Key result
Endothelin-1 increases M2 macrophage markers and MMP-9 production in cultured human macrophages versus controls.
Why the study?
The role of endothelin-1 in inducing the transition of cultured human macrophages into the alternatively activated M2 phenotype involved in fibrosis was investigated.
Does Endothelin-1 induce the transition of cultured human macrophages into the M2 phenotype?
Population
Cultured human monocytes (THP-1) and primary human peripheral blood monocyte-derived macrophages from healthy subjects
Comparison
Endothelin-1 treatment vs growth medium or interleukin-4
Design
Preclinical in vitro study
Follow-up
72 hours to 6 days
Authors
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Endothelin-1 may promote pro-fibrotic macrophage activity in vitro; leaves open relevance to human fibrosis and need for in vivo confirmation.
Does Endothelin-1 induce the transition of cultured human macrophages into the M2 phenotype?
p-value: p=<0.05
Endothelin-1 induces the alternatively activated (M2) pro-fibrotic macrophage phenotype in vitro, which can be blocked by an endothelin receptor antagonist like bosentan.
Soldano et al. (2016) studied Healthy subjects (in vitro macrophage study) (n=6). Endothelin-1 (ET-1) vs. Untreated cells (growth medium) was evaluated on Expression of M2 phenotype markers (CD204, CD206, CD163, IL-10, CCL-22) and MMP-9 production (p=<0.05). Endothelin-1 significantly increased the expression of M2 macrophage phenotype markers and MMP-9 production in cultured human macrophages compared to untreated controls.
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