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المؤلفOuhtit, Allal
المؤلفThouta, Rajesh
المؤلفZayed, Hatem
المؤلفGaur, Rajiv L
المؤلفFernando, Augusta
المؤلفRahman, Mizanur
المؤلفWelsh, David A
تاريخ الإتاحة2020-07-20T05:59:48Z
تاريخ النشر2020-05-01
اسم المنشورInternational Journal of Medical Sciences
المعرّفhttp://dx.doi.org/10.7150/ijms.33125
الاقتباسOuhtit A, Thouta R, Zayed H, Gaur RL, Fernando A, Rahman M, Welsh DA. CD44 mediates stem cell mobilization to damaged lung via its novel transcriptional targets, Cortactin and Survivin. Int J Med Sci 2020; 17(1):103-111. doi:10.7150/ijms.33125. Available from http://www.medsci.org/v17p0103.htm
معرّف المصادر الموحدhttp://hdl.handle.net/10576/15296
الملخصBeyond their role in bone and lung homeostasis, mesenchymal stem cells (MSCs) are becoming popular in cell therapy. Various insults may disrupt the repair mechanisms involving MSCs. One such insult is smoking, which is a major risk factor for osteoporosis and respiratory diseases. Upon cigarette smoke-induced damage, a series of reparatory mechanisms ensue; one such mechanism involves Glycosaminoglycans (GAG). One of these GAGs, namely hyaluronic acid (HA), serves as a potential therapeutic target in lung injury. However, much of its mechanisms of action through its major receptor CD44 remains unexplored. Our previous studies have identified and functionally validated that both cortactin (CTTN: marker of motility) and Survivin (BIRC5: required for cell survival) act as novel HA/CD44-downstream transcriptional targets underpinning cell motility. Here, human MSCs were treated with "" smoke to investigate the effects of cigarette smoke condensate (CSC) on these HA-CD44 novel signaling pathways. Our results show that CSC decreased the expression of both CD44 and its downstream targets CTTN and BIRC5 in MSCs, and that HA reversed these effects. Interestingly, CSC inhibited migration and invasion of MSCs upon CD44-targeted RNAi treatment. This shows the importance of CD44-HA/CTTN and CD44-HA/BIRC5 signaling pathways in MSC motility, and further suggests that these signaling pathways may provide a novel mechanism implicated in migration of MSCs during repair of lung tissue injury. These findings suggest that one should use caution before utilizing MSC from donors with history of smoking, and further pave the way towards the development of targeted therapeutic approaches against CD44-associated diseases.
اللغةen
الناشرIvyspring International Publisher
الموضوعCD44
Cortactin
Survivin
cigarette smoke
mesenchymal stem cells
العنوانCD44 mediates stem cell mobilization to damaged lung via its novel transcriptional targets, Cortactin and Survivin
النوعArticle
الصفحات103-111
رقم العدد1
رقم المجلد17
dc.accessType Open Access


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