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Am J Physiol Heart Circ Physiol 291: H496-H506, 2006. First published May 5, 2006; doi:10.1152/ajpheart.00114.2006
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Cytoskeletal Networks and the Regulation of Cardiac Contractility

Developmental changes in passive stiffness and myofilament Ca2+ sensitivity due to titin and troponin-I isoform switching are not critically triggered by birth

Martina Krüger,1 Thomas Kohl,2 and Wolfgang A. Linke1

1Physiology and Biophysics Unit, University of Muenster, Muenster; and 2German Center for Fetal Surgery and Minimally Invasive Therapy, Department of Obstetrics and Prenatal Medicine, University of Bonn, Bonn, Germany

Submitted 31 January 2006 ; accepted in final form 3 May 2006

The giant protein titin, a major contributor to myocardial mechanics, is expressed in two main cardiac isoforms: stiff N2B (3.0 MDa) and more compliant N2BA (>3.2 MDa). Fetal hearts of mice, rats, and pigs express a unique N2BA isoform (~3.7 MDa) but no N2B. Around birth the fetal N2BA titin is replaced by smaller-size N2BA isoforms and N2B, which predominates in adult hearts, stiffening their sarcomeres. Here we show that perinatal titin-isoform switching and corresponding passive stiffness (STp) changes do not occur in the hearts of guinea pig and sheep. In these species the shift toward "adult" proportions of N2B isoform is almost completed by midgestation. The relative contributions of titin and collagen to STp were estimated in force measurements on skinned cardiac muscle strips by selective titin proteolysis, leaving the collagen matrix unaffected. Titin-based STp contributed between 42% and 58% to total STp in late-fetal and adult sheep/guinea pigs and adult rats. However, only ~20% of total STp was titin based in late-fetal rat. Titin-borne passive tension and the proportion of titin-based STp generally scaled with the N2B isoform percentage. The titin isoform transitions were correlated to a switch in troponin-I (TnI) isoform expression. In rats, fetal slow skeletal TnI (ssTnI) was replaced by adult carciac TnI (cTnI) shortly after birth, thereby reducing the Ca2+ sensitivity of force development. In contrast, guinea pig and sheep coexpressed ssTnI and cTnI in fetal hearts, and skinned fibers from guinea pig showed almost no perinatal shift in Ca2+ sensitivity. We conclude that TnI-isoform and titin-isoform switching and corresponding functional changes during heart development are not initiated by birth but are genetically programmed, species-specific regulated events.

heart development; connectin; elasticity; myocardium


Address for reprint requests and other correspondence: W. A. Linke, Physiology and Biophysics Unit, Univ. of Muenster, Schlossplatz 5, D-48149 Muenster, Germany (e-mail: wlinke{at}uni-muenster.de)


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