This ANGII induced contractile response and change in traction force on the microposts was not observed in VSMCs lacking ILK.
In contrast, VSMCs lack their quiescence and "contractile" phenotype and acquire capacity to proliferate and migrate.
Recently, various genetically engineered mice, including mice lacking KATP channels (knockout mice) and mice expressing various mutant KATP channels (transgenic mice), have been generated.
We first ensured that we obtained the same effect in wild-type (C57BL/6J) mouse VSMCs as observed in human VSMCs.
Previously, we published that Msx1 is expressed in adult mouse VSMCs and pericytes and, in the embryo, in ECs and VSMCs (Goupille et al., 2008).
Furthermore, VSMC apoptosis, measured by quantification of cleaved caspase-3, was 43% lower in MMP-7 knockout mouse VSMCs compared with wild-type VSMCs following treatment with Fas-L.
However, some researchers have reported that Klotho has no effect on the calcification of human and mouse VSMCs [ 6, 7].
Mouse VSMCs were grown from explants of mouse aorta removed from either MMP knockout or wild-type mice or C57BL/6J controls, as described previously.
As seen in human VSMCs, we observed a significant increase in N-cadherin fragment and a decrease in full-length N-cadherin in mouse VSMCs following Fas-L treatment, and this increase was inhibited by BB-94.
As seen in the MMP-7 knockout mouse VSMCs, inhibition of MMP-7 in human VSMCs resulted in a significant reduction in cleaved caspase-3 following addition of Fas-L.
