| First Author | Mthunzi L | Year | 2023 |
| Journal | Am J Physiol Lung Cell Mol Physiol | Volume | 325 |
| Issue | 2 | Pages | L270-L276 |
| PubMed ID | 37401390 | Mgi Jnum | J:341245 |
| Mgi Id | MGI:7516478 | Doi | 10.1152/ajplung.00163.2023 |
| Citation | Mthunzi L, et al. (2023) Gremlin 1 is required for macrophage M2 polarization. Am J Physiol Lung Cell Mol Physiol 325(2):L270-L276 |
| abstractText | Pro-proliferative, M2-like polarization of macrophages is a critical step in the development of fibrosis and remodeling in chronic lung diseases such as pulmonary fibrosis and pulmonary hypertension. Macrophages in healthy and diseased lungs express gremlin 1 (Grem1), a secreted glycoprotein that acts in both paracrine and autocrine manners to modulate cellular function. Increased Grem1 expression plays a central role in pulmonary fibrosis and remodeling, however, the role of Grem1 in M2-like polarization of macrophages has not previously been explored. The results reported here show that recombinant Grem1 potentiated M2-like polarization of mouse macrophages and bone marrow-derived macrophages (BMDMs) in response to the Th2 cytokines IL4 and IL13. Genetic depletion of Grem1 in BMDMs inhibited M2 polarization while exogenous gremlin 1 could partially rescue this effect. Taken together, these findings reveal that gremlin 1 is required for M2-like polarization of macrophages.NEW & NOTEWORTHY We show here that gremlin 1 potentiated M2 polarization of mouse bone marrow-derived macrophages (BMDMs) in response to the Th2 cytokines IL4 and IL13. Genetic depletion of Grem1 in BMDMs inhibited M2 polarization while exogenous gremlin 1 partially rescued this effect. Taken together, these findings reveal a previously unknown requirement for gremlin 1 in M2 polarization of macrophages and suggest a novel cellular mechanism promoting fibrosis and remodeling in lung diseases. |
