modulate the function of other cells participating in the inflammatory response. [8][9][10][11][12] Given the potential for self-damage, a key feature of the inflammatory response is to confine ROS generation in time and space to areas where it is required. One way in which this is thought to occur is through a form of signal integration in which prior exposure to local proinflammatory factors is necessary for maximal activation by subsequent oxidase-triggering signals. [13][14][15][16][17] One of best studied examples of this "priming" phenomenon is the ability of tumor necrosis factor-␣ (TNF-␣), a cytokine released primarily by macrophages, to dramatically augment the oxidase response to bacterially derived peptides (eg, N-formyl-methionyl-leucylphenylal...

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Role of superoxide in hemorrhagic shock-induced P-selectin expression

Cited by 72 publications

References 30 publications

Lipopolysaccharide-binding protein modulates hepatic damage and the inflammatory response after hemorrhagic shock and resuscitation

Lipopolysaccharide-binding protein modulates hepatic damage and the inflammatory response after hemorrhagic shock and resuscitation

Modulation of the Inflammatory Response in Cardiovascular Disease

Sequential activation of class IB and class IA PI3K is important for the primed respiratory burst of human but not murine neutrophils

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