WITHDRAWN: Toll-like receptor-4 Signaling Improved the Migration of Sca-1+stem/progenitor Cells
| Autor: | Xiaogang Zhang, Daifu Zhang, Chunya Zhang, Ying Huang, Jinghua Shen, Jian-Qing Du |
|---|---|
| Rok vydání: | 2017 |
| Předmět: |
0301 basic medicine
Toll-like receptor Gene knockdown business.industry General Medicine Matrix metalloproteinase Cell biology 03 medical and health sciences 030104 developmental biology medicine.anatomical_structure Immunology TLR4 Medicine Surgery Bone marrow Progenitor cell Cardiology and Cardiovascular Medicine business Receptor Wound healing |
| Zdroj: | Annals of Vascular Surgery. |
| ISSN: | 0890-5096 |
| DOI: | 10.1016/j.avsg.2017.07.022 |
| Popis: | Atherosclerosis is considered as a chronic inflammatory process, during which macrophages and smooth muscle cells migrate into the vascular wall intima to initiate atherogenesis. Stem/progenitor cells (SPCs) have been demonstrated as a new source of monocytes/macrophages and smooth muscle cells (SMCs). However, the regulation of SPCs migration into atherosclerotic initiation sites to produce macrophages and SMCs in-situ is not fully elucidated. As toll-like receptor (TLRs) signaling plays essential role in migration of immunocytes, we wanted to explore the expression and function of TLRs in SPCs in detail. For this we isolated Sca-1 + bone marrow cells as SPCs, and TLRs were detected with quantitative RT-PCR and Western blotting. Our data show that multiple TLRs expressed on SPCs, with TLR4 as the most prominent one, and activation of TLR4 in SPCs is required for migration as assessed by conventional wound healing and transwell assays. Knockdown of TLR4 expression abrogates the migration of SPCs significantly, and re-expression restores it, further confirming functions of TLR4 in regulating SPCs biological behavior. In summary, our study shows the essential function of TLR4 signaling in SPC migration, strongly suggesting of its role in atherosclerotic lesion formation. Our data provide new insight into the biological regulators in SPC migration, with potential consequences for therapeutics of atherosclerosis. |
| Databáze: | OpenAIRE |
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