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1.

001-es BibID:BIBFORM048561
Első szerző:Antonella Nadalutti, Cristina
Cím:Thioredoxin Is Involved in Endothelial Cell Extracellular Transglutaminase 2 Activation Mediated by Celiac Disease Patient IgA / Cristina Antonella Nadalutti, Ilma Rita Korponay-Szabo, Katri Kaukinen, Zhuo Wang, Martin Griffin, Markku Mäki, Katri Lindfors
Dátum:2013
ISSN:1932-6203
Megjegyzések:PURPOSE:To investigate the role of thioredoxin (TRX), a novel regulator of extracellular transglutaminase 2 (TG2), in celiac patients IgA (CD IgA) mediated TG2 enzymatic activation.METHODS:TG2 enzymatic activity was evaluated in endothelial cells (HUVECs) under different experimental conditions by ELISA and Western blotting. Extracellular TG2 expression was studied by ELISA and immunofluorescence. TRX was analysed by Western blotting and ELISA. Serum immunoglobulins class A from healthy subjects (H IgA) were used as controls. Extracellular TG2 enzymatic activity was inhibited by R281. PX12, a TRX inhibitor, was also employed in the present study.RESULTS:We have found that in HUVECs CD IgA is able to induce the activation of extracellular TG2 in a dose-dependent manner. Particularly, we noted that the extracellular modulation of TG2 activity mediated by CD IgA occurred only under reducing conditions, also needed to maintain antibody binding. Furthermore, CD IgA-treated HUVECs were characterized by a slightly augmented TG2 surface expression which was independent from extracellular TG2 activation. We also observed that HUVECs cultured in the presence of CD IgA evinced decreased TRX surface expression, coupled with increased secretion of the protein into the culture medium. Intriguingly, inhibition of TRX after CD IgA treatment was able to overcome most of the CD IgA-mediated effects including the TG2 extracellular transamidase activity.CONCLUSIONS:Altogether our findings suggest that in endothelial cells CD IgA mediate the constitutive activation of extracellular TG2 by a mechanism involving the redox sensor protein TRX.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Thioredoxin
IgA
TG2
Megjelenés:Plos One. - 8 : 10 (2013), p. e77277. -
További szerzők:Korponay-Szabó Ilma (1959-) (gyermekgyógyász) Kaukinen, Katri Wang, Zhuo Griffin, Martin Mäki, Markku Lindfors, Katri
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2.

001-es BibID:BIBFORM011928
Első szerző:Caja, Sergio
Cím:Inhibition of transglutaminase 2 enzymatic activity ameliorates the anti-angiogenic effects of coeliac disease autoantibodies / Caja S., Myrsky E., Korponay-Szabo I., Nadalutti C., Sulic A. M., Lavric M., Sblattero D., Marzari R., Collighan R., Mongeot A., Griffin M., Maki M., Kaukinen K., Lindfors K.
Dátum:2010
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Scandinavian Journal of Gastroenterology. - 45 : 4 (2010), p. 421-427. -
További szerzők:Myrsky, Essi Korponay-Szabó Ilma (1959-) (gyermekgyógyász) Nadalutti, Cristina Sulic, Ana-Marija Lavric, Miha Sblattero, Daniele Marzari, Roberto Collighan, Russell Mongeot, Alexandre Griffin, Martin Mäki, Markku Kaukinen, Katri Lindfors, Katri
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3.

001-es BibID:BIBFORM048568
035-os BibID:Article ID: e65887
Első szerző:Kalliokoski, Suvi
Cím:Celiac Disease-Specific TG2-Targeted Autoantibodies Inhibit Angiogenesis Ex Vivo and In Vivo in Mice by Interfering with Endothelial Cell Dynamics / Suvi Kalliokoski, Ana-Marija Sulic, Ilma R. Korponay-Szabo, Zsuzsa Szondy, Rafael Frias, Mileidys Alea Perez, Stefania Martucciello, Anne Roivainen, Lauri J. Pelliniemi, Carla Esposito, Martin Griffin, Daniele Sblattero, Markku Mäki, Katri Kaukinen, Katri Lindfors, Sergio Caja
Dátum:2013
ISSN:1932-6203
Megjegyzések:A characteristic feature of celiac disease is the presence of circulating autoantibodies targeted against transglutaminase 2 (TG2), reputed to have a function in angiogenesis. In this study we investigated whether TG2-specific autoantibodies derived from celiac patients inhibit angiogenesis in both ex vivo and in vivo models and sought to clarify the mechanism behind this phenomenon. We used the ex vivo murine aorta-ring and the in vivo mouse matrigel-plug assays to address aforementioned issues. We found angiogenesis to be impaired as a result of celiac disease antibody supplementation in both systems. Our results also showed the dynamics of endothelial cells was affected in the presence of celiac antibodies. In the in vivo angiogenesis assays, the vessels formed were able to transport blood despite impairment of functionality after treatment with celiac autoantibodies, as revealed by positron emission tomography. We conclude that celiac autoantibodies inhibit angiogenesis ex vivo and in vivo and impair vascular functionality. Our data suggest that the anti-angiogenic mechanism of the celiac disease-specific autoantibodies involves extracellular TG2 and inhibited endothelial cell mobility.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Plos One [electronic resource]. - 8 : 6 (2013), [8] p. -
További szerzők:Sulic, Ana-Marija Korponay-Szabó Ilma (1959-) (gyermekgyógyász) Szondy Zsuzsanna (1959-) (molekuláris sejtbiológus, biokémikus) Frías, Rafael Perez, Mileidys Alea Martucciello, Stefania Roivainen, Anne Pelliniemi, Lauri J. Esposito, Carla Griffin, Martin Sblattero, Daniele Mäki, Markku Kaukinen, Katri Lindfors, Katri Caja, Sergio
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4.

001-es BibID:BIBFORM011940
Első szerző:Myrsky, Essi
Cím:Celiac disease IgA modulates vascular permeability in vitro through the activity of transglutaminase 2 and RhoA / Myrsky E., Caja S., Simon-Vecsei Z., Korponay-Szabo I., Nadalutti C., Collighan R., Mongeot A., Griffin M., Maki M., Kaukinen K., Lindfors K.
Dátum:2009
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Cellular and Molecular Life Sciences. - 66 : 20 (2009), p. 3375-3385. -
További szerzők:Caja, Sergio Simon-Vecsei Zsófia (1980-) (biológus) Korponay-Szabó Ilma (1959-) (gyermekgyógyász) Nadalutti, Cristina Collighan, Russell Mongeot, Alexandre Griffin, Martin Mäki, Markku Kaukinen, Katri Lindfors, Katri
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5.

001-es BibID:BIBFORM048567
Első szerző:Nadalutti, Cristina Antonella
Cím:Celiac disease patient IgA antibodies induce endothelial adhesion and cell polarization defects via extracellular transglutaminase 2 / Cristina Antonella Nadalutti, Ilma Rita Korponay-Szabo, Katri Kaukinen, Martin Griffin, Markku Mäki, Katri Lindfors
Dátum:2014
ISSN:1420-682X
Megjegyzések:We have recently found that celiac disease patient serum-derived autoantibodies targeted against transglutaminase 2 interfere with several steps of angiogenesis, including endothelial sprouting and migration, though the mechanism involved remained to be fully characterized. This study now investigated the processes underlying the antiangiogenic effects exerted by celiac disease patient antibodies on endothelial cells, with particular regard to the adhesion, migration, and polarization signaling pathway. We observed that celiac IgA reduced endothelial cell numbers by affecting adhesion without increasing apoptosis. Endothelial cells in the presence of celiac IgA showed weak attachment, a high susceptibility to detach from fibronectin, and a disorganized extracellular matrix due to a reduction of protein cross-links. Furthermore, celiac patient IgA led to secretion of active transglutaminase 2 from endothelial cells into the culture supernatants. Additionally, cell surface transglutaminase 2 mediated integrin clustering in the presence of celiac IgA was coupled to augmented expression of ?1-integrin. We also observed that celiac patient IgA-treated endothelial cells had migratory defects and a less polarized phenotype when compared to control groups, and this was associated with the RhoA signaling pathway. These biological effects mediated by celiac IgA on endothelial cells were partially influenced but not completely abolished by R281, an irreversible extracellular transglutaminase 2 enzymatic activity inhibitor. Taken together, our results imply that celiac patient IgA antibodies disturb the extracellular protein cross-linking function of transglutaminase 2, thus altering cell-extracellular matrix interactions and thereby affecting endothelial cell adhesion, polarization, and motility.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Cellular and Molecular Life Sciences. - 71 : 7 (2014), p. 1315-1326. -
További szerzők:Korponay-Szabó Ilma (1959-) (gyermekgyógyász) Kaukinen, Katri Griffin, Martin Mäki, Markku Lindfors, Katri
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6.

001-es BibID:BIBFORM044272
Első szerző:Rauhavirta, Tiina
Cím:Epithelial transport and deamidation of gliadin peptides : a role for coeliac disease patient immunoglobulin A / Rauhavirta, T., Qiao, S.-W., Jiang, Z., Myrsky, E., Loponen, J., Korponay-Szabó, I. R., Salovaara, H., Garcia-Horsman, J. A., Venäläinen, J., Männistö, P. T., Collighan, R., Mongeot, A., Griffin, M., Mäki, M., Kaukinen, K., Lindfors, K.
Dátum:2011
ISSN:0009-9104
Megjegyzések:In coeliac disease, the intake of dietary gluten induces small-bowel mucosal damage and the production of immunoglobulin (Ig)A class autoantibodies against transglutaminase 2 (TG2). We examined the effect of coeliac patient IgA on the apical-to-basal passage of gluten-derived gliadin peptides p31-43 and p57-68 in intestinal epithelial cells. We demonstrate that coeliac IgA enhances the passage of gliadin peptides, which could be abolished by inhibition of TG2 enzymatic activity. Moreover, we also found that both the apical and the basal cell culture media containing the immunogenic gliadin peptides were able to induce the proliferation of deamidation-dependent coeliac patient-derived T cells even in the absence of exogenous TG2. Our results suggest that coeliac patient IgA could play a role in the transepithelial passage of gliadin peptides, a process during which they might be deamidated.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Clinical And Experimental Immunology. - 164 : 1 (2011), p. 127-136. -
További szerzők:Qiao, Shuo-Wang Jiang, Z. Myrsky, Essi Loponen, J. Korponay-Szabó Ilma (1959-) (gyermekgyógyász) Salovaara, H. Garcia-Horsman, J. Arturo Venäläinen, Jarkko I. Männistö, Pekka T. Collighan, Russell Mongeot, Alexandre Griffin, Martin Mäki, Markku Kaukinen, Katri Lindfors, Katri
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