دورية أكاديمية
The Orphan Receptor Tyrosine Kinase ROR2 Facilitates MSCs to Repair Lung Injury in ARDS Animal Model
| العنوان: | The Orphan Receptor Tyrosine Kinase ROR2 Facilitates MSCs to Repair Lung Injury in ARDS Animal Model |
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| المؤلفون: | Shi-Xia Cai, Ai-Ran Liu, Song Chen, Hong-Li He, Qi-Hong Chen, Jing-Yuan Xu, Chun Pan, Yi Yang, Feng-Mei Guo, Ying-Zi Huang, Ling Liu, Hai-Bo Qiu |
| المصدر: | Cell Transplantation, Vol 25 (2016) |
| بيانات النشر: | SAGE Publishing, 2016. |
| سنة النشر: | 2016 |
| المجموعة: | LCC:Medicine |
| مصطلحات موضوعية: | Medicine |
| الوصف: | There are some limitations to the therapeutic effects of mesenchymal stem cells (MSCs) on acute respiratory distress syndrome (ARDS) due to their low engraftment and differentiation rates in lungs. We found previously that noncanonical Wnt5a signaling promoted the differentiation of mouse MSCs (mMSCs) into type II alveolar epithelial cells (AT II cells), conferred resistance to oxidative stress, and promoted migration of MSCs in vitro. As receptor tyrosine kinase-like orphan receptor 2 (ROR2) is an essential receptor for Wnt5a, it was reasonable to deduce that ROR2 might be one of the key molecules for the therapeutic effect of MSCs in ARDS. The mMSCs that stably overexpressed ROR2 or the green fluorescent protein (GFP) control were transplanted intratracheally into the ARDS mice [induced by intratracheal injection of lipopolysaccharide (LPS)]. The results showed that ROR2-overexpressing mMSCs led to more significant effects than the GFP controls, including the retention of the mMSCs in the lung, differentiation into AT II cells, improvement of alveolar epithelial permeability, improvement of acute LPS-induced pulmonary inflammation, and, finally, reduction of the pathological impairment of the lung tissue. In conclusion, MSCs that overexpress ROR2 could further improve MSC-mediated protection against epithelial impairment in ARDS. |
| نوع الوثيقة: | article |
| وصف الملف: | electronic resource |
| اللغة: | English |
| تدمد: | 0963-6897 1555-3892 |
| Relation: | https://doaj.org/toc/0963-6897; https://doaj.org/toc/1555-3892 |
| DOI: | 10.3727/096368915X689776 |
| URL الوصول: | https://doaj.org/article/880008a866f94dbb9a1bc96d0f248d27 |
| رقم الأكسشن: | edsdoj.880008a866f94dbb9a1bc96d0f248d27 |
| قاعدة البيانات: | Directory of Open Access Journals |
Full Text Finder | تدمد: | 09636897 15553892 |
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| DOI: | 10.3727/096368915X689776 |