LAUSR

Transforming growth factor β1 (TGFβ1) is a negative regulator of hematopoiesis, and yet, it is frequently found at the active sites of hematopoiesis. Here, we show for the first time that bone marrow‐derived mononuclear cells (BM MNCs) secrete TGFβ1 in response to erythropoietin (EPO). We further show that human bone marrow‐derived mesenchymal stromal cells (BMSCs) briefly exposed to the conditioned medium of EPO‐primed MNCs, or purified TGFβ1, gain significantly increased hematopoiesis‐supportive ability. Mechanistically, we show that this phenomenon involves TGFβ1‐mediated activation of nitric oxide (NO) signalling pathway in the BMSCs. The data suggest that EPO‐MNC‐TGFβ1 could be one of the regulatory axes operative in the bone marrow microenvironment involved in maintaining the functionality of the resident BMSCs.