Imperial College London

ProfessorMichaelSchneider

Faculty of MedicineNational Heart & Lung Institute

Chair in Cardiology
 
 
 
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Contact

 

+44 (0)013 34621727m.d.schneider Website

 
 
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Location

 

ICTEM buildingHammersmith Campus

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Summary

 

Publications

Publication Type
Year
to

173 results found

Weinreuter M, Kreusser MM, Beckendorf J, Schreiter FC, Leuschner F, Lehmann LH, Hofmann KP, Rostosky JS, Diemert N, Xu C, Volz HC, Jungmann A, Nickel A, Sticht C, Gretz N, Maack C, Schneider MD, Groene H-J, Mueller OJ, Katus HA, Backs Jet al., 2014, CaM Kinase II mediates maladaptive post-infarct remodeling and pro-inflammatory chemoattractant signaling but not acute myocardial ischemia/reperfusion injury, EMBO Molecular Medicine, Vol: 6, Pages: 1231-1245, ISSN: 1757-4676

Journal article

Lehmann LH, Rostosky JS, Buss SJ, Kreusser MM, Krebs J, Mier W, Enseleit F, Spiger K, Hardt SE, Wieland T, Haass M, Luescher TF, Schneider MD, Parlato R, Groene H-J, Haberkorn U, Yanagisawa M, Katus HA, Backs Jet al., 2014, Essential role of sympathetic endothelin A receptors for adverse cardiac remodeling, PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, Vol: 111, Pages: 13499-13504, ISSN: 0027-8424

Journal article

Kreusser MM, Lehmann LH, Keranov S, Hoting M-O, Oehl U, Kohlhaas M, Reil J-C, Neumann K, Schneider MD, Hill JA, Dobrev D, Maack C, Maier LS, Groene H-J, Katus HA, Olson EN, Backs Jet al., 2014, Cardiac CaM Kinase II Genes delta and gamma Contribute to Adverse Remodeling but Redundantly Inhibit Calcineurin-Induced Myocardial Hypertrophy, Circulation, Vol: 130, Pages: 1262-1273, ISSN: 0009-7322

Journal article

Chuang H-C, Sheu WH-H, Lin Y-T, Tsai C-Y, Yang C-Y, Cheng Y-J, Huang P-Y, Li J-P, Chiu L-L, Wang X, Xie M, Schneider MD, Tan T-Het al., 2014, HGK/MAP4K4 deficiency induces TRAF2 stabilization and Th17 differentiation leading to insulin resistance, Nature Communications, Vol: 5, ISSN: 2041-1723

Proinflammatory cytokines play important roles in insulin resistance. Here we report thatmice with a T-cell-specific conditional knockout of HGK (T-HGK cKO) develop systemicinflammation and insulin resistance. This condition is ameliorated by either IL-6 or IL-17neutralization. HGK directly phosphorylates TRAF2, leading to its lysosomal degradationand subsequent inhibition of IL-6 production. IL-6-overproducing HGK-deficient T cellsaccumulate in adipose tissue and further differentiate into IL-6/IL-17 double-positive cells.Moreover, CCL20 neutralization or CCR6 deficiency reduces the Th17 population or insulinresistance in T-HGK cKO mice. In addition, leptin receptor deficiency in T cells inhibits Th17differentiation and improves the insulin sensitivity in T-HGK cKO mice, which suggests thatleptin cooperates with IL-6 to promote Th17 differentiation. Thus, HGK deficiency inducesTRAF2/IL-6 upregulation, leading to IL-6/leptin-induced Th17 differentiation in adiposetissue and subsequent insulin resistance. These findings provide insight into the reciprocalregulation between the immune system and the metabolism.

Journal article

Johannesson B, Sattler S, Semenova E, Pastore S, Kennedy-Lydon TM, Sampson RD, Schneider MD, Rosenthal N, Bilbao Det al., 2014, Insulin-like growth factor-1 induces regulatory T cell-mediated suppression of allergic contact dermatitis in mice, DISEASE MODELS & MECHANISMS, Vol: 7, Pages: 977-985, ISSN: 1754-8403

Journal article

Liu Y, Kaneda R, Leja TW, Subkhankulova T, Tolmachov O, Minchiotti G, Schwartz RJ, Barahona M, Schneider MDet al., 2014, Hhex and Cer1 Mediate the Sox17 Pathway for Cardiac Mesoderm Formation in Embryonic Stem Cells, STEM CELLS, Vol: 32, Pages: 1515-1526, ISSN: 1066-5099

Journal article

Stuckey DJ, McSweeney SJ, Thin MZ, Habib J, Price AN, Fiedler LR, Gsell W, Prasad SK, Schneider MDet al., 2014, T-1 Mapping Detects Pharmacological Retardation of Diffuse Cardiac Fibrosis in Mouse Pressure-Overload Hypertrophy, CIRCULATION-CARDIOVASCULAR IMAGING, Vol: 7, Pages: 240-249, ISSN: 1941-9651

Journal article

Foeldes G, Mioulane M, Kodagoda T, Lendvai Z, Iqbal A, Ali NN, Schneider MD, Harding SEet al., 2014, Immunosuppressive Agents Modulate Function, Growth, and Survival of Cardiomyocytes and Endothelial Cells Derived from Human Embryonic Stem Cells, STEM CELLS AND DEVELOPMENT, Vol: 23, Pages: 467-476, ISSN: 1547-3287

Journal article

Fiedler LR, Maifoshie E, Schneider MD, 2014, Mouse Models of Heart Failure: Cell Signaling and Cell Survival, MOUSE MODELS OF THE NUCLEAR ENVELOPATHIES AND RELATED DISEASES, Vol: 109, Pages: 171-247, ISSN: 0070-2153

Journal article

Arechederra M, Carmona R, Gonzalez-Nunez M, Gutierrez-Uzquiza A, Bragado P, Cruz-Gonzalez I, Cano E, Guerrero C, Sanchez A, Miguel Lopez-Novoa J, Schneider MD, Maina F, Munoz-Chapuli R, Porras Aet al., 2013, Met signaling in cardiomyocytes is required for normal cardiac function in adult mice, BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE, Vol: 1832, Pages: 2204-2215, ISSN: 0925-4439

Journal article

Oakley RH, Ren R, Cruz-Topete D, Bird GS, Myers PH, Boyle MC, Schneider MD, Willis MS, Cidlowski JAet al., 2013, Essential role of stress hormone signaling in cardiomyocytes for the prevention of heart disease, PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, Vol: 110, Pages: 17035-17040, ISSN: 0027-8424

Journal article

McSweeney SJ, Schneider MD, 2013, Virgin birth: engineered heart muscle from parthenogenetic stem cells, JOURNAL OF CLINICAL INVESTIGATION, Vol: 123, Pages: 1010-1013, ISSN: 0021-9738

Journal article

Palacios JA, Schneider MD, 2013, Heart to heart: grafting cardiosphere-derived cells augments cardiac self-repair by both myocytes and stem cells, EMBO Molecular Medicine, Vol: 5, Pages: 177-179, ISSN: 1757-4676

Journal article

Lamothe B, Lai Y, Xie M, Schneider MD, Darnay BGet al., 2013, TAK1 Is Essential for Osteoclast Differentiation and Is an Important Modulator of Cell Death by Apoptosis and Necroptosis, MOLECULAR AND CELLULAR BIOLOGY, Vol: 33, Pages: 582-595, ISSN: 0270-7306

Journal article

Ibrahim M, Siedlecka U, Buyandelger B, Harada M, Rao C, Moshkov A, Bhargava A, Schneider M, Yacoub MH, Gorelik J, Knoll R, Terracciano CMet al., 2013, A critical role for Telethonin in regulating t-tubule structure and function in the mammalian heart, Hum Mol Genet, Vol: 22, Pages: 372-383, ISSN: 1460-2083

The transverse (t)-tubule system plays an essential role in healthy and diseased heart muscle, particularly in Ca(2+)-induced Ca(2+) release (CICR), and its structural disruption is an early event in heart failure. Both mechanical overload and unloading alter t-tubule structure, but the mechanisms mediating the normally tight regulation of the t-tubules in response to load variation are poorly understood. Telethonin (Tcap) is a stretch-sensitive Z-disc protein that binds to proteins in the t-tubule membrane. To assess its role in regulating t-tubule structure and function, we used Tcap knockout (KO) mice and investigated cardiomyocyte t-tubule and cell structure and CICR over time and following mechanical overload. In cardiomyocytes from 3-month-old KO (3mKO), there were isolated t-tubule defects and Ca(2+) transient dysynchrony without whole heart and cellular dysfunction. Ca(2+) spark frequency more than doubled in 3mKO. At 8 months of age (8mKO), cardiomyocytes showed progressive loss of t-tubules and remodelling of the cell surface, with prolonged and dysynchronous Ca(2+) transients. Ca(2+) spark frequency was elevated and the L-type Ca(2+) channel was depressed at 8 months only. After mechanical overload obtained by aortic banding constriction, the Ca(2+) transient was prolonged in both wild type and KO. Mechanical overload increased the Ca(2+) spark frequency in KO alone, where there was also significantly more t-tubule loss, with a greater deterioration in t-tubule regularity. In conjunction, Tcap KO showed severe loss of cell surface ultrastructure. These data suggest that Tcap is a critical, load-sensitive regulator of t-tubule structure and function.

Journal article

Lamothe B, Lai Y, Hur L, Orozco NM, Wang J, Campos AD, Xie M, Schneider MD, Lockworth CR, Jakacky J, Tran D, Ho M, Dawud S, Dong C, Lin H-K, Hu P, Estrov Z, Bueso-Ramos CE, Darnay BGet al., 2012, Deletion of TAK1 in the myeloid lineage results in the spontaneous development of myelomonocytic leukemia in mice, PLoS One, Vol: 7, Pages: 1-18, ISSN: 1932-6203

Previous studies of the conditional ablation of TGF-β activated kinase 1 (TAK1) in mice indicate that TAK1 has an obligatory role in the survival and/or development of hematopoietic stem cells, B cells, T cells, hepatocytes, intestinal epithelial cells, keratinocytes, and various tissues, primarily because of these cells’ increased apoptotic sensitivity, and have implicated TAK1 as a critical regulator of the NF-κB and stress kinase pathways and thus a key intermediary in cellular survival. Contrary to this understanding of TAK1’s role, we report a mouse model in which TAK1 deletion in the myeloid compartment that evoked a clonal myelomonocytic cell expansion, splenomegaly, multi-organ infiltration, genomic instability, and aggressive, fatal myelomonocytic leukemia. Unlike in previous reports, simultaneous deletion of TNF receptor 1 (TNFR1) failed to rescue this severe phenotype. We found that the features of the disease in our mouse model resemble those of human chronic myelomonocytic leukemia (CMML) in its transformation to acute myeloid leukemia (AML). Consequently, we found TAK1 deletion in 13 of 30 AML patients (43%), thus providing direct genetic evidence of TAK1’s role in leukemogenesis.

Journal article

Mioulane M, Foldes G, Ali NN, Schneider MD, Harding SEet al., 2012, Development of high content imaging methods for cell death detection in human pluripotent stem cell-derived cardiomyocytes, Journal of Cardiovascular Translational Research, Vol: 5, Pages: 593-604, ISSN: 1937-5387

Human pluripotent stem cell-derived cardiomyocytes (hPSC-CM) are being investigated as a new source of cardiac cells for drug safety assessment. We developed a novel scalable high content microscopy-based method for the detection of cell death in hPSC-CM that can serve for future predictive in vitro cardio-toxicological screens. Using rat neonatal ventricular cardiomyocytes (RVNC) or hPSC-CM, assays for nuclear remodelling, mitochondrial status, apoptosis and necrosis were designed using a combination of fluorescent dyes and antibodies on an automated microscopy platform. This allowed the observation of a chelerythrine-induced concentration-dependent apoptosis to necrosis switch and time-dependent progression of early apoptotic cells towards a necrotic-like phenotype. Susceptibility of hPSC-CM to chelerythrine-stimulated apoptosis varied with time after differentiation, but at most time points, hPSC-CM were more resistant than RVNC. This simple and scalable humanized high-content assay generates accurate cardiotoxicity profiles that can serve as a base for further assessment of cardioprotective strategies and drug safety.

Journal article

Fox K, Schneider M, Shurlock B, 2012, Centre of Excellence: Imperial College of Science, Technology, and Medicine, London, England, CIRCULATION, Vol: 125, Pages: F139-F144, ISSN: 0009-7322

Journal article

Schneider MD, 2012, Pioneer in Cardiovascular Research: Michael D. Schneider MD, FMedSci, FESC, FAHA, CIRCULATION, Vol: 125, Pages: F91-F95, ISSN: 0009-7322

Journal article

Genet G, Guilbeau-Frugier C, Honton B, Dague E, Schneider MD, Coatrieux C, Calise D, Cardin C, Nieto C, Payre B, Dubroca C, Marck P, Heymes C, Dubrac A, Arvanitis D, Despas F, Altie M-F, Seguelas M-H, Delisle M-B, Davy A, Senard J-M, Pathak A, Gales Cet al., 2012, Ephrin-B1 Is a Novel Specific Component of the Lateral Membrane of the Cardiomyocyte and Is Essential for the Stability of Cardiac Tissue Architecture Cohesion, CIRCULATION RESEARCH, Vol: 110, Pages: 688-U117, ISSN: 0009-7330

Journal article

Shukla PC, Singh KK, Quan A, Al-Omran M, Teoh H, Lovren F, Cao L, Rovira II, Pan Y, Brezden-Masley C, Yanagawa B, Gupta A, Deng C-X, Coles JG, Leong-Poi H, Stanford WL, Parker TG, Schneider MD, Finkel T, Verma Set al., 2011, BRCA1 is an essential regulator of heart function and survival following myocardial infarction, Nature Communications, Vol: 2, Pages: 1-11, ISSN: 2041-1723

The tumour suppressor BRCA1 is mutated in familial breast and ovarian cancer but its role in protecting other tissues from DNA damage has not been explored. Here we show a new role for BRCA1 as a gatekeeper of cardiac function and survival. In mice, loss of BRCA1 in cardiomyocytes results in adverse cardiac remodelling, poor ventricular function and higher mortality in response to ischaemic or genotoxic stress. Mechanistically, loss of cardiomyocyte BRCA1 results in impaired DNA double-strand break repair and activated p53-mediated pro-apoptotic signalling culminating in increased cardiomyocyte apoptosis, whereas deletion of the p53 gene rescues BRCA1-deficient mice from cardiac failure. In human adult and fetal cardiac tissues, ischaemia induces double-strand breaks and upregulates BRCA1 expression. These data reveal BRCA1 as a novel and essential adaptive response molecule shielding cardiomyocytes from DNA damage, apoptosis and heart dysfunction. BRCA1 mutation carriers, in addition to risk of breast and ovarian cancer, may be at a previously unrecognized risk of cardiac failure.

Journal article

Schneider MD, 2011, EPO and Super-EPO: Erythropoietins Direct Neoangiogenesis by Cardiac Progenitor Cells, CELL STEM CELL, Vol: 9, Pages: 95-96, ISSN: 1934-5909

Journal article

Schneider MD, 2011, A Cardiac Nonproliferation Treaty, SCIENCE, Vol: 332, Pages: 426-427, ISSN: 0036-8075

Journal article

Mercola M, Ruiz-Lozano P, Schneider MD, 2011, Cardiac muscle regeneration: lessons from development, GENES & DEVELOPMENT, Vol: 25, Pages: 299-309, ISSN: 0890-9369

Journal article

Noseda M, Peterkin T, Simoes FC, Patient R, Schneider MDet al., 2011, Cardiopoietic Factors Extracellular Signals for Cardiac Lineage Commitment, CIRCULATION RESEARCH, Vol: 108, Pages: 129-152, ISSN: 0009-7330

Journal article

Obeyesekere N, Ma F, Tesch G, Ozols E, Xie M, Schneider M, Nikolic-Paterson Det al., 2010, A POTENTIAL ROLE FOR TGF beta-ACTIVATED KINASE 1 (TAK1) EXPRESSION IN MONONUCLEAR PHAGOCYTES IN LPS-INDUCED ALBUMINURIA, NEPHROLOGY, Vol: 15, Pages: 94-94, ISSN: 1320-5358

Journal article

Kuroda J, Ago T, Matsushima S, Zhai P, Schneider MD, Sadoshima Jet al., 2010, NADPH oxidase 4 (Nox4) is a major source of oxidative stress in the failing heart, PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, Vol: 107, Pages: 15565-15570, ISSN: 0027-8424

Journal article

Greenblatt MB, Shim J-H, Zou W, Sitara D, Schweitzer M, Hu D, Lotinun S, Sano Y, Baron R, Park JM, Arthur S, Xie M, Schneider MD, Zhai B, Gygi S, Davis R, Glimcher LHet al., 2010, The p38 MAPK pathway is essential for skeletogenesis and bone homeostasis in mice, JOURNAL OF CLINICAL INVESTIGATION, Vol: 120, Pages: 2457-2473, ISSN: 0021-9738

Journal article

Lin S-C, Dolle P, Ryckebuesch L, Noseda M, Zaffran S, Schneider MD, Niederreither Ket al., 2010, Endogenous retinoic acid regulates cardiac progenitor differentiation, PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, Vol: 107, Pages: 9234-9239, ISSN: 0027-8424

Journal article

Noseda M, Schneider MD, 2010, Unleashing Cardiopoiesis: A Novel Role for G-CSF, CELL STEM CELL, Vol: 6, Pages: 188-189, ISSN: 1934-5909

Journal article

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