Table 1.
Gene Expression Profiling Reveals Alternative Activation of Macrophages in Laser-Induced Wound Healing
| Marker | Fold change |
|
|---|---|---|
| 0 vs 68 hours | 68 vs 116 hours | |
| Pan-macrophage markers | ||
| CD68 | 4.14 | 1.03 |
| CD11b | 5.62 | −1.27 |
| M2-type markers | ||
| Arg-1 | 81.23 | −13.23 |
| YM1 | 14.95 | −2.25 |
| CCL17 | 10.53 | −1.68 |
| IL-1RA | 24.36 | −1.42 |
| M1-type markers | ||
| iNOS | 1.06 | −2.19 |
| TNF-α | 1.30 | −1.03 |
| CXCL9 | 1.30 | 1.07 |
| CXCL11 | 1.23 | −1.05 |
| IL-12A | 1.03 | −1.12 |
| Growth factors | ||
| VEGF-A | −1.16 | −1.02 |
| IL-1β | 3.03 | −2.56 |
Gene expression profiling reveals that infiltrating macrophages in laser-induced CNV lesions are alternatively activated (M2-type macrophages), with strong upregulation of the prototypic M2-type markers arginase 1 (Arg-1, >80-fold) and YM1. Infiltration of alternatively activated macrophages into CNV lesions peaks at approximately 68 hours. IL-1β transcripts were also upregulated at 68 hours after laser injury. n = 3 per group.