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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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001-es BibID:	BIBFORM028773
Első szerző:	Korponay-Szabó Ilma (gyermekgyógyász)
Cím:	Missing endomysial and reticulin binding of coeliac antibodies in transglutaminase 2 knockout tissues / I. R. Korponay-Szabó, K. Laurila, Zs. Szondy, T. Halttunen, Z. Szalai, I. Dahlbom, I. Rantala, J. B. Kovács, L. Fésüs, M. Mäki
Dátum:	2003
ISSN:	0017-5749
Megjegyzések:	Autoantibodies against transglutaminase 2 (TG2) are thought to be responsible for the endomysial (EMA), reticulin (ARA), and jejunal antibody (JEA) tissue binding of serum samples from coeliac patients but the exclusive role of TG2 in these staining patterns has not yet been established. AIMS: To evaluate whether antigens other than TG2 contribute to EMA/ARA/JEA reactions. PATIENTS: Serum samples from 61 EMA/ARA/JEA positive untreated patients with coeliac disease, 40 dermatitis herpetiformis patients, and 34 EMA/ARA/JEA negative non-coeliac controls were tested. METHODS: TG2 knockout (TG2-/-) and wild-type mouse oesophagus, jejunum, liver, and kidney sections, and TG2-/- sections coated with human recombinant TG2 were used as substrates in single and double immunofluorescent studies for patient IgA binding and tissue localisation of TG2, fibronectin, actin, and calreticulin. RESULTS: None of the patient serum samples elicited EMA, ARA, or JEA binding in TG2-/- morphologically normal tissues. In contrast, 96 of 101 gluten sensitive patient samples (95%) reacted with wild-type mouse tissues and all 101 reacted in EMA/ARA/JEA patterns with TG2-/- mouse tissues coated with human TG2. Serum IgA binding to TG2-/- smooth muscle cells was observed in low titres in 31.1%, 27.5%, and 20.5%, and to TG2-/- epithelium in 26.3%, 5.0%, and 8.8% of coeliac, dermatitis herpetiformis, and control samples, respectively. These positivities partly colocalised with actin and calreticulin but not with TG2 or fibronectin. CONCLUSIONS: EMA/ARA/JEA antibody binding patterns are exclusively TG2 dependent both in coeliac and dermatitis herpetiformis patients. Actin antibodies are responsible for some positivities which are not part of the EMA/ARA/JEA reactions.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban egyetemen (Magyarországon) készült közlemény
Megjelenés:	Gut 52 : 2 (2003), p. 199-204. -
További szerzők:	Laurila, Kaija Szondy Zsuzsanna (1959-) (molekuláris sejtbiológus, biokémikus) Halttunen, Tuula Szalai Zoltán Dahlbom, Ingrid Rantala, I. Kovács B. J. Fésüs László (1947-) (orvos biokémikus) Mäki, Markku
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