Mesenchymal Stem Cells Seeded on Cross-Linked and Noncross-Linked Acellular Porcine Dermal Scaffolds for Long-Term Full-Thickness Hernia Repair in a Small Animal Model

2013 ◽  
Vol 38 (7) ◽  
pp. 572-579 ◽  
Author(s):  
Ondrej Mestak ◽  
Eva Matouskova ◽  
Zuzana Spurkova ◽  
Kamila Benkova ◽  
Pavel Vesely ◽  
...  
2020 ◽  
Vol 80 ◽  
pp. 105879 ◽  
Author(s):  
Somaye Sadeghi ◽  
Nariman Mosaffa ◽  
Seyed Mahmoud Hashemi ◽  
Mohammad Mehdi Naghizadeh ◽  
Tooba Ghazanfari

2017 ◽  
Vol 99 (4) ◽  
pp. 331-341 ◽  
Author(s):  
Claire D. Eliasberg ◽  
Ayelet Dar ◽  
Andrew R. Jensen ◽  
Iain R. Murray ◽  
Winters R. Hardy ◽  
...  

2000 ◽  
Vol 14 (6) ◽  
pp. 561-567 ◽  
Author(s):  
C. Kuntz ◽  
A. Wunsch ◽  
R. Rosch ◽  
F. Autschbach ◽  
J. Windeler ◽  
...  

2009 ◽  
Vol 44 (6) ◽  
pp. 1127-1133 ◽  
Author(s):  
Tamar L. Mirensky ◽  
Gregory N. Nelson ◽  
Matthew P. Brennan ◽  
Jason D. Roh ◽  
Narutoshi Hibino ◽  
...  

2021 ◽  
Vol 8 (1) ◽  
pp. e000879
Author(s):  
Premila Devi Leiphrakpam ◽  
Hannah R Weber ◽  
Tobi Ogun ◽  
Keely L Buesing

BackgroundAcute lung injury (ALI)/acute respiratory distress syndrome (ARDS) is a lethal disease with limited therapeutic options and an unacceptably high mortality rate. Understanding the complex pathophysiological processes involved in the development of ALI/ARDS is critical for developing novel therapeutic strategies. Smoke inhalation (SI) injury is the leading cause of morbidity and mortality in patients with burn-associated ALI/ARDS; however, to our knowledge few reliable, reproducible models are available for pure SI animal model to investigate therapeutic options for ALI/ARDS without the confounding variables introduced by cutaneous burn or other pathology.ObjectiveTo develop a small animal model of pure SI-induced ALI and to use this model for eventual testing of novel therapeutics for ALI.MethodsRats were exposed to smoke using a custom-made smoke generator. Peripheral oxygen saturation (SpO2), heart rate, arterial blood gas, and chest X-ray (CXR) were measured before and after SI. Wet/dry weight (W/D) ratio, lung injury score and immunohistochemical staining of cleaved caspase 3 were performed on harvested lung tissues of healthy and SI animals.ResultsThe current study demonstrates the induction of ALI in rats after SI as reflected by a significant, sustained decrease in SpO2 and the development of diffuse bilateral pulmonary infiltrates on CXR. Lung tissue of animals exposed to SI showed increased inflammation, oedema and apoptosis as reflected by the increase in W/D ratio, injury score and cleaved caspase 3 level of the harvested tissues compared with healthy animals.ConclusionWe have successfully developed a small animal model of pure SI-induced ALI. This model is offered to the scientific community as a reliable model of isolated pulmonary SI-induced injury without the confounding variables of cutaneous injury or other systemic pathology to be used for study of novel therapeutics or other investigation.


Cells ◽  
2021 ◽  
Vol 10 (1) ◽  
pp. 63
Author(s):  
Ji Hye Kwon ◽  
Miyeon Kim ◽  
Soyoun Um ◽  
Hyang Ju Lee ◽  
Yun Kyung Bae ◽  
...  

In order to provide a sufficient number of cells for clinical use, mesenchymal stem cells (MSCs) must be cultured for long-term expansion, which inevitably triggers cellular senescence. Although the small size of MSCs is known as a critical determinant of their fate, the main regulators of stem cell senescence and the underlying signaling have not been addressed. Umbilical cord blood-derived MSCs (UCB-MSCs) were obtained using size-isolation methods and then cultured with control or small cells to investigate the major factors that modulate MSC senescence. Cytokine array data suggested that the secretion of interukin-8 (IL-8) or growth-regulated oncogene-alpha (GROa) by senescent cells was markedly inhibited during incubation of small cells along with suppression of cognate receptor (C-X-C motif chemokine receptor2, CXCR2) via blockade of the autocrine/paracrine positive loop. Moreover, signaling via toll-like receptor 2 (TLR2) and TLR5, both pattern recognition receptors, drove cellular senescence of MSCs, but was inhibited in small cells. The activation of TLRs (2 and 5) through ligand treatment induced a senescent phenotype in small cells. Collectively, our data suggest that small cell from UCB-MSCs exhibit delayed cellular senescence by inhibiting the process of TLR signaling-mediated senescence-associated secretory phenotype (SASP) activation.


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