mCAT got youR TEF?
mCAT got youR TEF?
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DOI：
10.1161/circresaha.107.164053
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发表时间：
2007-10
影响因子：
20.1
通讯作者：
B. Herring;Jiliang Zhou
中科院分区：
文献类型：
--
作者：
B. Herring;Jiliang Zhou
See related article, pages 883–892 Adult smooth muscle cells are highly plastic and can exhibit a range of phenotypes in response to different environmental and developmental cues. Their phenotypes can range from quiescent highly contractile cells with high levels of characteristic contractile protein isoforms, to highly proliferative cells that secrete large amounts of extracellular matrix and express only low levels of smooth muscle-specific isoforms of contractile proteins. These two states are often referred to as differentiated and dedifferentiated or phenotypically modulated states.1 In reality the situation is more complex, with smooth muscle cells likely existing in a continuum of phenotypes between these two extremes. This smooth muscle cell plasticity often makes the unequivocal identification of smooth muscle cells challenging, particularly for the more dedifferentiated smooth muscle cells that are very similar to fibroblasts. The situation is further complicated by the existence of cell types with phenotypes part way between a fibroblast and a fully differentiated adult smooth muscle cell, namely myoepithelial and myofibroblast cells, and pericytes.2–4 A major challenge to developmental biologists is determining how these cells relate to each other, determining whether they are derived from common or distinct precursors, and whether myofibroblasts or pericytes can become smooth muscle cells. One approach to begin to answer these questions is to determine the molecular mechanisms that control the phenotype of each of these cell types. A new study by Gan and colleagues,5 described in this issue of Circulation Research , provides definitive molecular evidence that distinguishes myofibroblasts from adult smooth muscle cells by the distinct transcriptional mechanisms that they use to direct expression of a shared molecular marker, smooth muscle α-actin. In this elegant study, the authors demonstrate that the binding of RTEF-1 to MCAT elements within the smooth muscle α-actin promoter is required for transcription …
