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In addition, it has been shown that healthy ventricular tissue far from the acute injury also responds by increasing proliferation (hyperplasia), which is a compensatory mechanism of regeneration (FIGURE 22.26; Poss et al. 2002; Sallin et al. 2015).
Researchers working with zebrafish larvae induced severe injury to the ventricular tissue of the larval heart by causing apoptosis of the ventricular cardiomyocytes (Zhang et al. 2013).
This procedure severely ablated ventricular tissue in this larval heart.
Neighboring differentiated atrial cardiomyocytes responded to the injury by migrating into the damaged ventricular tissue and upregulating ven- tricule-specific genes such as vmhc (FIGURE 22.27A).
Twenty-four hours after ventricular cell ablation (right photograph), deltaD along with other related genes (blue stain) are highly upregulated in the atrial cardiomyocytes, particularly in those migrating toward the ventricular tissue.
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