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The in vitro nifedipine effect on the muscle force production was determined as the percentage of the remaining channel mediated contraction force.
PhE-induced contraction, however, was reduced in femoral arteries that lack smooth muscle cell AR from both SM-ARKO and SM/VE-ARKO mice, while there was a small reduction in ET-1 mediated contraction in all vascular ARKOs.
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These results affirm that collagen crosslinking treatments can prevent cell-mediated contraction of CDM scaffolds.
However, collagen hydrogels display relatively low stiffness and strength, are thrombogenic, and are highly susceptible to cell-mediated contraction.
Cell-mediated contraction plays a critical role in many physiological and pathological processes, notably organized contraction during wound healing.
In previous studies, we have demonstrated that collagen crosslinking techniques are capable of preventing cell-mediated contraction in CDM disks.
The current study examined the hypothesis that collagen crosslinking techniques could inhibit cell-mediated contraction of CDM scaffolds.
In the current study, we investigated the effects of CDM concentration and pore architecture on the ability of CDM scaffolds to resist cell-mediated contraction.
An in vitro co-culture system was devised to evaluate the effect of UEC on (i) SMC-mediated contraction of BAM discs, and (ii) SMC invasiveness into BAM.
Three-dimensional lattices of collagenase-resistant fibrils underwent cell-mediated contraction, but the fibrils did not organize into birefringent collagen bundles.
The degree and kinetics of chondrocyte-mediated contraction, chondrocyte proliferation, and protein and glycosaminoglycan synthesis were evaluated over a four-week period in vitro.
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