Elevated DAMP and pro-inflammatory cytokine release in an in vitro model of early placental insult

Placenta ◽  
2017 ◽  
Vol 57 ◽  
pp. 234-235
Author(s):  
Bernadette Baker ◽  
Helen Bischof ◽  
Frances Beards ◽  
Alexander Heazell ◽  
Colin Sibley ◽  
...  
2006 ◽  
Vol 20 (4) ◽  
Author(s):  
Cathy M Mueller ◽  
Yin‐yao Lin ◽  
Domenico Viterbo ◽  
Joelle Pierre ◽  
Shirley A Murray ◽  
...  

2012 ◽  
Vol 56 (6) ◽  
pp. 724-729 ◽  
Author(s):  
S. O. SCHNEIDER ◽  
A. E. BIEDLER ◽  
F. BEHMENBURG ◽  
T. VOLK ◽  
H. RENSING

2018 ◽  
Vol 96 (3) ◽  
pp. 304-307 ◽  
Author(s):  
Zahra Tavakoli Dargani ◽  
Reetu Singla ◽  
Taylor Johnson ◽  
Rakesh Kukreja ◽  
Dinender K. Singla

Doxorubicin (Dox) is an effective anticancer drug. Unfortunately, it causes cardiac and muscle toxicity due to increased oxidative stress and inflammation; however, it remains unknown whether Dox induces “pyroptosis” — an inflammation-mediated cell death. We investigated whether Dox induces pyroptosis in mouse soleus muscle (Sol 8) cells in vitro and to show the protective effect of embryonic stem cell exosomes (ES-exos) on pyroptosis. Dox and inflammation-induced in vitro model was generated. Pyroptosis was confirmed using immunohistochemistry (with putative markers caspase-1, IL-1β, and pro-inflammatory cytokine IL-18) and Western blotting of caspase-1 and IL-1β. The results show significant increase in the expression of caspase-1, IL-1β, and IL-18 following treatment with Dox, which was inhibited by ES-exos but not mouse embryonic fibroblast exosomes. Moreover, GW4869 compound inhibited functional activity of ES-exos, suggesting these vesicles are key players in the inhibition of pyroptosis. These results suggest that Dox induces inflammatory pyroptosis in Sol 8 cells, which is attenuated by ES-exos in vitro.


Author(s):  
Hoda Keshmiri Neghab ◽  
Mohammad Hasan Soheilifar ◽  
Gholamreza Esmaeeli Djavid

Abstract. Wound healing consists of a series of highly orderly overlapping processes characterized by hemostasis, inflammation, proliferation, and remodeling. Prolongation or interruption in each phase can lead to delayed wound healing or a non-healing chronic wound. Vitamin A is a crucial nutrient that is most beneficial for the health of the skin. The present study was undertaken to determine the effect of vitamin A on regeneration, angiogenesis, and inflammation characteristics in an in vitro model system during wound healing. For this purpose, mouse skin normal fibroblast (L929), human umbilical vein endothelial cell (HUVEC), and monocyte/macrophage-like cell line (RAW 264.7) were considered to evaluate proliferation, angiogenesis, and anti-inflammatory responses, respectively. Vitamin A (0.1–5 μM) increased cellular proliferation of L929 and HUVEC (p < 0.05). Similarly, it stimulated angiogenesis by promoting endothelial cell migration up to approximately 4 fold and interestingly tube formation up to 8.5 fold (p < 0.01). Furthermore, vitamin A treatment was shown to decrease the level of nitric oxide production in a dose-dependent effect (p < 0.05), exhibiting the anti-inflammatory property of vitamin A in accelerating wound healing. These results may reveal the therapeutic potential of vitamin A in diabetic wound healing by stimulating regeneration, angiogenesis, and anti-inflammation responses.


2011 ◽  
Vol 71 (05) ◽  
Author(s):  
M Salama ◽  
K Winkler ◽  
KF Murach ◽  
S Hofer ◽  
L Wildt ◽  
...  

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