研究表明，兩個微RNA,，即miR-145 和 miR-143,，存在于小鼠胚胎的多能心臟先祖細胞中。
miR-145是由心肌蛋白誘導的成年成纖維細胞向平滑肌細胞內的重新編程所必需的,，并且足以誘導神經冠干細胞分化成“血管平滑肌細胞”（VSMC）,。miR-145 和 miR-143一起以一個轉錄因子網(wǎng)絡為目標，來促進平滑肌細胞的分化和抑制其增殖,。這些發(fā)現(xiàn)提供的證據(jù)表明,，微RNA能夠起開關的作用，引導細胞向某個特定的體系分化,。另外,，miR-145 和 miR-143在調控VSMC的分化表現(xiàn)型和增殖表現(xiàn)型中所起作用在很多血管類疾病中可能是有關系的，因為VSMC在這兩種狀態(tài)之間的振蕩有助于血管閉塞,。（生物谷Bioon.com）
生物谷推薦原始出處：
Nature 460, 705-710 (6 August 2009) | doi:10.1038/nature08195
miR-145 and miR-143 regulate smooth muscle cell fate and plasticity
Kimberly R. Cordes1,2,3, Neil T. Sheehy1,2,3, Mark P. White1,2,3, Emily C. Berry1,2,3, Sarah U. Morton1,2,3, Alecia N. Muth1,2,3, Ting-Hein Lee4, Joseph M. Miano4, Kathryn N. Ivey1,2,3 & Deepak Srivastava1,2,3
1 Gladstone Institute of Cardiovascular Disease, San Francisco, California 94158, USA
2 Department of Pediatrics, University of California, San Francisco, California 94543, USA
3 Department of Biochemistry & Biophysics, University of California, San Francisco, California 94143, USA
4 Aab Cardiovascular Research Institute, University of Rochester School of Medicine and Dentistry, Rochester, New York 14642, USA
MicroRNAs (miRNAs) are regulators of myriad cellular events, but evidence for a single miRNA that can efficiently differentiate multipotent stem cells into a specific lineage or regulate direct reprogramming of cells into an alternative cell fate has been elusive. Here we show that miR-145 and miR-143 are co-transcribed in multipotent murine cardiac progenitors before becoming localized to smooth muscle cells, including neural crest stem-cell-derived vascular smooth muscle cells. miR-145 and miR-143 were direct transcriptional targets of serum response factor, myocardin and Nkx2-5 (NK2 transcription factor related, locus 5) and were downregulated in injured or atherosclerotic vessels containing proliferating, less differentiated smooth muscle cells. miR-145 was necessary for myocardin-induced reprogramming of adult fibroblasts into smooth muscle cells and sufficient to induce differentiation of multipotent neural crest stem cells into vascular smooth muscle. Furthermore, miR-145 and miR-143 cooperatively targeted a network of transcription factors, including Klf4 (Kruppel-like factor 4), myocardin and Elk-1 (ELK1, member of ETS oncogene family), to promote differentiation and repress proliferation of smooth muscle cells. These findings demonstrate that miR-145 can direct the smooth muscle fate and that miR-145 and miR-143 function to regulate the quiescent versus proliferative phenotype of smooth muscle cells.
