| Literature DB >> 28181347 |
Miguel F Diaz1,2, Abishek B Vaidya1,2, Siobahn M Evans1,2, Hyun J Lee1,2, Benjamin M Aertker1, Alexander J Alexander1,2,3, Katherine M Price1,2,3, Joyce A Ozuna1,2,3, George P Liao1, Kevin R Aroom1, Hasen Xue1, Liang Gu1,2, Rui Omichi1,2,4, Supinder Bedi1, Scott D Olson1, Charles S Cox1,2, Pamela L Wenzel1,2.
Abstract
Mesenchymal stromal cells (MSCs) are believed to mobilize from the bone marrow in response to inflammation and injury, yet the effects of egress into the vasculature on MSC function are largely unknown. Here we show that wall shear stress (WSS) typical of fluid frictional forces present on the vascular lumen stimulates antioxidant and anti-inflammatory mediators, as well as chemokines capable of immune cell recruitment. WSS specifically promotes signaling through NFκB-COX2-prostaglandin E2 (PGE2 ) to suppress tumor necrosis factor-α (TNF-α) production by activated immune cells. Ex vivo conditioning of MSCs by WSS improved therapeutic efficacy in a rat model of traumatic brain injury, as evidenced by decreased apoptotic and M1-type activated microglia in the hippocampus. These results demonstrate that force provides critical cues to MSCs residing at the vascular interface which influence immunomodulatory and paracrine activity, and suggest the potential therapeutic use of force for MSC functional enhancement. Stem Cells 2017;35:1259-1272.Entities:
Keywords: Biomechanical force; Immunomodulation; Inflammation; Mesenchymal stromal cells; Shear stress; Traumatic brain injury
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Year: 2017 PMID： 28181347 PMCID： PMC5405000 DOI： 10.1002/stem.2587
Source DB: PubMed Journal: Stem Cells ISSN： 1066-5099 Impact factor: 6.277