Role of the actin cytoskeleton during respiratory burst in chemoattractant‐stimulated neutrophils

Bengtsson, Torbjörn; Orselius, Kristina; Wetterö, Jonas

doi:10.1016/j.cellbi.2005.10.017

Cited by 39 publications

(31 citation statements)

References 49 publications

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“…Earlier studies have suggested that disruption of actin fibers at the plasma membrane and phagosomes enhances the fMLP-triggered oxidative burst in phagocytes (26). These observations are further supported in the present study of lung ECs by our demonstration that disruption or depolymerization of actin filaments by cytochalasin D or latrunculin A markedly increased basal and hyperoxia-mediated ROS production, whereas stabilization of actin filaments with phalloidin blocked the oxidative response.…”

Section: Discussionsupporting

confidence: 80%

“…Accumulating evidence supports a link between the actin cytoskeleton and actin-binding proteins in the activation of phagocytic and non-phagocytic NADPH oxidase (23)(24)(25)(26)(27). Stimulation of neutrophils with phorbol ester induces translocation of p47 phox to the cytoskeleton without altering the distribution of either p40 phox or p67 phox and increases the oxidase activity that co-sediments with a heavy plasma membrane fraction consisting of actin and fodrin (28,29).…”

Section: Discussionmentioning

confidence: 99%

“…These observations are further supported in the present study of lung ECs by our demonstration that disruption or depolymerization of actin filaments by cytochalasin D or latrunculin A markedly increased basal and hyperoxia-mediated ROS production, whereas stabilization of actin filaments with phalloidin blocked the oxidative response. The molecular mechanisms of cytochalasin D-and latrunculin A-mediated modulation of ROS production are unclear; however, in neutrophils cytochalasin B is known to potentiate the fMLP-induced accumulation of diacylglycerol, which could activate NADPH oxidase via protein kinase C (26,39). In the present study, we did not evaluate diacyglycerol levels after pretreatment of HPAECs with cytochalasin D, but we observed that cytochalasin D activated Rac1, a key regulator and activator of NADPH oxidase in non-phagocytic cells (data not shown).…”

Section: Discussionmentioning

confidence: 99%

“…Actin cytoskeleton and other cytoskeletal proteins may play a role in phagocytic and non-phagocytic assembly and the activation of NADPH oxidase (23)(24)(25)(26)(27). In phorbol ester-stimulated neutrophils, oxidase activity has been shown to co-sediment with the heavy plasma membrane fraction that contains actin and fodrin; furthermore, the labile oxidase can be stabilized by chemical cross-linking and is not extractable by Triton X-100, suggesting that an interaction occurs between the NADPH oxidase complex and actin filaments (28,29).…”

mentioning

confidence: 99%

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Regulation of Hyperoxia-induced NADPH Oxidase Activation in Human Lung Endothelial Cells by the Actin Cytoskeleton and Cortactin

Usatyuk

Romer

et al. 2007

Journal of Biological Chemistry

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Although the actin cytoskeleton has been implicated in the control of NADPH oxidase in phagocytosis, very little is known about the cytoskeletal regulation of endothelial NADPH oxidase assembly and activation. Here, we report a role for cortactin and the tyrosine phosphorylation of cortactin in hyperoxiainduced NADPH oxidase activation and ROS production in human pulmonary artery ECs (HPAECs). Exposure of HPAECs to hyperoxia for 3 h induced NADPH oxidase activation, as demonstrated by enhanced superoxide production. Hyperoxia also caused a thickening of the subcortical dense peripheral F-actin band and increased the localization of cortactin in the cortical regions and lamellipodia at cell-cell borders that protruded under neighboring cells. Pretreatment of HPAECs with the actin-stabilizing agent phallacidin attenuated hyperoxia-induced cortical actin thickening and ROS production, whereas cytochalasin D and latrunculin A enhanced basal and hyperoxia-induced ROS formation. In HPAECs, a 3-h hyperoxic exposure enhanced the tyrosine phosphorylation of cortactin and interaction between cortactin and p47 phox , a subcomponent of the EC NADPH oxidase, when compared with normoxic cells. Furthermore, transfection of HPAECs with cortactin small interfering RNA or myristoylated cortactin Src homology domain 3 blocking peptide attenuated ROS production and the hyperoxia-induced translocation of p47 phox to the cell periphery. Similarly, down-regulation of Src with Src small interfering RNA attenuated the hyperoxia-mediated phosphorylation of cortactin tyrosines and blocked the association of cortactin with actin and p47phox . In addition, the hyperoxia-induced generation of ROS was significantly lower in ECs expressing a tyrosine-deficient mutant of cortactin than in vector control or wild-type cells. These data demonstrate a novel function for cortactin and actin in hyperoxiainduced activation of NADPH oxidase and ROS generation in human lung endothelial cells. production that is dependent on NADPH oxidase activation and independent of the mitochondrial electron transport or xanthine/xanthine oxidase systems (10). The mechanisms of NADPH oxidase activation are complex. In phagocytes, activation of NADPH oxidase requires serine phosphorylation of the cytosolic p47 phox , p67 phox , and p40 phox components, assembly of the phosphorylated subunits with Rac2, and translocation to the phagosomes for association with cytochrome b 558. Here, one-electron reduction of molecular O 2 to O 2 . occurs with NADPH as the electron donor (7). In leukocytes, formyl-Met-Leu-Phe-OH or phorbol ester stimulates phosphorylation of p47 phox at multiple serine residues through reactions involving several protein kinases such as protein kinase C, protein kinase A, and mitogen-activated protein kinases (14 -17). In HPAECs, tumor necrosis factor-␣-medi-*This work was supported by National Institutes of Health Grants RO1 HL 69909 (to V. N.), PO1 HL 58064 (to V. N. and J. G. N. G.) and DE13079-01 and AI061042 (to L. H. R.). The costs of publication...

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Section: Discussionsupporting

confidence: 80%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

See 2 more Smart Citations

Regulation of Hyperoxia-induced NADPH Oxidase Activation in Human Lung Endothelial Cells by the Actin Cytoskeleton and Cortactin

Usatyuk

Romer

et al. 2007

Journal of Biological Chemistry

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“…For example, actin depolymerization was shown to promote p47 phox -dependent, Nox2-mediated superoxide production in neutrophils (65) and endothelial cells (66). The underlying mechanism is likely 2-fold as follows: actin depolymerization enhances receptorinduced signaling pathways leading to the assembly of Nox2 from cytosolic and membrane-bound components, and it may also remove physical constraints from the association of these.…”

Section: Discussionmentioning

confidence: 99%

Myocardin-related Transcription Factor Regulates Nox4 Protein Expression

Rozycki

Bialik

Speight

et al. 2016

Journal of Biological Chemistry

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Background: Generation of myofibroblasts, the culprit of fibrosis, requires cytoskeleton remodeling and Nox4 (NADPH oxidase) expression. The link between these events is unknown. Results: Down-regulation/inhibition of the cytoskeleton-controlled transcriptional coactivators, myocardin-related transcription factor (MRTF), and TAZ/YAP abrogates Nox4 expression. Conclusion: MRTF and TAZ/YAP are essential for Nox4 expression. Significance: We show new mechanisms whereby the cytoskeleton regulates cellular redox state and fibrogenesis.

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Chemotherapy-associated hepatotoxicity and surgery for colorectal liver metastases

Zorzi

Laurent

Pawlik

et al. 2007

British Journal of Surgery

480

276

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Background: Preoperative systemic chemotherapy is increasingly used in patients who undergo hepatic resection for colorectal liver metastases (CLM). Although chemotherapy-related hepatic injury has been reported, the incidence and the effect of such injury on patient outcome remain ill defined.Methods: A systematic review of relevant studies published before May 2006 was performed. Studies that reported on liver injury associated with preoperative chemotherapy for CLM were identified and data on chemotherapy-specific liver injury and patient outcome following hepatic resection were synthesized and tabulated.Results: Hepatic steatosis, a mild manifestation of non-alcoholic fatty liver disease (NAFLD), may occur after treatment with 5-fluorouracil and is associated with increased postoperative morbidity. Nonalcoholic steatohepatitis, a serious complication of NAFLD that includes inflammation and hepatocyte damage, can occur after treatment with irinotecan, especially in obese patients. Irinotecan-associated steatohepatitis can affect hepatic reserve and increase morbidity and mortality after hepatectomy. Hepatic sinusoidal obstruction syndrome can occur in patients treated with oxaliplatin, but does not appear to be associated with an increased risk of perioperative death. Conclusion:Preoperative chemotherapy for CLM induces regimen-specific hepatic changes that can affect patient outcome. Both response rate and toxicity should be considered when selecting preoperative chemotherapy in patients with CLM.

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Role of the actin cytoskeleton during respiratory burst in chemoattractant‐stimulated neutrophils

Cited by 39 publications

References 49 publications

Regulation of Hyperoxia-induced NADPH Oxidase Activation in Human Lung Endothelial Cells by the Actin Cytoskeleton and Cortactin

Regulation of Hyperoxia-induced NADPH Oxidase Activation in Human Lung Endothelial Cells by the Actin Cytoskeleton and Cortactin

Myocardin-related Transcription Factor Regulates Nox4 Protein Expression

Chemotherapy-associated hepatotoxicity and surgery for colorectal liver metastases

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