Serafim  Papadimitriou

Takeshi Tsuda

Associate Professor

Pennsylvania,United States

biography

Dr. Takeshi Tsuda is a Staff Pediatric Cardiologist at Nemours Cardiac Center, Nemours/duPont Hospital for Children, Wilmington, DE.
He also serves as an Associate Professor of Pediatrics, Thomas Jefferson University, Jefferson Medical College. Dr. Tsuda is a Physician Scientist who has been studying a role of extracellular matrix protein, fibulin-2, in developing myocardial remodeling and heart failure in the mouse model.
His recent findings suggest that fibulin-2 mediates tissue activation of TGF-ββ and its downstream signaling. Dr. Tsuda’s team also has established a bioassay system to measure TGF-ββ activity in the tissue.
His clinical interest includes congenital heart disease, valvar heart disease, cardiomyopathy, heart failure, and exercise physiology.

 

Area of Interest

Heart failure
Remodeling
Extracellular matrix
Signal transduction TGF-β
Myocardial fibrosis
Congenital heart disease
Valvar heart disease (mitral regurgitation)
Hemodynamics
Cardiomyopathy
Exercise physiology


top publication

1. Aonuma K, Tsuda T, Komiyama A, Akabane T, Tokunaga S, Tada A, Zenda, H. A pediatric case of paraquat poisoning successfully treated with direct hemoperfusion (Japanese).Shinshu Med. J37; 173-176, 1989.

2. Tsuda T, Komiyama A, Aonuma K, Akabane T, Nakayama T. Transient abnormal myelopoiesis and diffuse hepatic necrosis in Down's syndrome with prominent bleeding diathesis Acta Paedtr Scand. 79; 241-243, 1990.

3. Tsuda T, Philp N, Zile MH, Linask KK. Left-right asymmetric localization of flectin in the extracellular matrix during heart looping. Developmental Biology 173: 39-50, 1996.

4. Tsuda T. Majumder K, Linask KK. Differential expression of flectin in the extracellular matrix and left-right asymmetry in mouse embryonic heart during looping stages. Developmental Genetics 23: 203-14, 1998.

5. Tsuda T, Wang H, Timpl R, Chu, M-L. Fibulin-2 expression marks transformed mesenchymal cells in developing cardiac valves, aortic arch vessels and coronary vessels. Developmental Dynamics 222: 89-100, 2001.

6. Tsuda T, Pan T-C, Evangelisti L, Chu M-L. Prominent expression of lysyl oxidase during mouse embryonic cardiovascular development. Anatomical Record 270A; 93-96, 2003.

7. Tsuda T†, Gao E, Markova D, Evangelisti L, Ma X-L, Chu M-L.. Post-ischemic ventricular remodeling occurs independent of hemodynamic changes. Cardiovascular Research 59: 926-33, 2003. (†Corresponding author)

8. Tsuda T, Markova D, Evangelisti L, Wang H, Chu, M-L. The zinc finger protein zac1 is expressed in chondrogeneic sites of the mouse. Developmental Dynamics 229: 340-348, 2004.

9. Chu M-L, Tsuda T,. Fibulins in Development and Heritable Disease. Birth Defects Research (Part C) Embryo Today 72:25-36, March 2004.

10. Miller TL, Altman AR, Tsuda T, Shaffer TH. A Novel Ultrasound Imaging Method and Preparation for the in vivo Evaluation of Tracheal Kinetics and Mechanics. Journal of Biomechanics 40; 1615-1621, 2007.

11. Kobayashi N, Kostka G, Garbe JHO, Keene DR, Bächinger, Hanisch F-G, Markova D, Tsuda T, Timpl R, Chu M-L, Sasaki T. A comparative analysis of the fibulin protein family: Biochemical characterization, binding interactions and tissue localization. J Biol Chem 282; 11805-11816, 2007.

12. Akins RE, GrattonK, Quezada E, Rutter H, Tsuda T, Soteropoulos P. Gene expression profile of bioreactor-cultured cardiac cells: Activation of morphogenetic pathways for tissue engineering. DNA Cell Biol 26; 425-434, 2007.

13. Mizuno J, Akune T, Tsuda T, Fukui Y, Otsuji M, Kin N, Saito Y, Orii R, Hayashida M, Arita H, Hanaoka K. Time course of systolic and diastolic blood pressure decreases during the preintubation period of anesthesia induction: Modeling with a logistic function. J Clin Anesthesia 19:497-505, 2007.

14. Sicot F-X*, Tsuda T,* Markova D, Klemment JF, Birk D, Chu M-L. Fibulin-2 is a dispensable for mouse development and elastic fiber formation. Mol Cell Biology 28; 1061-1067, 2008 (*equal contribution).

15. Mizuno J, Tsuda T, Otsuji M, Arita H, Hanaoka K. Assessment by Logistic Model of Hemodynamic Changes during General Anesthesia (Japanese). Masui (Anesthesiology) 57: 341-351, 2008.

16. Tsuda T†, Wu J, Gao E, Joyce J, Markova D, Dong H-L, Liu Y, Zhang H-Z, Zou Y, Gao F, Miller T, Koch W, Ma X-L, Chu M-L. Loss of fibulin-2 protects against progressive ventricular failure after myocardial infarction. J Mol Cell Card 52: 273-282, 2012 († Corresponding author).

17. Khan SA, Joyce J, Tsuda T†. Quantification of active and total transforming growth factor-b levels in serum and solid organ tissues by bioassay. BMC Research Notes 5: 636-645, 2012.

18. Dong H-L, Rutter H, Gao E, Akins R, Gidding S, Tsuda T†. Integrated wall stress for assessing ventricular workload during ventricular remodeling. J Translational Medicine 11: 183, 2013 doi: 10.1186/1479-5876-11-183.

19. Zhang H-X, Wu J. Dong H-L, Khan SA, Chu M-L, Tsuda T†. Fibulin-2 deficiency attenuates Angiotensin II-induced cardiac hypertrophy by reducing Transforming Growth Factor- signaling. Clin Sci (Lond)126: 275-288, 2014 .

20. Khan SA, Joyce J, Margulies K, Tsuda T†. Enhanced bioactive transforming growth factor (TGF)- levels in advanced human heart failure. Submitted.

21. Longmate WM, Monichan R, Chu M-L, Tsuda T, Mahoney M, DiPersio CM. Reduced fibulin-2 contributes to loss of basement membrane integrity and skin blistering in mice lacking integrin 31 in the epidermis. J Invest Dermatol 2014, online published (doi:10.1038/jid.2014.10).

22. Olijnyk D, Ferrier R, Ibrahim AM, Tsuda T, Chu M-L, Gusterson BA, Stein TS, Morris JS. Fibulin-2 is involved in early extra-cellular matrix development of the outgrowing mouse mammary epithelium. J Mol Cell Sci 2014, online published (doi: 10.1007/s00018-014-1577-4).

23. Tsuda T†, Dunn S, Radtke W. Acquired discrete subaortic stenosis in solid organ transplant recipients. Pedtr Transplant, in press. († Corresponding author)

24. Tsuda T†, Fitzgerald K, Scavena M, Gidding S, Flanigan K, Marks H, Moore SA. Early progressive dilated cardiomyopathy in a family with Becker muscular dystrophy related to a novel frameshift mutation in the dystrophin gene exon 27. Submitted