Does alpha ( v ) beta ( 3 ) integrin engagement enhance cell invasiveness in human multiple myeloma?
This ability of myeloma plasma cells to interact with VN and FN via avb3 integrin engagement suggests a novel mechanism for their invasion and spreading, since this interaction allows them to adhere to the substratum and enhances their proliferation and protease secretion.
These results implicate a tissue degeneration triggered by Nav1.5 deficiency manifesting as a TGF-β(1)-mediated fibrosis accompanied by electric remodeling in the sinus node dysfunction associated with Scn5a disruption or aging. The latter effects interact to produce the most severe phenotype in old Scn5a(+/-) mice. In demonstrating this, our findings suggest a novel regulatory role for Nav1.5 in cellular biological processes in addition to its electrophysiologic function.