frodo wrote:Could this be the real mechanism of action of the beta-interferon?
The abstract indicates that interferon-beta blocks collateral arteriogenesis. In CCSVI, we often discuss collateral veins. However, this article covers collateral arteries. They are saying that interferon-beta blocks the growth of new collateral arteries. I don't see that this paper is related to treating MS with interferon-beta except that the effect it discusses could be seen as a negative side effect of the medication.
Schirmer et al. wrote:Treatment of vascular smooth muscle cells (VSMC) with IFNbeta resulted in an attenuated proliferation, cell-cycle arrest and increased expression of cyclin-dependent kinase inhibitor-1A (p21). Growth-inhibitory effect of IFNbeta was attenuated by inhibition of p21 by RNA-interference. IFNbeta-treated THP1 monocytes showed enhanced apoptosis.
Schirmer et al. wrote:RNA-interference of the IFNbeta receptor-1 (IFNAR1) increased VSMC proliferation, cell cycle progression, and reduced p21 gene expression. IFNbeta-signaling and FAS and TRAIL expression were attenuated in monocytes from IFNAR1-/- mice, indicating reduced monocyte apoptosis. Hindlimb perfusion restoration one week after femoral artery ligation was improved in IFNAR1-/- mice compared to wildtype mice as assessed by infusion of fluorescent microspheres
They blocked the cellular production of the interferon-beta receptor using RNA interference. This would make any added interferon-beta less effective. They found that blocking the activity of interferon-beta increased vascular smooth muscle cell proliferation.
In addition, they also used mice that deficient for the interferon-beta receptor gene (IFNAR1-/- mice) and found that restoration of blood flow to the hind limb following femoral artery ligation was enhanced compared to control mice.
In retrospect to CCSVI, veins do not have the layer of smooth muscle cells that are found in arteries. Here is a nice comparison of the structure of arteries and veins