Search

Your search keyword '"Blankesteijn, W. Matthijs"' showing total 243 results
Start Over Author "Blankesteijn, W. Matthijs"
243 results on '"Blankesteijn, W. Matthijs"'

4. Urocortin 2 Gene Transfer Improves Heart Function in Aged Mice

Author

Giamouridis, Dimosthenis, Gao, Mei Hua, Lai, N Chin, Guo, Tracy, Miyanohara, Atsushi, Blankesteijn, W Matthijs, Biessen, Erik AL, and Hammond, H Kirk

Subjects
Medical Physiology, Biomedical and Clinical Sciences, Aging, Cardiovascular, Prevention, Gene Therapy, Genetics, Heart Disease, Aetiology, 2.1 Biological and endogenous factors, Animals, Calcium-Calmodulin-Dependent Protein Kinase Type 2, Corticotropin-Releasing Hormone, Female, Gene Transfer Techniques, Genetic Therapy, Genetic Vectors, HEK293 Cells, Humans, Male, Mice, Mice, Inbred C57BL, Sarcoplasmic Reticulum Calcium-Transporting ATPases, Stroke Volume, Urocortins, Ventricular Dysfunction, Left, Ventricular Function, Left, AAV, HFpEF, LV strain, age-related LV dysfunction, contractile function, diastolic function, gene transfer, urocortin 2, Biological Sciences, Technology, Medical and Health Sciences, Biotechnology, Clinical sciences, Medical biotechnology
Abstract

Prevalence of left ventricular (LV) systolic and diastolic dysfunction increases with aging. We previously reported that urocortin 2 (Ucn2) gene transfer increases heart function in mice with heart failure with reduced ejection fraction. Here, we test the hypotheses that (1) Ucn2 gene transfer will increase LV function in aged mice and that (2) Ucn2 gene transfer given in early life will prevent age-related LV dysfunction. Nineteen-month-old (treatment study) and 3-month-old (prevention study) mice received Ucn2 gene transfer or saline. LV function was examined 3-4 months (treatment study) or 20 months (prevention study) after Ucn2 gene transfer or saline injection. In both the treatment and prevention strategies, Ucn2 gene transfer increased ejection fraction, reduced LV volume, increased LV peak -dP/dt and peak +dP/dt, and reduced global longitudinal strain. Ucn2 gene transfer-in both treatment and prevention strategies-was associated with higher levels of LV SERCA2a protein, reduced phosphorylation of LV CaMKIIa, and reduced LV α-skeletal actin mRNA expression (reflecting reduced cardiac stress). In conclusion, Ucn2 gene transfer restores normal cardiac function in mice with age-related LV dysfunction and prevents development of LV dysfunction.

Published
2020

7. Wnt Signaling in Cardiac Remodeling and Heart Failure

Author

Stylianidis, Vasili, Hermans, Kevin C. M., Blankesteijn, W. Matthijs, Barrett, James E., Editor-in-chief, Flockerzi, Veit, Series editor, Frohman, Michael A., Series editor, Geppetti, Pierangelo, Series editor, Hofmann, Franz B., Series editor, Michel, Martin C., Series editor, Page, Clive P, Series editor, Rosenthal, Walter, Series editor, Wang, KeWei, Series editor, Bauersachs, Johann, editor, Butler, Javed, editor, and Sandner, Peter, editor

Published
2017
Full Text
View/download PDF

15. Intermittent pacing therapy favorably modulates infarct remodeling

Author

Uitterdijk, André, Springeling, Tirza, Hermans, Kevin C. M., Merkus, Daphne, de Beer, Vincent J., Gorsse-Bakker, Charlotte, Mokelke, Eric, Daskalopoulos, Evangelos P., Wielopolski, Piotr A., Cleutjens, Jack P. M., Blankesteijn, W. Matthijs, Prinzen, Frits W., van der Giessen, Willem J., van Geuns, Robert-Jan M., and Duncker, Dirk J.

Published
2017
Full Text
View/download PDF

16. Preface

Author

Blankesteijn, W. Matthijs, primary and Altara, Raffaele, additional

Published
2015
Full Text
View/download PDF

17. Contributors

Author

Altara, Raffaele, primary, Beaudoin, Jonathan, additional, Blankesteijn, W. Matthijs, additional, Brunner-La Rocca, Hans-Peter, additional, Buys, Emmanuel, additional, Carbone, Federico, additional, Cicero, Arrigo F.G., additional, Daskalopoulos, Evangelos P., additional, de Castro Brás, Lisandra E., additional, Deleon-Pennell, Kristine Y., additional, Eisel, Uli L.M., additional, Favari, Elda, additional, Frangogiannis, Nikolaos G., additional, Frantz, Stefan, additional, Frunza, Olga, additional, Hall, Michael E., additional, Hermans, Kevin C.M., additional, Heymans, Stephane, additional, Iyer, Rugmani Padmanabhan, additional, Kusters, Dennis H.M., additional, Lange, Richard A., additional, Lindsey, Merry L., additional, Ma, Yonggang, additional, Mann, Douglas L., additional, Montecucco, Fabrizio, additional, Planavila, Anna, additional, Reutelingsperger, Chris P.M., additional, Ronda, Nicoletta, additional, Scherrer-Crosbie, Marielle, additional, Schoemaker, Regien G., additional, Schroen, Blanche, additional, Schurgers, Leon J., additional, Tegtmeier, Jan, additional, Thoonen, Robrecht, additional, Toba, Hiroe, additional, van Bilsen, Marc, additional, van Delft, Lieke, additional, van Empel, Vanessa, additional, Vandenwijngaert, Sara, additional, Weirather, Johannes, additional, Yabluchanskiy, Andriy, additional, and Zimetti, Francesca, additional

Published
2015
Full Text
View/download PDF

21. Molecular Imaging of Interstitial Alterations in Remodeling Myocardium After Myocardial Infarction

Author

van den Borne, Susanne W.M., Isobe, Satoshi, Verjans, Johan W., Petrov, Artiom, Lovhaug, Dagfinn, Li, Peng, Zandbergen, H. Reinier, Ni, Youping, Frederik, Peter, Zhou, Jun, Arbo, Bente, Rogstad, Astri, Cuthbertson, Alan, Chettibi, Salah, Reutelingsperger, Chris, Blankesteijn, W. Matthijs, Smits, Jos F.M., Daemen, Mat J.A.P., Zannad, Faiez, Vannan, Mani A., Narula, Navneet, Pitt, Bertram, Hofstra, Leonard, and Narula, Jagat

Published
2008
Full Text
View/download PDF

25. The Wnt/frizzled/GSK-3[beta] pathway: a novel therapeutic target for cardiac hypertrophy

Author

Blankesteijn, W. Matthijs, van de Schans, Veerle A.M., ter Horst, Paul, and Smits, Jos F.M.

Subjects
Heart enlargement -- Care and treatment, Heart enlargement -- Complications and side effects, Heart failure -- Risk factors, Protein kinases -- Health aspects, Biological sciences, Chemistry, Pharmaceuticals and cosmetics industries
Abstract

An excessive hypertrophic response of the heart to an increased workload is a leading cause of heart failure. At present, cardiac hypertrophy is treated with inhibitors of the renin-angiotensin system or with [beta]-adrenoceptor antagonists. These current therapeutic strategies inhibit prohypertrophic signaling pathways, but this therapy is inadequate in a substantial number of patients. However, the hypertrophic response of the heart is the net result of activation of prohypertrophic and antihypertrophic pathways. Glycogen synthase kinase-3[beta] (GSK-3[beta]) has a powerful antihypertrophic effect, but is inhibited by growth factors and hypertrophic stimuli through phosphorylation at the [Ser.sup.9] residue of GSK-3[beta]. Activation of the Wnt/frizzled pathway also results in inactivation of GSK-3[beta] through sequestration of the kinase rather than phosphorylation at [Ser.sup.9]. In this Opinion article we will review the current evidence for the involvement of Wnt/frizzled signaling and the activation of GSK-3[beta] in the regulation of cardiac hypertrophy, and subsequently discuss the potential of this pathway to serve as a novel therapeutic approach for cardiac hypertrophy.

Published
2008

30. Pharmacological depletion of microglia prevents vascular cognitive impairment in Ang II-induced hypertension

Author

Kerkhofs, Danielle, primary, van Hagen, Britt T., additional, Milanova, Irina V., additional, Schell, Kimberly J., additional, van Essen, Helma, additional, Wijnands, Erwin, additional, Goossens, Pieter, additional, Blankesteijn, W. Matthijs, additional, Unger, Thomas, additional, Prickaerts, Jos, additional, Biessen, Erik A., additional, van Oostenbrugge, Robert J., additional, and Foulquier, Sebastien, additional

Published
2020
Full Text
View/download PDF

31. Pharmacological depletion of microglia and perivascular macrophages prevents vascular Cognitive Impairment in Ang II-induced Hypertension

Author

Kerkhofs, Danielle, primary, van Hagen, Britt T., additional, Milanova, Irina V., additional, Schell, Kimberly J., additional, van Essen, Helma, additional, Wijnands, Erwin, additional, Goossens, Pieter, additional, Blankesteijn, W. Matthijs, additional, Unger, Thomas, additional, Prickaerts, Jos, additional, Biessen, Erik A., additional, van Oostenbrugge, Robert J., additional, and Foulquier, Sébastien, additional

Published
2020
Full Text
View/download PDF

41. Treatment strategies for post-infarction left ventricular free-wall rupture

Author

Matteucci, Matteo, primary, Fina, Dario, additional, Jiritano, Federica, additional, Meani, Paolo, additional, Blankesteijn, W Matthijs, additional, Raffa, Giuseppe Maria, additional, Kowaleski, Mariusz, additional, Heuts, Samuel, additional, Beghi, Cesare, additional, Maessen, Jos, additional, and Lorusso, Roberto, additional

Published
2019
Full Text
View/download PDF

43. The Therapeutic Potential of Blocking Galectin-3 Expression in Acute Myocardial Infarction and Mitigating Inflammation of Infarct Region: A Clinical Outcome-Based Translational Study

Author

Mosleh, Wassim, primary, Chaudhari, Milind R, additional, Sonkawade, Swati, additional, Mahajan, Supriya, additional, Khalil, Charl, additional, Frodey, Kevin, additional, Shah, Tanvi, additional, Dahal, Suraj, additional, Karki, Roshan, additional, Katkar, Rujuta, additional, Blankesteijn, W Matthijs, additional, Page, Brian, additional, Pokharel, Saraswati, additional, Kim, Minhyung, additional, and Sharma, Umesh C, additional

Published
2018
Full Text
View/download PDF

45. Urocortin 2Gene Transfer Improves Heart Function in Aged Mice

Author

Giamouridis, Dimosthenis, Gao, Mei Hua, Lai, N. Chin, Guo, Tracy, Miyanohara, Atsushi, Blankesteijn, W. Matthijs, Biessen, Erik A.L., and Hammond, H. Kirk

Abstract

Prevalence of left ventricular (LV) systolic and diastolic dysfunction increases with aging. We previously reported that urocortin 2(Ucn2) gene transfer increases heart function in mice with heart failure with reduced ejection fraction. Here, we test the hypotheses that (1) Ucn2gene transfer will increase LV function in aged mice and that (2) Ucn2gene transfer given in early life will prevent age-related LV dysfunction. Nineteen-month-old (treatment study) and 3-month-old (prevention study) mice received Ucn2gene transfer or saline. LV function was examined 3–4 months (treatment study) or 20 months (prevention study) after Ucn2gene transfer or saline injection. In both the treatment and prevention strategies, Ucn2gene transfer increased ejection fraction, reduced LV volume, increased LV peak −dP/dt and peak +dP/dt, and reduced global longitudinal strain. Ucn2gene transfer—in both treatment and prevention strategies—was associated with higher levels of LV SERCA2a protein, reduced phosphorylation of LV CaMKIIa, and reduced LV α-skeletal actin mRNA expression (reflecting reduced cardiac stress). In conclusion, Ucn2gene transfer restores normal cardiac function in mice with age-related LV dysfunction and prevents development of LV dysfunction.

Published
2020
Full Text
View/download PDF

46. Interventions in WNT Signaling to Induce Cardiomyocyte Proliferation: Crosstalk with Other Pathways

Author

Blankesteijn, W. Matthijs

Abstract

Myocardial infarction is a frequent cardiovascular event and a major cause for cardiomyocyte loss. In adult mammals, cardiomyocytes are traditionally considered to be terminally differentiated cells, unable to proliferate. Therefore, the wound-healing response in the infarct area typically yields scar tissue rather than newly formed cardiomyocytes. In the last decade, several lines of evidence have challenged the lack of proliferative capacity of the differentiated cardiomyocyte: studies in zebrafish and neonatal mammals have convincingly demonstrated the regenerative capacity of cardiomyocytes. Moreover, multiple signaling pathways have been identified in these models that—when activated in adult mammalian cardiomyocytes—can reactivate the cell cycle in these cells. However, cardiomyocytes frequently exit the cell cycle before symmetric division into daughter cells, leading to polyploidy and multinucleation. Now that there is more insight into the reactivation of the cell cycle machinery, other prerequisites for successful symmetric division of cardiomyocytes, such as the control of sarcomere disassembly to allow cytokinesis, require more investigation. This review aims to discuss the signaling pathways involved in cardiomyocyte proliferation, with a specific focus on wingless/int-1 protein signaling. Comparing the conflicting results from in vitro and in vivo studies on this pathway illustrates that the interaction with other cells and structures around the infarct is likely to be essential to determine the outcome of these interventions. The extensive crosstalk with other pathways implicated in cardiomyocyte proliferation calls for the identification of nodal points in the cell signaling before cardiomyocyte proliferation can be moved forward toward clinical application as a cure of cardiac disease.SIGNIFICANCE STATEMENTEvidence is mounting that proliferation of pre-existing cardiomyocytes can be stimulated to repair injury of the heart. In this review article, an overview is provided of the different signaling pathways implicated in cardiomyocyte proliferation with emphasis on wingless/int-1 protein signaling, crosstalk between the pathways, and controversial results obtained in vitro and in vivo.

Published
2020
Full Text
View/download PDF

49. Wnt signaling in atherosclerosis

Author

Blankesteijn, W. Matthijs and Blankesteijn, W. Matthijs

Abstract

Atherosclerosis is a disease of the vascular wall that forms the basis for a large spectrum of pathologies of various organs and tissues. Although massive research efforts in the last decades have yielded valuable information about its underlying molecular mechanisms, this has not led to a translation info effective therapeutic interventions that can stop the progression or even can induce regression of atherosclerosis. This underscores the importance of investigations on the involvement of novel signaling pathways in the development and progression of this condition. In this review we focus on the role of Wnt signaling in atherosclerosis. Experimental evidence is presented that Writ signaling is involved in many aspects of the development and progression of vascular lesions including endothelial dysfunction, macrophage activation and the proliferation and migration of vascular smooth muscle cells. Subsequently, we will discuss the role of Wnt signaling in myocardial infarction and stroke, two Common pathologies resulting from the progression of atherosclerotic lesions towards an unstable phenotype. Despite the fact that the published data sometimes are ambiguous or even conflicting, a picture is emerging that an attenuation of Wnt signaling is beneficial for the cardiovascular system that is compromised by atherosclerosis.

Published
2015

Catalog

Books, media, physical & digital resources
See catalog results