| First Author | Wasson R | Year | 2024 |
| Journal | Physiol Rep | Volume | 12 |
| Issue | 14 | Pages | e16139 |
| PubMed ID | 39016176 | Mgi Jnum | J:351633 |
| Mgi Id | MGI:7702869 | Doi | 10.14814/phy2.16139 |
| Citation | Wasson R, et al. (2024) Bone marrow monocytes and macrophages from mice lacking betaENaC and ASIC2 have a reduced chemotactic migration response and polarization. Physiol Rep 12(14):e16139 |
| abstractText | The monocyte-macrophage system plays an important role in phagocytosis of pathogens and cellular debris following infection or tissue injury in several pathophysiological conditions. We examined ENaC/ASIC subunit transcript expression and the importance of select subunits in migration of bone marrow derived monocytes (freshly isolated) and macrophages (monocytes differentiated in culture). We also examined the effect of select subunit deletion on macrophage phenotype. BM monocytes were harvested from the femurs of male and female WT and KO mice (6-12 weeks of age). Our results show that alpha, beta, gammaENaC, and ASIC1-5 transcripts are expressed in BM macrophages and monocytes to varying degrees. At least alphaENaC, betaENaC, and ASIC2 subunits contribute to chemotactic migration responses in BM monocyte-macrophages. Polarization markers (CD86, soluble TNFalpha) in BM macrophages from mice lacking ASIC2a plus betaENaC were shifted towards the M1 phenotype. Furthermore, select M1 phenotypic markers were recovered with rescue of betaENaC or ASIC2. Taken together, these data suggest that betaENaC and ASIC2 play an important role in BM macrophage migration and loss of betaENaC and/or ASIC2 partially polarizes macrophages to the M1 phenotype. Thus, targeting ENaC/ASIC expression in BM macrophages may regulate their ability to migrate to sites of injury. |
