Reoxygenation of Hypoxic Human Umbilical Vein Endothelial Cells Activates the Classic Complement Pathway

Collard, Charles D.; Väkevä, Antti; Büküşoğlu, Cüneyt; Zünd, Gregor; Sperati, C. John; Colgan, Sean P.; Stahl, Gregory L.

doi:10.1161/01.cir.96.1.326

Cited by 85 publications

(88 citation statements)

References 36 publications

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“…Furthermore CD55 expression on endothelial cells was upregulated in the presence of both VEGF and tumour-conditioned media. Similar increases in expression of CD55 have also been reported with TNF-α, IL-1β, IL-4 and hypoxia (Collard et al, 1997;Hindmarsh and Marks 1998). Our data suggests that the tumour environment causes upregulation of CD55 on tumour-associated endothelium.…”

Section: Discussionsupporting

confidence: 87%

CD55 is over-expressed in the tumour environment

Spendlove

Morgan

et al. 2001

Br J Cancer

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Summary CD55 is a protein that protects cells from complement-mediated attack. 791Tgp72 is an antigen which has been used succesfully as a target for both tumour imaging and cancer vaccines. 791Tgp72 has recently been identified as CD55. Quantitative expression of CD55 in the tumour environment was therefore studied. Tumour cells showed a 4-100-fold increase in CD55 cell surface expression when compared to normal cells. Immunohistochemical staining of colorectal tumours also revealed high expression of CD55 in the stroma. To examine the source of this stromal CD55 the ability of both epithelial cells and endothelial cells to produce extracellular CD55 was measured. Tumour cell lines deposit CD55 into their extracellular matrix (ECM) in direct proportion to their cell surface expression. In contrast the ECM from HUVEC cells contained large amounts of CD55 despite expressing low levels of CD55 on their cell surface. Furthermore expression of CD55 on HUVEC cells was increased by exposure to VEGF. Although it remains unclear why CD55 is upregulated in the tumour environment its high level of expression on tumour cells and associated endothelium may explain why it is a good target for both imaging and immunotherapy. © 2001 Cancer Research Campaign http://www.bjcancer.com Keywords: CD55 (DAF), tumour expression; endothelium; stroma; vascular endothelial growth factor (VEGF) 80Received 27 September 1999 Revised 3 February 2000 Accepted 15 March 2000 Correspondence to : LG Durrant British Journal of Cancer (2001) 84(1), 80-86 © 2001 Cancer Research Campaign doi: 10.1054/ bjoc.2000.1570, available online at http://www.idealibrary.com on http://www.bjcancer.com and tumour-conditioned medium or VEGF (10-300 µg ml -1 : Zeneca, Alderley Park, UK) respectively for 48 h prior to harvesting the HUVECs. Tumour-conditioned media was derived from the MDA 231 breast cancer cell line. These were grown to confluence and the media replaced with serum free M199:Hams F12 medium. Following 24 h incubation the resultant conditioned media was filtered for use with the HUVEC. Fresh media was used to culture the control HUVECs. Freshly resected tumours were finely minced and dissociated in collagenase (0.05%; Boehringer Mannheim) and DNase (0.1%; Boehringer Mannheim) for 1 h at 37˚C. Monoclonal antibodiesMonoclonal antibodies 791T/36 (IgG2b anti-791Tgp72;Embleton et al, 1981), BRIC 216 (IgG1 anti-SCR 3 of CD55; Tate et al, 1989), BRIC 220 (IgG1 anti-SCR 1 of CD55; Tate et al, 1989), BRIC 110 (IgG1 anti-SCR 2 of CD55; Spring et al, 1987;Coyne et al, 1992) have been reported previously. BRIC 229 and E4.3 (Sparrow and Mckenzie, 1983) recognize CD59 and CD46 respectively. The BRIC antibodies were purchased from the Blood Group Reference laboratory (Bristol, UK). Normal mouse IgG (Sigma, Dorset, UK) and 708 monoclonal antibody (IgG2b) was used as negative control antibodies. Indirect immunofluorescenceCell lines were incubated with monoclonal antibody for 1 h at 4˚C. Cells were washed twice in fresh media containing 1% FCS and then incubat...

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Section: Discussionsupporting

confidence: 87%

CD55 is over-expressed in the tumour environment

Spendlove

Morgan

et al. 2001

Br J Cancer

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“…Although the above evidence suggests a pivotal role of the classical pathway of complement for reperfusion injury, studies of the lectin pathways have suggested it is also involved (32,33). In vitro studies of endothelium found that both classical and lectin pathways may be activated under hypoxia/reperfusion condition.…”

Section: Activation Of the Lectin Pathway By Natural Igm In A Modelmentioning

confidence: 99%

Activation of the Lectin Pathway by Natural IgM in a Model of Ischemia/Reperfusion Injury

Zhang

Takahashi

Alicot

et al. 2006

The Journal of Immunology

129

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Reperfusion of ischemic tissues elicits an acute inflammatory response involving serum complement, which is activated by circulating natural IgM specific to self-Ags exposed by ischemia. Recent reports demonstrating a role for the lectin pathway raise a question regarding the initial events in complement activation. To dissect the individual roles of natural IgM and lectin in activation of complement, mice bearing genetic deficiency in early complement, IgM, or mannan-binding lectin were characterized in a mesenteric model of ischemia reperfusion injury. The results reveal that IgM binds initially to ischemic Ag providing a binding site for mannan-binding lectin which subsequently leads to activation of complement and injury.

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“…There were no statistical differences between groups in any of the measures. 6). This is a normal finding in mice and is unlikely to be of pathogenic importance as glomeruli were histologically normal (see Fig.…”

Section: Effects Of Ig-and T-lymphocyte Deficiencies On Renal Functiomentioning

confidence: 99%

Injury in renal ischemia-reperfusion is independent from immunoglobulins and T lymphocytes

Park

Haas

Cunningham

et al. 2002

American Journal of Physiology-Renal Physiology

120

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Ischemia-reperfusion injury (IRI) is a complex and incompletely understood process involving a cascade of events that culminates in apoptotic and/or necrotic cell death. Natural IgM antibodies and complement have been implicated in the pathogenesis of IRI in a variety of organ systems as have T lymphocytes in renal IRI. To investigate the role of Ig and T lymphocytes in renal IRI, recombination-activating gene (RAG)-1-deficient mice were studied. RAG-1(−/−) mice were not protected from acute renal failure induced by 27.5 min of bilateral renal ischemia and subsequent reperfusion [serum urea nitrogen levels 30 h after reperfusion, 155.2 ± 5.6 and 152.8 ± 11.4 mg/dl in RAG-1(−/−) and wild-type mice, respectively; n = 13 each]. Histological examination showed acute tubular necrosis and neutrophilic infiltration with no significant differences between groups. In contrast with other organ systems, Igs were not found in kidneys at time points ranging from 1 min to 30 h after ischemia. Thus Igs and mature T lymphocytes do not appear to play a significant role in the pathogenesis of IRI in the kidney.

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Reoxygenation of Hypoxic Human Umbilical Vein Endothelial Cells Activates the Classic Complement Pathway

Cited by 85 publications

References 36 publications

CD55 is over-expressed in the tumour environment

CD55 is over-expressed in the tumour environment

Activation of the Lectin Pathway by Natural IgM in a Model of Ischemia/Reperfusion Injury

Injury in renal ischemia-reperfusion is independent from immunoglobulins and T lymphocytes

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