Post-ischaemic angiogenic therapy usingin vivoprevascularized ascorbic acid-enriched myocardial artificial grafts improves heart function in a rat model

2011 ◽  
Vol 7 (3) ◽  
pp. 203-212 ◽  
Author(s):  
Eliana C. Martinez ◽  
Jing Wang ◽  
Shera Lilyanna ◽  
Lieng H. Ling ◽  
Shu U. Gan ◽  
...  
2012 ◽  
Vol 18 (8) ◽  
pp. S9
Author(s):  
Mareike Poetsch ◽  
Anika Tschirner ◽  
Sandra Palus ◽  
John Beadle ◽  
Andrew J.S. Coats ◽  
...  

2020 ◽  
Vol 12 (2-4) ◽  
pp. 212
Author(s):  
M. Canu ◽  
A. Carabelli ◽  
M. Debiossat ◽  
A. Broisat ◽  
M. Desvignes ◽  
...  

2020 ◽  
Vol 21 (24) ◽  
pp. 9603
Author(s):  
Konstantin V. Dergilev ◽  
Evgeny K. Shevchenko ◽  
Zoya I. Tsokolaeva ◽  
Irina B. Beloglazova ◽  
Ekaterina S. Zubkova ◽  
...  

Cell therapy of the post-infarcted myocardium is still far from clinical use. Poor survival of transplanted cells, insufficient regeneration, and replacement of the damaged tissue limit the potential of currently available cell-based techniques. In this study, we generated a multilayered construct from adipose-derived mesenchymal stromal cells (MSCs) modified to secrete stem cell factor, SCF. In a rat model of myocardium infarction, we show that transplantation of SCF producing cell sheet induced activation of the epicardium and promoted the accumulation of c-kit positive cells in ischemic muscle. Morphometry showed the reduction of infarct size (16%) and a left ventricle expansion index (0.12) in the treatment group compared to controls (24–28%; 0.17–0.32). The ratio of viable myocardium was more than 1.5-fold higher, reaching 49% compared to the control (28%) or unmodified cell sheet group (30%). Finally, by day 30 after myocardium infarction, SCF-producing cell sheet transplantation increased left ventricle ejection fraction from 37% in the control sham-operated group to 53%. Our results suggest that, combining the genetic modification of MSCs and their assembly into a multilayered construct, we can provide prolonged pleiotropic effects to the damaged heart, induce endogenous regenerative processes, and improve cardiac function.


PLoS ONE ◽  
2017 ◽  
Vol 12 (10) ◽  
pp. e0187345 ◽  
Author(s):  
Ivan Bernardo ◽  
James Wong ◽  
Mary E. Wlodek ◽  
Ross Vlahos ◽  
Paul Soeding

2016 ◽  
Vol 64 (S 02) ◽  
Author(s):  
K. Blanke ◽  
F. Schlegel ◽  
A. Salameh ◽  
W. Raasch ◽  
M. Bader ◽  
...  

Blood ◽  
1977 ◽  
Vol 49 (3) ◽  
pp. 471-475 ◽  
Author(s):  
T Udomratn ◽  
MH Steinberg ◽  
GD Jr Campbell ◽  
FJ Jr Oelshlegel

Abstract There is little information available concerning the possible effects of ascorbic acid on glucose-6-phosphate dehydrogenase (G-6-PD) - deficient erythrocytes. We therefore studied the survival of G-6-PD- deficient cells, incubated with ascorbic acid, in rats with partial reticuloendothelial and complement blockade. Animals were pretreated with ethyl palmitate and cobra venom factor. They were then transfused with 51Cr-labeled erythrocytes which had been incubated in the presence or absence of ascorbic acid. G-6-PD-deficient cells, incubated with ascorbic acid, had impaired survival when compared to that of controls. G-6-PD-deficient cells, in the absence of ascorbic acid, had survival times equal to those of normal control erythrocytes. At the concentrations used, ascorbic acid did not appear to alter the survival of normal cells. Ascorbic acid causes premature loss of G-6-PD- deficient human erythrocytes in this rat model. On the basis of previous clinical and experimental observations, as well as this study, caution should be used when administering ascorbic acid in large doses to individuals who might be G-6-PD deficient.


Lipids ◽  
2015 ◽  
Vol 51 (5) ◽  
pp. 635-642 ◽  
Author(s):  
Naser H. M. Ibrahim ◽  
Sijo J. Thandapilly ◽  
Yong Jia ◽  
Thomas Netticadan ◽  
Harold Aukema

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