Noncanonical TGFβ signaling contributes to aortic aneurysm progression in marfan syndrome mice

Science

Volumn 332, Issue 6027, 2011, Pages 358-361

  Holm, Tammy M ^a   Habashi, Jennifer P ^a   Doyle, Jefferson J ^a   Bedja, Djahida ^a   Chen, YiChun ^a   Van Erp, Christel ^a   Lindsay, Mark E ^a   Kim, David ^a   Schoenhoff, Florian ^a   Cohn, Ronald D ^a   Loeys, Bart L ^b   Thomas, Craig J ^c   Patnaik, Samarjit ^c   Marugan, Juan J ^c   Judge, Daniel P ^a   Dietz, Harry C ^a  

^a JOHNS HOPKINS UNIVERSITY SCHOOL OF MEDICINE   (United States)

^b GHENT UNIVERSITY HOSPITAL   (Belgium)

^c NATIONAL INSTITUTES OF HEALTH   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

MITOGEN ACTIVATED PROTEIN KINASE 1; MITOGEN ACTIVATED PROTEIN KINASE 3; SMAD2 PROTEIN; STRESS ACTIVATED PROTEIN KINASE 1; TRANSFORMING GROWTH FACTOR BETA;

ENZYME ACTIVITY; GROWTH RATE; INHIBITION; RODENT;

ANIMAL EXPERIMENT; ANIMAL MODEL; AORTA ANEURYSM; ARTICLE; COMPARATIVE STUDY; MARFAN SYNDROME; MOUSE; NONHUMAN; PRIORITY JOURNAL; PROTEIN EXPRESSION; TISSUE GROWTH; WESTERN BLOTTING;

ANIMALS; ANTHRACENES; AORTA; AORTIC ANEURYSM; DIPHENYLAMINE; DISEASE MODELS, ANIMAL; DISEASE PROGRESSION; ENZYME ACTIVATION; LOSARTAN; MAP KINASE SIGNALING SYSTEM; MARFAN SYNDROME; MICE; MITOGEN-ACTIVATED PROTEIN KINASE 1; MITOGEN-ACTIVATED PROTEIN KINASE 3; MITOGEN-ACTIVATED PROTEIN KINASE 8; PROTEIN KINASE INHIBITORS; SMAD2 PROTEIN; SMAD4 PROTEIN; SULFONAMIDES; TRANSFORMING GROWTH FACTOR BETA;

MUS;

EID: 79954625123     PISSN: 00368075     EISSN: 10959203     Source Type: Journal    
DOI: 10.1126/science.1192149     Document Type: Article

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29. Supported by the National Institutes of Health (H.C.D. and D.P.J), Howard Hughes Medical Institute (H.C.D.), National Marfan Foundation (H.C.D., J.P.H., and J.J.D.), Cellular and Molecular Medicine Training Program (J.J.D.), National Human Genome Research Institute Intramural Research Program and the NIH Therapeutics for Rare and Neglected Diseases Program (C.J.T., S.P., and J.J.M.), and the Smilow Center for Marfan Syndrome Research (H.C.D.). We thank Dr. C. Deng for the Smad4-targeted mice. Johns Hopkins University and the authors (H.C.D., J.P.H., D.P.J., and R.C.) have filed a patent relating to the use of TGFb antagonists, including angiotensin II type 1 receptor blockers, for the treatment of Marfan syndrome.