scholarly journals Repeated Thermal Therapy Up-Regulates Endothelial Nitric Oxide Synthase and Augments Angiogenesis in a Mouse Model of Hindlimb Ischemia

2006 ◽  
Vol 70 (4) ◽  
pp. 463-470 ◽  
Author(s):  
Yuichi Akasaki ◽  
Masaaki Miyata ◽  
Hideyuki Eto ◽  
Takahiro Shirasawa ◽  
Narisato Hamada ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Mouse Model ◽  
Endothelial Nitric Oxide Synthase ◽  
Thermal Therapy ◽  
Hindlimb Ischemia ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide

scholarly journals Insulin-like growth factor 1 signaling in the placenta requires endothelial nitric oxide synthase to support trophoblast function and normal fetal growth

2020 ◽  
Author(s):  
Rebecca L Wilson ◽  
Weston Troja ◽  
Emily K Sumser ◽  
Alec Maupin ◽  
Kristin Lampe ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Growth Factor ◽  
Nitric Oxide Synthase ◽  
Mouse Model ◽  
Fetal Growth ◽  
Endothelial Nitric Oxide Synthase ◽  
Genetic Model ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide

AbstractCurrently, there is no effective treatment for placenta dysfunction in utero. In a ligated mouse model of fetal growth restriction (FGR), nanoparticle-mediated human insulin-like 1 growth factor (hIGF1) gene delivery (NP-Plac1-hIGF1) increased hIGF1 expression and maintained fetal growth. However, whether it can restore fetal growth remains to be determined. Using the endothelial nitric oxide synthase knockout (eNOS−/−) mouse model, a genetic model of FGR, we found that despite inducing expression of hIGF1 in the placentas treated with NP-Plac1-hIGF1 (P=0.0425), FGR did not resolve. This was associated with no change to the number of fetal capillaries in the placenta labyrinth; an outcome increased with NP-Plac1-hIGF1 treatment in the ligated mouse model, despite increased expression of angiopoietin 1 (P=0.05) and suggested IGF1 signaling in the placenta requires eNOS to modulate placenta angiogenesis. To further assess this hypothesis, we used the BeWo Choriocarcinoma cell line and human placenta explant cultures that were treated with NP-Plac1-hIGF1, oxidative stress was induced with hydrogen peroxide (H2O2) and NOS activity inhibited using the inhibitor L-NMMA. In both BeWo and explants, the protective effect of NP-Plac1-hIGF1 treatment against H2O2 induced cell death/lactate dehydrogenase release was prevented by eNOS inhibition (P=0.003 and P<0.0001, respectively). This was associated with an increase in mRNA expression of oxidative stress markers HIF1α (P<0.0001) and ADAM10 (P=0.0002) in the NP-Plac1-hIGF1+H2O2+L-NMMA treated BeWo cells. These findings show for the first time the requirement of eNOS/NOS in IGF1 signaling in placenta cells that may have implications for placental angiogenesis and fetal growth.

scholarly journals Waon Therapy Upregulates Hsp90 and Leads to Angiogenesis Through the Akt-Endothelial Nitric Oxide Synthase Pathway in Mouse Hindlimb Ischemia

2012 ◽  
Vol 76 (7) ◽  
pp. 1712-1721 ◽  
Author(s):  
Takahiro Miyauchi ◽  
Masaaki Miyata ◽  
Yoshiyuki Ikeda ◽  
Yuichi Akasaki ◽  
Narisato Hamada ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Endothelial Nitric Oxide Synthase ◽  
Hindlimb Ischemia ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide
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