Remodeling of cell-cell and cell-extracellular matrix communications during tissue injury

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Remodeling of cell-cell and cell-extra cellular matrix interactions at the border zone of rat myocardial infarctsWe conducted experimental infarction in rats and performed three-dimensional analysis of the localization of gap junctions (connexin43), desmosomes (desmoplakin), adherents junctions (cadherin) and integrins (β1-integrin) by immunoconfocal microscopy. After myocardial infarction, changes in the distribution of gap junctions, desmosomes and adherens junctions showed a similar but nonidentical tendency. In the early phase, gap junctions almost disappeared at stumps (longitudinal edges of cardiomyocytes facing the infarct), and, although desmosomes and adherents junctions decreased, they still remained. In the healing phase, at stumps, connexin43, desmoplakin and cadherin were closely associated between multiple cell processes originating from a single cardiomyocyte. (β1-Integrin at the cell process increased during the formation of papillary myotendinous junction-like structures. Abnormal localization of connexin43 was often accompanied by desmoplakin and cadherin on lateral surfaces of surviving cardiomyocytes. These findings suggested that remodeling of gap junction distribution was closely linked to changes in desmosomes and adherents junctions, and that temporary formation of intracellular junctional complexes was an element of the remodeling of cell-cell and cell-extra cellular matrix interactions after myocardial infarction.Abnormalities in intracellular calcium dynamics in cardiomyocytes at the border zone of rat myocardial infarctsReal time confocal Ca^<2+> imaging showed frequent Ca^<2+> waves in cardiomyocytes at border zones at early phases postligation (2-4 hours). These results suggest that abnormal expression and function of gap junctions could be associated with Ca^<2+> waves at the border zone of myocardial infarcts.