Interesting New Paper out on MS>LESIONS and Endothelial c
Posted: Wed Dec 30, 2009 2:56 pm
Sure like to get my mitts on this one, anyone have anything or is this a repeat, seems to be from yesterday. Plus would appreciate tips on how to shorten the url's lol.
Copyright © 2009 Published by Elsevier Ireland Ltd.
Increased blood vessel density and endothelial cell proliferation in multiple sclerosis cerebral white matter
"Angiogenesis" is mentioned + stiffened blood vessel linings. Wonder if that would extend to other veins like in the neck for instance, and at some point, that accounts for loss of flexibility, and inability (all structural considerations aside like bone pushing into it for example) of the vessel to "bounce back", and at that point, the stenosis stays that way, with minimal amount of re-inflation to it's ordinary diameter, almost like the difference between a flexible hose that collapses, but inflates when water goes through it, and a solid copper pipe with a dent in it that doesn't readily assume it's normal shape without angioplasty.
What the heck I'll just put the abstract in here:
Abstract
Multiple sclerosis (MS) is primarily considered an inflammatory demyelinating disease, however the role of vasculature in MS pathogenesis is now receiving much interest. MS lesions often develop along blood vessels and alterations in blood brain barrier structure and function, with associated changes in the basement membrane, are pathological features. Nevertheless, the possibility of angiogenesis occurring in MS has received little attention. In this study we used triple label enzyme immunohistochemistry to investigate blood vessel density and endothelial cell proliferation in MS samples (n = 39) compared with control tissue to explore evidence of angiogenesis in MS. The results showed that in all MS samples examined blood vessel density increased compared with controls. The greatest increase was found in subacute lesions where numbers of positively stained vessels increased from 43.9 ± 8.5% in controls to 84.2 ± 13.3% (P = 0.001). Furthermore, using an antibody against endoglin (CD105), a specific marker of proliferating endothelial cells, which are characteristic of angiogenesis, we have shown that vessels containing proliferating endothelial cells were more pronounced in all MS tissue examined (normal-appearing white matter, acute, subacute and chronic lesions, P ≥ 0.027) compared with control and this was greatest in the MS normal-appearing white matter (68.8 ± 19.8% versus 10.58 ± 6.4%, P = 0.003). These findings suggest that angiogenesis may play a role in lesion progression, failure of repair and scar formation.
Copyright © 2009 Published by Elsevier Ireland Ltd.
Increased blood vessel density and endothelial cell proliferation in multiple sclerosis cerebral white matter
"Angiogenesis" is mentioned + stiffened blood vessel linings. Wonder if that would extend to other veins like in the neck for instance, and at some point, that accounts for loss of flexibility, and inability (all structural considerations aside like bone pushing into it for example) of the vessel to "bounce back", and at that point, the stenosis stays that way, with minimal amount of re-inflation to it's ordinary diameter, almost like the difference between a flexible hose that collapses, but inflates when water goes through it, and a solid copper pipe with a dent in it that doesn't readily assume it's normal shape without angioplasty.
What the heck I'll just put the abstract in here:
Abstract
Multiple sclerosis (MS) is primarily considered an inflammatory demyelinating disease, however the role of vasculature in MS pathogenesis is now receiving much interest. MS lesions often develop along blood vessels and alterations in blood brain barrier structure and function, with associated changes in the basement membrane, are pathological features. Nevertheless, the possibility of angiogenesis occurring in MS has received little attention. In this study we used triple label enzyme immunohistochemistry to investigate blood vessel density and endothelial cell proliferation in MS samples (n = 39) compared with control tissue to explore evidence of angiogenesis in MS. The results showed that in all MS samples examined blood vessel density increased compared with controls. The greatest increase was found in subacute lesions where numbers of positively stained vessels increased from 43.9 ± 8.5% in controls to 84.2 ± 13.3% (P = 0.001). Furthermore, using an antibody against endoglin (CD105), a specific marker of proliferating endothelial cells, which are characteristic of angiogenesis, we have shown that vessels containing proliferating endothelial cells were more pronounced in all MS tissue examined (normal-appearing white matter, acute, subacute and chronic lesions, P ≥ 0.027) compared with control and this was greatest in the MS normal-appearing white matter (68.8 ± 19.8% versus 10.58 ± 6.4%, P = 0.003). These findings suggest that angiogenesis may play a role in lesion progression, failure of repair and scar formation.