Subsequent to generation of null allele of α7 gene (itga7) in mouse germline by homologous recombination in embryonic stem cells (Mayer U et al., Nat Genet 17:318,1997), skeletal muscle was found to correlate with some alterations and specific damage of the myotendinous junctions. Besides detailed assessment of the distribution of this protein in (i) a series of different skeletal muscles (SSM), including mimic ones, (ii) myocardium (CSM), and (iii) smooth muscular tissues (SM) in wild type, further ultrastructural information was here added on cell-matrix interface in−/− type. Concerning SSM, myodermal junctions showed the most severe alterations including myofilament disarrangement, mitochondrium damages, and drastic increase of sarcolemmal indentations. Tissue suffering was found to affect CSM according to variable extents in different animals as well as specific heart areas in the same animal. The most severe alterations affected the junctions between papillary muscles and "chordae tendineae" including overgrowth of connective tissue, abnormous increase in the interdigitations at the myotendinous junctions and topical detachments between degenerating cardiomyocytes. Concerning SM, more prominent sarcolemmal indentations for vessel SM than visceral SM and higher α3-integrin-chain expression for visceral SM were appearent as alternative, compensatory features versus the α7-integrin-chain deficiency.
