Increased expression of gelatinases and alteration of basement membrane in rat soleus muscle following femoral artery ligation

2000 ◽  
Vol 26 (1) ◽  
pp. 11-21 ◽  
Author(s):  
E. Frisdal ◽  
E. Teiger ◽  
J. -P. Lefaucheur ◽  
S. Adnot ◽  
E. Planus ◽  
...  
2007 ◽  
Vol 39 (Supplement) ◽  
pp. S429
Author(s):  
William L. Sexton ◽  
Kyra Carpenter-Timm ◽  
Marietta Squire ◽  
Neja Valeja ◽  
Matthew J. Wessner ◽  
...  

2003 ◽  
Vol 284 (3) ◽  
pp. R792-R801 ◽  
Author(s):  
Martin Flück ◽  
Matthias Chiquet ◽  
Silvia Schmutz ◽  
Marie-Hélène Mayet-Sornay ◽  
Dominique Desplanches

The hypothesis was tested that mechanical loading, induced by hindlimb suspension and subsequent reloading, affects expression of the basement membrane components tenascin-C and fibronectin in the belly portion of rat soleus muscle. One day of reloading, but not the previous 14 days of hindlimb suspension, led to ectopic accumulation of tenascin-C and an increase of fibronectin in the endomysium of a proportion (8 and 15%) of muscle fibers. Large increases of tenascin-C (40-fold) and fibronectin (7-fold) mRNA within 1 day of reloading indicates the involvement of pretranslational mechanisms in tenascin-C and fibronectin accumulation. The endomysial accumulation of tenascin-C was maintained up to 14 days of reloading and was strongly associated with centrally nucleated fibers. The observations demonstrate that an unaccustomed increase of rat soleus muscle loading causes modification of the basement membrane of damaged muscle fibers through ectopic endomysial expression of tenascin-C.


2020 ◽  
pp. 1-12 ◽  
Author(s):  
Yuji Kanazawa ◽  
Mamoru Nagano ◽  
Satoshi Koinuma ◽  
Mitsugu Sujino ◽  
Yoichi Minami ◽  
...  

Diabetes ◽  
1987 ◽  
Vol 36 (9) ◽  
pp. 1041-1046 ◽  
Author(s):  
S. Sasson ◽  
D. Edelson ◽  
E. Cerasi

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Sonia Selbonne ◽  
Celina Madjene ◽  
Benjamin Salmon ◽  
Yacine Boulaftali ◽  
Marie-Christine Bouton ◽  
...  

AbstractWe previously identified the inhibitory serpin protease nexin-1 (PN-1) as an important player of the angiogenic balance with anti-angiogenic activity in physiological conditions. In the present study, we aimed to determine the role of PN-1 on pathological angiogenesis and particularly in response to ischemia, in the mouse model induced by femoral artery ligation. In wild-type (WT) muscle, we observed an upregulation of PN-1 mRNA and protein after ischemia. Angiography analysis showed that femoral artery perfusion was more rapidly restored in PN-1−/− mice than in WT mice. Moreover, immunohistochemistry showed that capillary density increased following ischemia to a greater extent in PN-1−/− than in WT muscles. Moreover, leukocyte recruitment and IL-6 and MCP-1 levels were also increased in PN-1−/− mice compared to WT after ischemia. This increase was accompanied by a higher overexpression of the growth factor midkine, known to promote leukocyte trafficking and to modulate expression of proinflammatory cytokines. Our results thus suggest that the higher expression of midkine observed in PN-1- deficient mice can increase leukocyte recruitment in response to higher levels of MCP-1, finally driving neoangiogenesis. Thus, PN-1 can limit neovascularisation in pathological conditions, including post-ischemic reperfusion of the lower limbs.


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