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Cardiovascular Research 2000 46(2):346-355; doi:10.1016/S0008-6363(00)00034-1
© 2000 by European Society of Cardiology
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Copyright © 2000, European Society of Cardiology

Expression of laminin {alpha}2 chain during normal and pathological growth of myocardium in rat and human

Patricia Oliviéroa, Catherine Chassagnea, Nathalie Salichona, Alain Corbierb, Gilles Hamonb, Françoise Marottea, Danièle Charlemagnea, Lydie Rappaporta and Jane-Lise Samuela,*

aU127 INSERM, IFR—Circulation Paris VII, Hopital Lariboisière, 41 Bd Chapelle, Université D. Diderot, 75475 Paris, France
bHoechst Marion Roussel, 111 route de Noisy, Romainville, France

* Corresponding author. Tel.: +33-144-631-741; fax: +33-148-742-315

Objectives: Fibrosis is a classical feature of cardiac hypertrophy. To date changes within the basal lamina during normal and pathological cardiac growth have been poorly investigated. The goal of the present study was to determine if the expression of the muscle specific subunit of merosin (laminin {alpha}2 chain) together with that of fibronectin (FN) is modified in the diseased human heart. Laminin {alpha}2 chain expression was also investigated during physiological and pathological cardiac growth in the rat. Methods: In ten normal human hearts and ten hearts with idiopathic dilated cardiomyopathy (IDCM), the laminin-{alpha}2 and FN mRNA levels were quantified by slot-blot using total RNA and the protein distribution was analysed using an immunofluorescence approach. In Wistar rats, laminin {alpha}2 and FN mRNA expression was analyzed using RNase protection assay (RPA) and slot-blot assays. Results: The amount of laminin {alpha}2 mRNA did not vary in normal and pathological human hearts whereas it was significantly decreased in renovascular hypertensive rats (–20%) P<0.05 versus normal tissue). The amount of fibronectin mRNA increased in IDMC patients (x2, P<0.05 versus normal tissue), but was unchanged in hypertensive rats. A negative correlation was found between the cardiac laminin-{alpha}2 level and the age of the patients whatever the cardiac status. During postnatal development in the rat, a similar decrease in cardiac laminin-{alpha}2 level was observed between 3 and 30 weeks of age. Finally, the immunofluorescent approach failed to detect any alteration in laminin {alpha}2 distribution within the human myocardium. Conclusion: These data indicate that an imbalance between myocyte hypertrophy and the level of laminin-{alpha}2 might contribute to alterations in sarcolemmal properties, which occur during the development of cardiac hypertrophy and its transition to cardiac failure.

KEYWORDS Extracellular matrix; Hypertrophy


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