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1. Male patients affected by mosaic PCDH19 mutations: five new cases

Author

de Lange, I. M., Rump, P., Neuteboom, R. F., Augustijn, P. B., Hodges, K., Kistemaker, A. I., Brouwer, O. F., Mancini, G. M. S., Newman, H. A., Vos, Y. J., Helbig, K. L., Peeters-Scholte, C., Kriek, M., Knoers, N. V., Lindhout, D., Koeleman, B. P. C., van Kempen, M. J. A., and Brilstra, E. H.

Published
2017
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2. Clinical presentation, disease course, and outcome of COVID-19 in hospitalized patients with and without pre-existing cardiac disease: a cohort study across 18 countries

Author

Linschoten, M., Uijl, A., Schut, A., Jakob, C. E. M., Romao, L. R., Bell, R. M., McFarlane, E., Stecher, M., Zondag, A. G. M., van Iperen, E. P. A., Hermans-van Ast, J. F., Lea, N. C., Schaap, J., Jewbali, L. S., Smits, P. C., Patel, R. S., Aujayeb, A., van Smeden, M., Siebelink, H. J., Williams, S., Pilgram, L., Tieleman, R. G., Williams, B., Asselbergs, F. W., Al-Ali, A. K., Al-Muhanna, F. A., Al-Rubaish, A. M., Al-Windy, N. Y. Y., Alkhalil, M., Almubarak, Y. A., Al Nafie, A. N., Al Shahrani, M., Al Shehri, A. M., Anning, C., Anthonio, R. L., Badings, E. A., Ball, C., Van Beek, E. A., Ten Berg, J. M., Von Bergwelt-Baildon, M., Bianco, M., Blagova, O., V, Bleijendaal, H., Bor, W. L., Borgmann, S., van Boxem, A. J. M., van den Brink, F. S., Bucciarelli-Ducci, C., Van Bussel, B. C. T., Byrom-Goulthorp, R., Captur, G., Caputo, M., Charlotte, N., vom Dahl, J., Dark, P., De Sutter, J., Degenhardt, C., Delsing, C. E., Dolff, S., Dorman, H. G. R., Drost, J. T., Eberwein, L., Emans, M. E., Er, A. G., Ferreira, J. B., Forner, M. J., Friedrichs, A., Gabriel, L., Groenemeijer, B. E., Groenendijk, A. L., Gruener, B., Guggemos, W., Haerkens-Arends, H. E., Hanses, F., Hedayat, B., Heigener, D., van der Heijden, D. J., Hellou, E., Hellwig, K., Henkens, M. T. H. M., Hermanides, R. S., Hermans, W. R. M., van Hessen, M. W. J., Heymans, S. R. B., Hilt, A. D., van der Horst, I. C. C., Hower, M., van Ierssel, S. H., Isberner, N., Jensen, B., Kearney, M. T., Kielstein, J. T., Kietselaer, B. L. J. H., Kochanek, M., Kolk, M. Z. H., Koning, A. M. H., Kopylov, P. Y., Kuijper, A. F. M., Kwakkel-van, E. R. P. J. M., Lanznaster, J., van der Linden, M. M. J. M., van der Lingen, A. C. J., Linssen, G. C. M., Lomas, D., Maarse, M., Magdelijns, F. J. H., Magro, M., Markart, P., Martens, F. M. A. C., Mazzilli, S. G., McCann, G. P., van der Meer, P., Meijs, M. F. L., Merle, U., Messiaen, P., Milovanovic, M., Monraats, P. S., Montagna, L., Moriarty, A., Moss, A. J., Mosterd, A., Nadalin, S., Nattermann, J., Neufang, M., Nierop, P. R., Offerhaus, J. A., Van Ofwegen-Hanekamp, C. E. E., Parker, E., Persoon, A. M., Piepel, C., Pinto, Y. M., Poorhosseini, H., Prasad, S., Raafs, A. G., Raichle, C., Rauschning, D., Redon, J., Reidinga, A. C., Ribeiro, M. I. A., Riedel, C., Rieg, S., Ripley, D. P., Rommele, C., Rothfuss, K., Ruddel, J., Ruthrich, M. M., Salah, R., Saneei, E., Saxena, M., Schellings, D. A. A. M., Scholte, N. T. B., Schubert, J., Seelig, J., Shafiee, A., Shore, A. C., Spinner, C., Stieglitz, S., Strauss, R., Sturkenboom, N. H., Tessitore, E., Thomson, R. J., Timmermans, P. J. R., Tio, R. A., Tjong, F. V. Y., Tometten, L., Trauth, J., Van Craenenbroeck, E. M., van Veen, H. P. A. A., den Uil, C. A., Vehreschild, M. J. G. T., Veldhuis, L., I, Veneman, T., Verschure, D. O., Voigt, I, Walter, L., vande Watering, D. J., de Vries, J. K., vande Wal, R. M. A., Westendorp, I. C. D., Westendorp, P. H. M., Westhoff, T., Weytjens, C., Wierda, E., Wille, K., de With, K., Worm, M., Woudstra, P., Wu, K. W., Zaal, R., Zaman, A. G., van der Zee, P. M., Zijlstra, L. E., Alling, T. E., Ahmed, R., Bayraktar-Verver, E. C. E., van Aken, K., Jimenes, Bermudez F. J., Biole, C. A., Den Boer-Penning, P., Bontje, M., Bos, M., Bosch, L., Broekman, M., Broeyer, F. J. F., de Bruijn, E. A. W., Bruinsma, S., Cardoso, N. M., Cosyns, B., Len, van Da D. H., Dekimpe, E., Domange, J., van Doorn, J. L., van DOorn, P., Dormal, F., Drost, I. M. J., Dunnink, A., van Eck, J. W. M., Elshinawy, K., Gevers, R. M. M., Gognieva, D. G., van der Graaf, M., Grangeon, S., Guclu, A., Habib, A., Haenen, N. A., Hamilton, K., Handgraaf, S., Heidbuchel, H., Hendriks-van Woerden, M., Hessels-Linnemeijer, B. M., Hosseini, K., Huisman, J., Jacobs, T. C., Jansen, S. E., Janssen, A., Jourdan, K., ten Kate, G. L., van Kempen, M. J., Kievit, C. M., Kleikers, P., Knufman, N., van der Kooi, S. E., Koole, B. A. S., Koole, M. A. C., Kui, K. K., Kuipers-Elferink, L., Lemoine, I, Lensink, E., van Marrewijk, V, Meijer, E. J., Melein, A. J., Mesitskaya, D. F., van Nes, C. P. M., Paris, F. M. A., Perrelli, M. G., Pieterse-Rots, A., Pisters, R., Polkerman, B. C., van Poppel, A., Reinders, S., Reitsma, M. J., Ruiter, A. H., Selder, J. L., van der Sluis, A., Sousa, A. I. C., Tajdini, M., Sanchez, Tercedor L., Van de Heyning, C. M., Vial, H., Vlieghe, E., Vonkeman, H. E., Vreugdenhil, P., de Vries, T. A. C., Willems, A. M., Wils, A. M., Zoet-Nugteren, S. K., Linschoten, M., Uijl, A., Schut, A., Jakob, C. E. M., Romao, L. R., Bell, R. M., McFarlane, E., Stecher, M., Zondag, A. G. M., van Iperen, E. P. A., Hermans-van Ast, J. F., Lea, N. C., Schaap, J., Jewbali, L. S., Smits, P. C., Patel, R. S., Aujayeb, A., van Smeden, M., Siebelink, H. J., Williams, S., Pilgram, L., Tieleman, R. G., Williams, B., Asselbergs, F. W., Al-Ali, A. K., Al-Muhanna, F. A., Al-Rubaish, A. M., Al-Windy, N. Y. Y., Alkhalil, M., Almubarak, Y. A., Al Nafie, A. N., Al Shahrani, M., Al Shehri, A. M., Anning, C., Anthonio, R. L., Badings, E. A., Ball, C., Van Beek, E. A., Ten Berg, J. M., Von Bergwelt-Baildon, M., Bianco, M., Blagova, O., V, Bleijendaal, H., Bor, W. L., Borgmann, S., van Boxem, A. J. M., van den Brink, F. S., Bucciarelli-Ducci, C., Van Bussel, B. C. T., Byrom-Goulthorp, R., Captur, G., Caputo, M., Charlotte, N., vom Dahl, J., Dark, P., De Sutter, J., Degenhardt, C., Delsing, C. E., Dolff, S., Dorman, H. G. R., Drost, J. T., Eberwein, L., Emans, M. E., Er, A. G., Ferreira, J. B., Forner, M. J., Friedrichs, A., Gabriel, L., Groenemeijer, B. E., Groenendijk, A. L., Gruener, B., Guggemos, W., Haerkens-Arends, H. E., Hanses, F., Hedayat, B., Heigener, D., van der Heijden, D. J., Hellou, E., Hellwig, K., Henkens, M. T. H. M., Hermanides, R. S., Hermans, W. R. M., van Hessen, M. W. J., Heymans, S. R. B., Hilt, A. D., van der Horst, I. C. C., Hower, M., van Ierssel, S. H., Isberner, N., Jensen, B., Kearney, M. T., Kielstein, J. T., Kietselaer, B. L. J. H., Kochanek, M., Kolk, M. Z. H., Koning, A. M. H., Kopylov, P. Y., Kuijper, A. F. M., Kwakkel-van, E. R. P. J. M., Lanznaster, J., van der Linden, M. M. J. M., van der Lingen, A. C. J., Linssen, G. C. M., Lomas, D., Maarse, M., Magdelijns, F. J. H., Magro, M., Markart, P., Martens, F. M. A. C., Mazzilli, S. G., McCann, G. P., van der Meer, P., Meijs, M. F. L., Merle, U., Messiaen, P., Milovanovic, M., Monraats, P. S., Montagna, L., Moriarty, A., Moss, A. J., Mosterd, A., Nadalin, S., Nattermann, J., Neufang, M., Nierop, P. R., Offerhaus, J. A., Van Ofwegen-Hanekamp, C. E. E., Parker, E., Persoon, A. M., Piepel, C., Pinto, Y. M., Poorhosseini, H., Prasad, S., Raafs, A. G., Raichle, C., Rauschning, D., Redon, J., Reidinga, A. C., Ribeiro, M. I. A., Riedel, C., Rieg, S., Ripley, D. P., Rommele, C., Rothfuss, K., Ruddel, J., Ruthrich, M. M., Salah, R., Saneei, E., Saxena, M., Schellings, D. A. A. M., Scholte, N. T. B., Schubert, J., Seelig, J., Shafiee, A., Shore, A. C., Spinner, C., Stieglitz, S., Strauss, R., Sturkenboom, N. H., Tessitore, E., Thomson, R. J., Timmermans, P. J. R., Tio, R. A., Tjong, F. V. Y., Tometten, L., Trauth, J., Van Craenenbroeck, E. M., van Veen, H. P. A. A., den Uil, C. A., Vehreschild, M. J. G. T., Veldhuis, L., I, Veneman, T., Verschure, D. O., Voigt, I, Walter, L., vande Watering, D. J., de Vries, J. K., vande Wal, R. M. A., Westendorp, I. C. D., Westendorp, P. H. M., Westhoff, T., Weytjens, C., Wierda, E., Wille, K., de With, K., Worm, M., Woudstra, P., Wu, K. W., Zaal, R., Zaman, A. G., van der Zee, P. M., Zijlstra, L. E., Alling, T. E., Ahmed, R., Bayraktar-Verver, E. C. E., van Aken, K., Jimenes, Bermudez F. J., Biole, C. A., Den Boer-Penning, P., Bontje, M., Bos, M., Bosch, L., Broekman, M., Broeyer, F. J. F., de Bruijn, E. A. W., Bruinsma, S., Cardoso, N. M., Cosyns, B., Len, van Da D. H., Dekimpe, E., Domange, J., van Doorn, J. L., van DOorn, P., Dormal, F., Drost, I. M. J., Dunnink, A., van Eck, J. W. M., Elshinawy, K., Gevers, R. M. M., Gognieva, D. G., van der Graaf, M., Grangeon, S., Guclu, A., Habib, A., Haenen, N. A., Hamilton, K., Handgraaf, S., Heidbuchel, H., Hendriks-van Woerden, M., Hessels-Linnemeijer, B. M., Hosseini, K., Huisman, J., Jacobs, T. C., Jansen, S. E., Janssen, A., Jourdan, K., ten Kate, G. L., van Kempen, M. J., Kievit, C. M., Kleikers, P., Knufman, N., van der Kooi, S. E., Koole, B. A. S., Koole, M. A. C., Kui, K. K., Kuipers-Elferink, L., Lemoine, I, Lensink, E., van Marrewijk, V, Meijer, E. J., Melein, A. J., Mesitskaya, D. F., van Nes, C. P. M., Paris, F. M. A., Perrelli, M. G., Pieterse-Rots, A., Pisters, R., Polkerman, B. C., van Poppel, A., Reinders, S., Reitsma, M. J., Ruiter, A. H., Selder, J. L., van der Sluis, A., Sousa, A. I. C., Tajdini, M., Sanchez, Tercedor L., Van de Heyning, C. M., Vial, H., Vlieghe, E., Vonkeman, H. E., Vreugdenhil, P., de Vries, T. A. C., Willems, A. M., Wils, A. M., and Zoet-Nugteren, S. K.

Abstract

Aims Patients with cardiac disease are considered high risk for poor outcomes following hospitalization with COVID-19. The primary aim of this study was to evaluate heterogeneity in associations between various heart disease subtypes and in-hospital mortality. Methods and results We used data from the CAPACITY-COVID registry and LEOSS study. Multivariable Poisson regression models were fitted to assess the association between different types of pre-existing heart disease and in-hospital mortality. A total of 16 511 patients with COVID-19 were included (21.1% aged 66-75 years; 40.2% female) and 31.5% had a history of heart disease. Patients with heart disease were older, predominantly male, and often had other comorbid conditions when compared with those without. Mortality was higher in patients with cardiac disease (29.7%; n= 1545 vs. 15.9%; n= 1797). However, following multivariable adjustment, this difference was not significant [adjusted risk ratio (aRR) 1.08, 95% confidence interval (CI) 1.02-1.15; P = 0.12 (corrected for multiple testing)]. Associations with in-hospital mortality by heart disease subtypes differed considerably, with the strongest association for heart failure (aRR 1.19, 95% CI 1.10-1.30; P <0.018) particularly for severe (New York Heart Association class III/IV) heart failure (aRR 1.41, 95% CI 1.20-1.64; P < 0.018). None of the other heart disease subtypes, including ischaemic heart disease, remained significant after multivariable adjustment. Serious cardiac complications were diagnosed in <1% of patients. Conclusion Considerable heterogeneity exists in the strength of association between heart disease subtypes and in-hospital mortality. Of all patients with heart disease, those with heart failure are at greatest risk of death when hospitalized with COVID-19. Serious cardiac complications are rare during hospitalization. [GRAPHICS] .

Published
2022

3. Clinical and genetic aspects of PCDH19-related epilepsy syndromes and the possible role of PCDH19 mutations in males with autism spectrum disorders

Author

van Harssel, J. J. T., Weckhuysen, S., van Kempen, M. J. A., Hardies, K., Verbeek, N. E., de Kovel, C. G. F., Gunning, W. B., van Daalen, E., de Jonge, M. V., Jansen, A. C., Vermeulen, R. J., Arts, W. F. M., Verhelst, H., Fogarasi, A., de Rijk-van Andel, J. F., Kelemen, A., Lindhout, D., De Jonghe, P., Koeleman, B. P. C., Suls, A., and Brilstra, E. H.

Published
2013
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7. Male patients affected by mosaic PCDH19 mutations : five new cases

Author

de Lange, I M, Rump, P., Neuteboom, Rinze F., Augustijn, Paul B., Hodges, K, Kistemaker, A I, Brouwer, Oebele F., Mancini, Grazia M S, Newman, H A, Vos, Yvonne J., Helbig, Katherine L, Peeters-Scholte, C.M.P.C.D., Kriek, M., Knoers, N V, Lindhout, D, Koeleman, B P C, van Kempen, M J A, Brilstra, E H, de Lange, I M, Rump, P., Neuteboom, Rinze F., Augustijn, Paul B., Hodges, K, Kistemaker, A I, Brouwer, Oebele F., Mancini, Grazia M S, Newman, H A, Vos, Yvonne J., Helbig, Katherine L, Peeters-Scholte, C.M.P.C.D., Kriek, M., Knoers, N V, Lindhout, D, Koeleman, B P C, van Kempen, M J A, and Brilstra, E H

Published
2017

8. Male patients affected by mosaic PCDH19 mutations: five new cases

Author

Genetica Klinische Genetica, Child Health, Genetica, Genetica Groep Koeleman, Circulatory Health, Brain, Genetica Oper. Mangt Genoom Diagnostiek, de Lange, I M, Rump, P., Neuteboom, Rinze F., Augustijn, Paul B., Hodges, K, Kistemaker, A I, Brouwer, Oebele F., Mancini, Grazia M S, Newman, H A, Vos, Yvonne J., Helbig, Katherine L, Peeters-Scholte, C.M.P.C.D., Kriek, M., Knoers, N V, Lindhout, D, Koeleman, B P C, van Kempen, M J A, Brilstra, E H, Genetica Klinische Genetica, Child Health, Genetica, Genetica Groep Koeleman, Circulatory Health, Brain, Genetica Oper. Mangt Genoom Diagnostiek, de Lange, I M, Rump, P., Neuteboom, Rinze F., Augustijn, Paul B., Hodges, K, Kistemaker, A I, Brouwer, Oebele F., Mancini, Grazia M S, Newman, H A, Vos, Yvonne J., Helbig, Katherine L, Peeters-Scholte, C.M.P.C.D., Kriek, M., Knoers, N V, Lindhout, D, Koeleman, B P C, van Kempen, M J A, and Brilstra, E H

Published
2017

9. Discontinuous conduction in mouse bundle branches is caused by bundle-branch architecture

Author

van Veen, T. A., van Rijen, H. V., van Kempen, M. J., Miquerol, L., Opthof, T., Gros, D., Vos, M. A., Jongsma, H. J., de Bakker, J. M., Institut de Biologie du Développement de Marseille (IBDM), Aix Marseille Université (AMU)-Centre National de la Recherche Scientifique (CNRS), and Aix Marseille Université (AMU)-Collège de France (CdF (institution))-Centre National de la Recherche Scientifique (CNRS)

Subjects
[SDV.BC]Life Sciences [q-bio]/Cellular Biology
Published
2005

10. Impaired conduction in the bundle branches of mouse hearts lacking the gap junction protein connexin40

Author

van Rijen, H. V., van Veen, T. A., van Kempen, M. J., Wilms-Schopman, F. J., Potse, M., Krueger, O., Willecke, K., Opthof, T., Jongsma, H. J., de Bakker, J. M., Other departments, ACS - Amsterdam Cardiovascular Sciences, and Cardiology

Subjects
sense organs
Abstract

Connexin (Cx)40 and Cx45 are the major protein subunits of gap junction channels in the conduction system of mammals. To determine the role of Cx40, we correlated cardiac activation with Connexin distribution in normal and Cx40-deficient mice hearts. Epicardial and septal activation was recorded in Langendorff-perfused adult mice hearts with a 247-point compound electrode (interelectrode distance, 0.3 mm). After electrophysiological measurements, hearts were prepared for immunohistochemistry and histology to determine Connexin distribution and fibrosis. In both wild-type and Cx40-deficient animals, epicardial activation patterns were similar. The right and left ventricular septum was invariably activated from base to apex. Histology revealed a continuity of myocytes from the common bundle to the septal myocardium. Within this continuity, colocalization was found of Cx43 and Cx45 but not of Cx40 and Cx43. Both animals showed similar His-bundle activation. In Cx40-deficient mice, the proximal bundle branches expressed Cx45 only. The absence of Cx40 in the proximal bundles correlated with right bundle-branch block. Conduction in the left bundle branch was impaired as compared with wild-type animals. Our data show that (1) in mice, a continuity exists between the common bundle and the septum, and (2) Cx40 deficiency results in right bundle-branch block and impaired left bundle-branch conduction

Published
2001

11. Heart defects in connexin43-deficient mice

Author

Ya, J., Erdtsieck-Ernste, E. B., de Boer, P. A., van Kempen, M. J., Jongsma, H., Gros, D., Moorman, A. F., Lamers, W. H., and Other departments

Subjects
cardiovascular system
Abstract

Cardiac malformation in connexin43 (CX43)-disrupted mice is restricted to the junction between right ventricle and outflow tract, even though CX43 is also expressed abundantly elsewhere. We analyzed cardiac morphogenesis in immunohistochemically and hybridohistochemically stained and three-dimensionally reconstructed serial sections of CX43-deficient embryos between embryonic day (ED) 10 and birth. The establishment of the D configuration in the ascending loop of CX43-deficient hearts is markedly retarded, so that the right ventricle retains a craniomedial position and is connected with the outflow tract by a more acute bend in ED10 and ED11 embryos. Because of the subsequent growth of the right ventricle, this condition usually evolves into a D loop, but when it persists, a "crisscross" configuration develops, with the atrioventricular cushions rotated 90 degrees, a horizontal muscular ventricular septum, and a parallel course of the endocardial ridges of the outflow tract. After ED12, large intertrabecular pouches develop at the ventricular side of both shelflike myocardial structures that support the endocardial ridges of the outflow tract, ie, at the location that was earlier characterized by the acute bend between the right ventricle and the outflow tract and that subsequently develops into the anterosuperior leaflet of the tricuspid valve. Retarded development of the D configuration in the ascending loop of the embryonic heart predisposes the myocardium at the junction of the right ventricle and outflow tract to excessive development of intertrabecular pouches during subsequent development

Published
1998

12. Gap junctions in human umbilical cord endothelial cells contain multiple connexins

Author

van Rijen, H., van Kempen, M. J., Analbers, L. J., Rook, M. B., van Ginneken, A. C., Gros, D., Jongsma, H. J., and Other departments

Subjects
cardiovascular system
Abstract

We investigated the expression pattern of gap junctional proteins (connexins, Cx) in situ and in vitro and their functional characteristics in cultured human umbilical vein endothelial cells (HUVEC) and cultured human umbilical artery endothelial cells (HUAEC). In both arteries and veins, Cx37, Cx40, and Cx43 could be detected in situ and in vitro (passages 2-4). Distribution patterns of Cx40 and Cx43 were homogeneous in situ but more heterogeneous in vitro. Cx37 is heterogeneously expressed both in situ and in vitro. Among most cells, no Cx37 staining could be detected; when present, it was found as bright spots between some clusters of cells. Cx40 was more abundant in cultured arterial endothelium than in cultured venous endothelium. Dye-coupling experiments with Lucifer yellow CH revealed extensive dye spread in HUVEC (15.2 +/- 0.4, mean +/- SE, n = 110) but was significantly restricted in HUAEC (9.8 +/- 0.3, n = 110). Electrophysiological gap junctional characteristics were determined in cultured HUVEC and HUAEC pairs by use of the dual voltage-clamp technique. In contrast to the dye-coupling experiments, mean macroscopic electrical conductance was significantly larger for HUAEC pairs (31.4 +/- 6.0 nS, n = 12) than for HUVEC pairs (16.6 +/- 2.8, n = 18). In HUVEC, we measured multiple single gap junctional channel conductances in the range of 19-75 pS. Interestingly, additional conductances of 80-200 pS were measured in HUAEC, possibly partially reflecting activity of channels formed of Cx40, which are more abundant in the cultured arterial endothelial cells

Published
1997

13. Developmental changes of connexin40 and connexin43 mRNA distribution patterns in the rat heart

Author

van Kempen, M. J., Vermeulen, J. L., Moorman, A. F., Gros, D., Paul, D. L., Lamers, W. H., and Other departments

Subjects
cardiovascular system, sense organs
Abstract

OBJECTIVES: Gap junctions have been demonstrated ultrastructurally in cardiac regions where connexin40 (Cx40) and connexin43 (Cx43) protein could not be detected immunohistochemically. We investigated therefore the distribution of their mRNAs with more sensitive techniques. METHODS: In situ hybridizations with Cx40 and Cx43 cRNA probes were performed on sections of rat hearts from 9 embryonic days (ED 9) to adults. RESULTS: From ED 13, Cx40 and Cx43 mRNA are detectable in atria and ventricles, but not in their flanking myocardium (inflow tract, atrioventricular canal and outflow tract). Even though Cx40 and Cx43 mRNA eventually become expressed in the inflow tract, they remain undetectable in the sinoatrial node, the atrioventricular canal (including atrioventricular node) and outflow tract. Expression of Cx40 is maximal in the fetal period and declines towards birth. Cx40 expression in the left and right ventricles evolves independently, its mRNA disappearing 4 days earlier from the right than from the left ventricle, and earlier from the free wall than from the trabeculations. Expression of Cx43 mRNA increases during development and changes postnatally from uniform to punctate. Prenatally, Cx43 mRNA was strongest in the subepicardial layer of the ventricular free wall. Nevertheless, we did not detect protein in this layer. CONCLUSIONS: Cardiac regions without detectable Cx40 or Cx43 mRNA either have extremely low levels of expression or express a different connexin. The temporally separate disappearance of Cx40 mRNA from the fetal ventricles implies that left and right ventricles mature independently with respect to gap-junctional communication. The division of the developing heart in compartments where Cx40 and Cx43 mRNA can and cannot be detected, implies pretranslationally regulated gene expression. The postnatally observed subcellular redistribution of Cx43 mRNA coincides with a reported increase in protein expression

Published
1996

19. The Immune Response in Adenoids and Tonsils.

Author

Van Kempen, M. J. P., Rijkers, G. T., and Van Cauwenberge, P. B.

Subjects
*IMMUNE response, *ADENOIDS, *TONSILS, *DENDRITIC cells, *IMMUNOLOGY, *PHARYNX
Abstract

The adenoid and tonsils are lymphoid tissues located in the pharynx that play an important role in host defense against invading antigens of the upper respiratory tract. Histologically, these structures consist of four well-defined microcompartments which all participate in the immune response: the cryptepithelium, the follicular germinal center with the mantle zone and interfollicular area. With the uptake of antigen by M-cells present in the cryptepithelium a process is initiated which ultimately results in the generation and dissemination of antigen-specific memory and mainly dimeric IgA-producing effector B-lymphocytes. This process requires successful cognate interactions between antigen-presenting cells and lymphocytes and mutually between lymphocytes, which depend not only on antigen-specific signals but also on the expression of various complementary adhesion and costimulatory molecules.Copyright © 2000 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Published
2000
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20. Endothelial-specific deletion of connexin40 promotes atherosclerosis by increasing CD73-dependent leukocyte adhesion.

Author

Chadjichristos CE, Scheckenbach KE, van Veen TA, Richani Sarieddine MZ, de Wit C, Yang Z, Roth I, Bacchetta M, Viswambharan H, Foglia B, Dudez T, van Kempen MJ, Coenjaerts FE, Miquerol L, Deutsch U, Jongsma HJ, Chanson M, and Kwak BR

Subjects
Animals, Atherosclerosis immunology, Atherosclerosis pathology, Cell Adhesion immunology, Cells, Cultured, Connexins metabolism, Endothelial Cells metabolism, Gap Junctions metabolism, Green Fluorescent Proteins genetics, Mice, Mice, Transgenic, Monocytes metabolism, Monocytes pathology, RNA, Small Interfering, Signal Transduction immunology, Vasculitis immunology, Vasculitis pathology, Gap Junction alpha-5 Protein, 5'-Nucleotidase metabolism, Atherosclerosis physiopathology, Connexins genetics, Endothelial Cells pathology, Vasculitis physiopathology
Abstract

Background: Endothelial dysfunction is the initiating event of atherosclerosis. The expression of connexin40 (Cx40), an endothelial gap junction protein, is decreased during atherogenesis. In the present report, we sought to determine whether Cx40 contributes to the development of the disease., Methods and Results: Mice with ubiquitous deletion of Cx40 are hypertensive, a risk factor for atherosclerosis. Consequently, we generated atherosclerosis-susceptible mice with endothelial-specific deletion of Cx40 (Cx40del mice). Cx40del mice were indeed not hypertensive. The progression of atherosclerosis was increased in Cx40del mice after 5 and 10 weeks of a high-cholesterol diet, and spontaneous lesions were observed in the aortic sinuses of young mice without such a diet. These lesions showed monocyte infiltration into the intima, increased expression of vascular cell adhesion molecule-1, and decreased expression of the ecto-enzyme CD73 in the endothelium. The proinflammatory phenotype of Cx40del mice was confirmed in another model of induced leukocyte recruitment from the lung microcirculation. Endothelial CD73 is known to induce antiadhesion signaling via the production of adenosine. We found that reducing Cx40 expression in vitro with small interfering RNA or antisense decreased CD73 expression and activity and increased leukocyte adhesion to mouse endothelial cells. These effects were reversed by an adenosine receptor agonist., Conclusions: Cx40-mediated gap junctional communication contributes to a quiescent nonactivated endothelium by propagating adenosine-evoked antiinflammatory signals between endothelial cells. Alteration in this mechanism by targeting Cx40 promotes leukocyte adhesion to the endothelium, thus accelerating atherosclerosis.

Published
2010
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