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1.

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
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
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2.

001-es BibID:BIBFORM044274
Első szerző:Martucciello, Stefania
Cím:RhoB is associated with the anti-angiogenic effects of celiac patient transglutaminase 2-targeted autoantibodies / Martucciello Stefania, Lavric Miha, Toth Boglarka, Korponay-Szabo Ilma, Nadalutti Cristina, Myrsky Essi, Rauhavirta Tiina, Esposito Carla, Sulic Ana-Marija, Sblattero Daniele, Marzari Roberto, Mäki Markku, Kaukinen Katri, Lindfors Katri, Caja Sergio
Dátum:2012
ISSN:0946-2716
Megjegyzések:Celiac patient-derived anti-transglutaminase 2 (TG2) antibodies disturb several steps in angiogenesis, but the detailed molecular basis is not known. Therefore, we here analyzed by microarray technology the expression of a set of genes related to angiogenesis and endothelial cell biology in order to identify factors that could explain our previous data related to vascular biology in the context of celiac disease. To this end, in vitro models using human umbilical vein endothelial cells (HUVECs) or in vivo models of angiogenesis were used. A total of 116 genes were analyzed after treatment with celiac patient autoantibodies against TG2. Compared to treatment with control IgA celiac patient, total IgA induced a consistent expression change of 10 genes, the up-regulation of four and down-regulation of six. Of these genes the up-regulated RhoB was selected for further studies. RhoB expression was found to be up-regulated at both messenger RNA and protein level in response to celiac patient total IgA as well as anti-TG2-specific antibody derived from a celiac patient. Interestingly, down-regulation of RhoB by specific small interfering RNA treatment in endothelial cells could rescue the deranged endothelial length and tubule formation caused by celiac disease autoantibodies. RhoB function is controlled by its post-translational modification by farnesylation. This modification of RhoB required for its correct function can be prevented by the cholesterol lowering drug simvastatin, which was also able to abolish the anti-angiogenic effects of celiac anti-TG2 autoantibodies. Taken together, our results would suggest that RhoB plays a key role in the response of endothelial cells to celiac disease-specific anti-TG2 autoantibodies
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Journal Of Molecular Medicine-Jmm. - 90 : 7 (2012), p. 817-826. -
További szerzők:Lavric, Miha Tóth Boglárka Korponay-Szabó Ilma (1959-) (gyermekgyógyász) Nadalutti, Cristina Myrsky, Essi Rauhavirta, Tiina Esposito, Carla Sulic, Ana-Marija Sblattero, Daniele Marzari, Roberto Mäki, Markku Kaukinen, Katri Lindfors, Katri Caja, Sergio
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3.

001-es BibID:BIBFORM025026
Első szerző:Myrsky, Essi
Cím:Altered small-bowel mucosal vascular network in untreated coeliac disease / Myrsky E., Syrjänen M., Korponay-Szabo I. R., Mäki M., Kaukinen K., Lindfors K.
Dátum:2009
ISSN:0036-5521
Megjegyzések:It has recently been shown that serum autoantibodies targeted against transglutaminase 2 derived from untreated coeliac patients can disturb several steps of angiogenesis in vitro. The purpose of this study was to establish whether the small-bowel mucosal vasculature is altered in coeliac disease and whether the putative changes are gluten dependent. MATERIAL AND METHODS: The small-bowel mucosal microvessel architecture was examined in duodenal biopsy samples from coeliac patients before and after a gluten-free diet and from non-coeliac controls. In addition, the vasculature was subjected to a detailed morphometric analysis. Double immunofluorescent stainings of the vasculature with anti- alpha-smooth muscle actin antibody were performed in order to assess the maturity of mucosal vessels. Coeliac disease-specific transglutaminase 2-targeted autoantibody deposits in the vessel wall were studied using triple immunofluorescent stainings. RESULTS: On a gluten-containing diet the mucosal vasculature in the small intestine of untreated coeliac disease patients was altered in overall organization as well as in the number and maturity of the vessels when compared to healthy subjects. In patients on a gluten-free diet, the vasculature normalized parallel to mucosal recovery. CONCLUSIONS: In coeliac disease, ingestion of gluten leads to altered appearance of small-bowel mucosal microvasculature. It is thus conceivable that the small-bowel mucosal vascular biology might be involved in the pathogenesis of coeliac disease.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Scandinavian Journal Of Gastroenterology. - 44 : 2 (2009), p. 162-167. -
További szerzők:Syrjänen, Mari Korponay-Szabó Ilma (1959-) (gyermekgyógyász) Mäki, Markku Kaukinen, Katri Lindfors, Katri
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4.

001-es BibID:BIBFORM025025
Első szerző:Myrsky, Essi
Cím:Coeliac disease-specific autoantibodies targeted against transglutaminase 2 disturb angiogenesis / Myrsky, E., Kaukinen, K., Syrjänen, M., Korponay-Szabó, I. R., Mäki, M., Lindfors, K.
Dátum:2008
ISSN:0009-9104
Megjegyzések:Coeliac disease is characterized by immunoglobulin-A (IgA)-class autoantibodies targeted against transglutaminase 2 (TG2), a multi-functional protein also with a role in angiogenesis. These antibodies are present in patient serum but are also found bound to TG2 below the epithelial basement membrane and around capillaries in the small intestinal mucosa. Based on these facts and the information that the mucosal vasculature of coeliac patients on a gluten-containing diet is disorganized, we studied whether the coeliac disease-specific autoantibodies targeted against TG2 would disturb angiogenesis. The effects of coeliac disease-specific autoantibodies on in vitro angiogenesis were studied in angiogenic cell cultures. The binding of the antibodies to cells, endothelial sprouting, migration of both endothelial and vascular mesenchymal cells, the integrity of the actin cytoskeleton in both cell types and the differentiation of vascular mesenchymal cells were recorded. In vitro, IgA derived from coeliac disease patients on a gluten-containing diet binds to surface TG2 on endothelial and vascular mesenchymal cells and this binding can be inhibited by the removal of TG2. In addition, coeliac disease-specific autoantibodies targeting TG2 disturb several steps of angiogenesis: endothelial sprouting and the migration of both endothelial and vascular mesenchymal cells. Furthermore, the autoantibodies cause disorganization of the actin cytoskeleton in both capillary cell types that account most probably for the defective cellular migration. We conclude that coeliac disease-specific autoantibodies recognizing TG2 inhibit angiogenesis in vitro. This disturbance of the angiogenic process could lead in vivo to the disruption of the mucosal vasculature seen in coeliac disease patients on a gluten-containing diet.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:Clinical And Experimental Immunology. - 152 : 1 (2008), p. 111-119. -
További szerzők:Kaukinen, Katri Syrjänen, Mari Korponay-Szabó Ilma (1959-) (gyermekgyógyász) Mäki, Markku Lindfors, Katri
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5.

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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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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