Scientific Personnel

Brief Bio

Capetanaki studied Biology in the University of Athens, she received her M.Sc. from CUNY and her Ph.D from University of Heidelberg in 1980. She did her post doctoral and senior research fellowship at CALTECH. In 1986 she joined the faculty of the Department of Molecular and Cellular Biology of Baylor College of Medicine at Houston, where she stayed for 16 years and climbed up all the professorship ranks. Leaving Houston for Greece, she was offered an adjunct professorship in the same Department which she still holds. She is now head of the Cell Biology Division and director of the Center of Basic Research I of the Foundation of Biomedical Research of the Academy of Athens. Capetanaki's research goal is the use of Molecular and Cell Biology, Genomics and Transgenesis in mice to a) develop models and study the molecular and cellular mechanisms responsible for Cardiomyopathy and Heart Failure development and b) contribute in the development of gene and cell therapy strategies to prevent or reverse the developement or the responsible pathologic processes. Several discoveries from Capetanaki's group the last 10 years have provided very important insight into the role of desmin intermediate filaments (IFs) in protection against mitochondrial defect accumulation and cardiomyocyte death. Her group’s hypothesis is that desmin in muscle cells and generally IF cytoskeleton in other cells, functions as a part of a cellular internet, a scaffold that facilitates mechanochemical signaling and transport processes and cross-talk between different membranous organelles, including among others, mitochondria, ER/SR, nucleus and plasma membrane. Protein and lipid complex formation and stabilization of crucial organelle microdomain structures might be a potential mechanism of its action. Disturbance of these processes lead to disease and understanding them will provide unprecedented insight into the biology of the disease. Recent studies from Capetanaki's lab demonstrated that in addition to deficiency or mutations, TNF-a induced caspase cleavage of desmin plays also a major role in heart failure development with similar mitochondrial defects . Therefore, the focus of her lab has been the elucidation of the mechanism by which perturbations in cardiomyocyte cytoskeletal network, specifically due to deficiency or collapse of its IF components, including desmin and its associated partners, lead to defects in mitochondrial structure and function, cardiomyocyte death, myocardial degeneration, dilated cardiomyopathy and heart failure. It is a long term goal of her lab to use the generated knowledge towards the development of effective strategies targeting particularly mitochondrial protection in order to prevent or reverse cardiomyopathy and heart failure.

Selected Publications

Weitzer, G., Kim, J.-U. Bradley, A. and Capetanaki, Y.(1995) Cytoskeletal control of myogenesis: a desmin null mutation blocks the myogenic pathway during embryonic stem cell differentiation. Dev. Biol.172, 422-439.

Milner, D., Weitzer, G., Tran, D., Bradley, A. and Capetanaki, Y. (1996)  Disruption of muscle architecture and myocardial degeneration in mice lacking desmin. J. Cell Biol. 134, 1255-1270.

Milner, D. J., Mavroidis, M., Weisleder, N. and Capetanaki, Y. (2000). Desmin cytoskeleton linked to muscle mitochondrial distribution and respiratory function . J. Cell  Biol. 150: 1283-1297.

Weisleder, N, Taffet, G. and Capetanaki, Y. (2004)  Over-expression of Bcl-2 corrects motichondrial defects and ameliorates  inherited desmin null cardiomyopathy. Proc. Nat. Acad. Sci., USA. 101:769-774.

Weisleder, N., Soumaka, E., Abbasi, S., Heinrich Taegtmeyer, H., and Capetanaki, Y.(2004). Cardiomyocyte-specific desmin rescue of desmin null cardiomyopathy excludes vascular involvement. J. Mol. Cell. Cardiol. 36:121-128.

Capetanaki, Y, Bloch,RJ., Kouloumenta, A., Mavroidis, M.,Psarras, S. (2007).  Muscle intermediate filaments and their links to membranes and membranous organelles. Exp. Cell Res. 313: 2063-2076.

Kouloumenta, A., Mavroidis, M and Capetanaki, Y. (2007). Proper perinuclear localization of the TRIM-like protein myospryn requires its binding partner desmin. J. Biol. Chem. 282:35211-35221.

Panagopoulou, P. , Davos, C., Milner, D., Varela, E., J., Mann, D. and Capetanaki, Y. (2008). Desmin mediates TNF-a induced aggregate formation and intercalated disk reorganization in heart failure J. Cell Biol. 181: 761-775.

Psarras, S., Mavroidis, M., Sanoudou, D., Davos, C., Xanthou, G., Varela, E., Panoutsakopoulou, V, and Capetanaki,Y. (2012). Regulation of Adverse Remodeling by Osteopontin in a Genetic Heart Failure Model. Eur. Heart J. 33:1954-1963. doi:10.1093/eurheart/erh119. Epub 2011 (Apr 26).

Capetanaki Y, Papathanasiou S, Diokmetzidou A, Vatsellas G, Tsikitis M. 2015. Desmin related disease: a matter of  cell survival failure. Curr Opin Cell Biol. 32: 113-120.

Papathanasiou, S, Rickelt, S, Soriano, ME, Schips , TG, Maier , HJ, Davos, CH, Varela, A, Kaklamanis ,L, Mann , DL, Capetanaki,Y. (2015). Tumor necrosis factor-α confers cardioprotection through ectopic expression of keratins K8 and K18.   Nature Med. 21:1076-1084. doi:10.1038/nm.3925.

Diokmetzidou A, Soumaka E, Kloukina I, Tsikitis M, Makridakis M, Varela A, Davos CH, Georgopoulos S,  Anesti A, Vlachou A and  Capetanaki Y (2016). Desmin and αB-Crystallin Interplay in Maintenance of Mitochondrial Homeostasis and Cardiomyocyte Survival. J. Cell Sci. 129: 3705-3720. Doi: 10.1242/jcs.192203.

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