التفاصيل البيبلوغرافية
| العنوان: |
Extramedullary hematopoiesis generates Ly-6C(high) monocytes that infiltrate atherosclerotic lesions. |
| المؤلفون: |
Robbins CS (AUTHOR), Chudnovskiy A (AUTHOR), Rauch PJ (AUTHOR), Figueiredo JL (AUTHOR), Iwamoto Y (AUTHOR), Gorbatov R (AUTHOR), Etzrodt M (AUTHOR), Weber GF (AUTHOR), Ueno T (AUTHOR), van Rooijen N (AUTHOR), Mulligan-Kehoe MJ (AUTHOR), Libby P (AUTHOR), Nahrendorf M (AUTHOR), Pittet MJ (AUTHOR), Weissleder R (AUTHOR), Swirski FK (AUTHOR), Robbins, Clinton S1 (AUTHOR), Chudnovskiy, Aleksey (AUTHOR), Rauch, Philipp J (AUTHOR), Figueiredo, Jose-Luiz (AUTHOR) |
| المصدر: |
Circulation. 1/17/2012, Vol. 125 Issue 2, p364-374. 11p. |
| مستخلص: |
Background: Atherosclerotic lesions are believed to grow via the recruitment of bone marrow-derived monocytes. Among the known murine monocyte subsets, Ly-6C(high) monocytes are inflammatory, accumulate in lesions preferentially, and differentiate. Here, we hypothesized that the bone marrow outsources the production of Ly-6C(high) monocytes during atherosclerosis.Methods and Results: Using murine models of atherosclerosis and fate-mapping approaches, we show that hematopoietic stem and progenitor cells progressively relocate from the bone marrow to the splenic red pulp, where they encounter granulocyte macrophage colony-stimulating factor and interleukin-3, clonally expand, and differentiate to Ly-6C(high) monocytes. Monocytes born in such extramedullary niches intravasate, circulate, and accumulate abundantly in atheromata. On lesional infiltration, Ly-6C(high) monocytes secrete inflammatory cytokines, reactive oxygen species, and proteases. Eventually, they ingest lipids and become foam cells.Conclusions: Our findings indicate that extramedullary sites supplement the hematopoietic function of the bone marrow by producing circulating inflammatory cells that infiltrate atherosclerotic lesions. [ABSTRACT FROM AUTHOR] |
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