| First Author | Kim JI | Year | 2009 |
| Journal | Histochem Cell Biol | Volume | 132 |
| Issue | 2 | Pages | 191-8 |
| PubMed ID | 19437030 | Mgi Jnum | J:151682 |
| Mgi Id | MGI:4354722 | Doi | 10.1007/s00418-009-0604-2 |
| Citation | Kim JI, et al. (2009) Expression of CPI-17 in smooth muscle during embryonic development and in neointimal lesion formation. Histochem Cell Biol 132(2):191-8 |
| abstractText | Ca(2+) sensitivity of smooth muscle (SM) contraction is determined by CPI-17, an inhibitor protein for myosin light chain phosphatase (MLCP). CPI-17 is highly expressed in mature SM cells, but the expression level varies under pathological conditions. Here, we determined the expression of CPI-17 in embryonic SM tissues and arterial neointimal lesions using immunohistochemistry. As seen in adult animals, the predominant expression of CPI-17 was detected at SM tissues on mouse embryonic sections, whereas MLCP was ubiquitously expressed. Compared with SM alpha-actin, CPI-17 expression doubled in arterial SM from embryonic day E10 to E14. Like SM alpha-actin and other SM marker proteins, CPI-17 was expressed in embryonic heart, and the expression was down-regulated at E17. In adult rat, CPI-17 expression level was reduced to 30% in the neointima of injured rat aorta, compared with the SM layers, whereas the expression of MLCP was unchanged in both regions. Unlike other SM proteins, CPI-17 was detected at non-SM organs in the mouse embryo, such as embryonic neurons and epithelium. Thus, CPI-17 expression is reversibly controlled in response to the phenotype transition of SM cells that restricts the signal to differentiated SM cells and particular cell types. |
