Dermal ECM

In other cases, where elastin serves in ECM to control cell and matrix function, elastin has lesser tropoelastin chains and, along with collagen, plays very important roles in the regulation of cells, especially in elastic tissues such as blood vessels [96]. Several studies have shown the roles of elastin during arterial morphogenesis, via knockout experiments. Significant differences in SMC proliferation were observed in cases where tropoelastin was knocked out [96,97]. In another study, elastin knockout mitigated SMC proliferation and the effect was shown to be dose-dependent [98]. Similar effects have been demonstrated in other studies with endothelial cells [99]. Cell proliferation and differentiation was reduced due to elastin knockout. Several other studies have also shown very similar effects with dermal fibroblasts, where elastin plays a very important role in the matrix as a defense mechanism as described earlier. Dermal fibroblasts failed to attach and proliferate on the elastin deprived matrices [89,100]. 

In addition to MEFs, several human cell lines have been shown to be suitable feeders for hPSC culture. It is rational to assume that adhesion-based cultures of hPSCs rely on the natural ECM polymers deposited by the feeder cells for attachment and proliferation. On the basis of this idea, researchers began to use the ECM components secreted by feeder cells. There are two types of ECMs that are employed for hPSC culture decellu-larized ECMs prepared from human fibroblasts from foreskin, dermal, or other human cell lines (which are chemically undefined but not xenogenic) [28,43-46] and single or mixed components of chemically defined ECMs, such as fibronectin, laminin, and vitronectin [47]. These ECMs are used as coating materials on cell culture dishes or scalfolds [48]. 

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