The official MedZine Blog

Interpretation of medical news

Macrophage proliferation in atherosclerosis and microRNA triggers lymphoma

Macrophage proliferation in atherosclerosis and microRNA triggers lymphoma

Also this week MedZine brings you the latest medical news on various medical specialisms. In this editorial two striking studies are highlighted. The first identifies macrophage proliferation as a driving force in atherosclerosis. The second shows how microRNAs trigger lymphoma.

Atherosclerosis and macrophage proliferation

Previously, it was thought that atherosclerotic plaques grow by drawing monocytes in from the circulation. The monocytes mature into macrophages and each monocyte generates one macrophage. The macrophages ingest lipid and cholesterol molecules, which leads to the buildup of a fatty core that contributes to the risk of plaque rupture. Heart attacks and strokes can be the result. In a publication in Nature Medicine, Robbins and colleagues describe that proliferation of new macrophages within plaques is a major driver of their growth. The atherosclerotic lesion is a very dynamic environment. In a series of experiments in mice, the researchers found that existing plaques within the aortas of animals fed a high-cholesterol diet showed evidence of a rapid and constant proliferation of macrophages, which did not require the presence of monocytes in the blood. Although monocytes were needed for the initiation of atherosclerosis, once plaques had formed, macrophage proliferation became the primary mechanism for the further growth of plaques. In addition, a receptor on macrophages that appears to contribute to their proliferation within plaques was identified. Furthermore, the researchers found evidence of macrophage proliferation in plaques from human carotid arteries.

Lymphoma triggered by microRNAs

MicroRNAs (miRNAs) have been broadly implicated in cancer, but their exact function remains unclear. A cluster of miRNAs, miR-17~92, is often overexpressed in human cancers. In a publication in EMBO Journal, Jin and colleagues show that miR-17~92 triggers lymphoma. The researchers showed that 80% of transgenic mice overexpressing miR-17~92 in B cells develop lymphoma within one year. In addition, in a mouse model of Burkitt lymphoma deletion of miR-17~92 delayed the development of lymphoma and prolonged survival of the mice. The lymphomas that did develop where derived from cells that still expressed miR-17~92. By analyzing the binding sites of miR-17~92 to messenger RNA, genes that are suppressed by miR-17~92 were identified. Many of these inhibit cell growth and survival programs. Chemical inhibitors of two of these genes could lead to shrinkage of tumors and prolonged survival when injected in mice with miR-17~92-driven lymphoma. The researchers conclude that miR-17~92 is a powerful cancer driver that coordinates the activation of multiple oncogenic pathways. These findings also indicate that chemical inhibition of miRNA downstream pathways has therapeutic value.

Sources: Eurekalert, Nature Medicine and EMBO Journal

Read more testimonials by health care professionals and advertisers

Follow us