Macrophages become polarized by cues in their environment and this polarization causes a functional change in their behavior. Two main subsets of polarized macrophages have been described. M1, or "classically activated" macrophages, are pro-inflammatory and M2, or "alternatively activated" macrophages, are anti-inflammatory. In this study, we investigated the motility and force generation of primary human macrophages polarized down the M1 and M2 pathways using chemokinesis assays and traction force microscopy on polyacrylamide gels. We found that M1 macrophages are significantly less motile and M2 macrophages are significantly more motile than unactivated M0 macrophages. We also showed that M1 macrophages generate significantly less force than M0 or M2 macrophages. We further found that M0 and M2, but not M1, macrophage force generation is dependent on ROCK signaling, as identified using the chemical inhibitor Y27632. Finally, using the chemical inhibitor blebbistatin, we found that myosin contraction is required for force generation by M0, M1, and M2 macrophages. This study represents the first investigation of the changes in the mechanical motility mechanisms used by macrophages after polarization.
Effect of M1-M2 Polarization on the Motility and Traction Stresses of Primary Human Macrophages
Creators
Laurel E. Hind - University of Pennsylvania
Emily B. Lurier - Drexel University
Micah Dembo - Department of Biomedical Engineering Boston University Boston MA
Kara L. Spiller - Drexel University
Daniel A. Hammer - University of Pennsylvania
Publication Details
Cellular and molecular bioengineering, v 9(3), pp 455-465
Publisher
Springer Nature
Number of pages
11
Grant note
GM1094287; HL18208 / NIH; United States Department of Health & Human Services; National Institutes of Health (NIH) - USA
P01HL018208 / NATIONAL HEART, LUNG, AND BLOOD INSTITUTE; United States Department of Health & Human Services; National Institutes of Health (NIH) - USA; NIH National Heart Lung & Blood Institute (NHLBI)
R01GM104287 / NATIONAL INSTITUTE OF GENERAL MEDICAL SCIENCES; United States Department of Health & Human Services; National Institutes of Health (NIH) - USA; NIH National Institute of General Medical Sciences (NIGMS)
Resource Type
Journal article
Language
English
Academic Unit
School of Biomedical Engineering, Science, and Health Systems
Web of Science ID
WOS:000381594700013
Scopus ID
2-s2.0-84964344260
Other Identifier
991019168590404721
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