2016
DOI: 10.1016/j.tvjl.2016.05.014
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Effects of pro-inflammatory cytokines on chondrogenesis of equine mesenchymal stromal cells derived from bone marrow or synovial fluid

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Cited by 29 publications
(33 citation statements)
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“…Besides, the cells carry limited potential to produce glycosaminoglycans (Zayed, Schumacher, Misk, & Dhar, 2016). Thus, to avoid such adverse effects of the inflammation, drugs to reduce the same may be used.…”
Section: Osteoarthritismentioning
confidence: 99%
“…Besides, the cells carry limited potential to produce glycosaminoglycans (Zayed, Schumacher, Misk, & Dhar, 2016). Thus, to avoid such adverse effects of the inflammation, drugs to reduce the same may be used.…”
Section: Osteoarthritismentioning
confidence: 99%
“…anti-microbial properties [59]), but might at the same time be involved in catabolic pathways [60]. Moreover, the leukocyte fraction in L-PRF has been reported to be accountable for the overproduction of several growth factors, including VEGF and inflammatory cytokines [59,61], which have been described to negatively impact chondrogenesis in vitro [31,[62][63][64][65][66][67]. In contrast, many other growth factors present in L-PRF ex and L-PRF CM are reported to have beneficial influences on MSC chondrogenesis [31,34,68,69].…”
Section: Discussionmentioning
confidence: 99%
“…However, the use of xenogenic MSCs is currently not recommended in clinical trials. MSCs have anti-inflammatory properties but high-end inflammation usually reduces their ability for chondrogenic differentiation without affecting their phenotypic characteristics and proliferation potential (Ando et al 2012;Zayed et al 2016). In equine OA, the limited efficacy of their MSCs may be explained by an increased expression of the adhesion molecule, a decrease in the migration of related genes (Barrachina et al 2016;Reesink et al 2017), and the production of glycosaminoglycans (Zayed et al 2016).…”
Section: In Vivo Preclinical Experimental Models/ Clinical Studiesmentioning
confidence: 99%
“…MSCs have anti-inflammatory properties but high-end inflammation usually reduces their ability for chondrogenic differentiation without affecting their phenotypic characteristics and proliferation potential (Ando et al 2012;Zayed et al 2016). In equine OA, the limited efficacy of their MSCs may be explained by an increased expression of the adhesion molecule, a decrease in the migration of related genes (Barrachina et al 2016;Reesink et al 2017), and the production of glycosaminoglycans (Zayed et al 2016). Pro-inflammatory cytokines like IL-1b, IL-17, and TNF-a decrease the expression levels of cartilage-specific genes like SOX-9 and TGF-b1, and those encoding aggrecan, collagen II (Kondo et al 2013;Zayed et al 2016), and galactin (Reesink et al 2017) in the MSCs.…”
Section: In Vivo Preclinical Experimental Models/ Clinical Studiesmentioning
confidence: 99%