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Diez-Torre A.,University of the Basque Country | Diaz-Nunez M.,University of the Basque Country | Eguizabal C.,Center for Regenerative Medicine Barcelona | Silvan U.,ETH Zurich | Arechaga J.,University of the Basque Country
Andrology | Year: 2013

Summary: Understanding the mechanisms that enable migrating cells to reach their targets is of vital importance, as several pathologies, including cardiac defects and some tumours, are consequences of altered cell migration. With a view to evaluating if matrix metalloproteinases (MMPs) and their tissue inhibitors (TIMPs) play a role in the active migration of primordial germ cells (PGCs) from their place of origin in extra-embryonic sites towards their final destination in the developing gonads, we analysed the expression of mRNAs encoding nine MMPs and four TIMPs in migrating (E10.5) and post-migrating (E12.5) PGCs by means of quantitative polymerase chain reaction and the presence of MT1-MMP in the membrane of these cells. Our results show that PGCs express MMP-2, MMP-9, MMP-11, MT1-MMP, TIMP-1, TIMP-2 and TIMP-3 at both migrating and non-migrating stages. Comparing expression levels of MMP genes between E10.5 and E12.5 PGCs revealed higher expression in migrating PGCs of MT1- MMP (10.3-fold), MMP-2 (4.8-fold), MMP-11 (3.2-fold) and MMP-9 (2.1-fold). Similarly, the levels of TIMP gene expression were always higher in E12.5 genital ridge somatic cells: TIMP-3 (3.4-fold), TIMP-1 (2.4-fold) and TIMP-2 (1.8-fold). Moreover, the analysis at protein level showed the presence of MT1-MMP in the membrane of migrating PGCs whereas the expression of these metalloproteinase is not detected once the PGCs have reach the urogenital ridges and stop migrating. These results suggest that the change from the motile to non-motile phenotype that occurs during PGC maturation to gonocytes may be mediated in part by enhanced expression of MMPs in migrating PGCs together with higher expression of TIMPs in E12.5 genital ridges. © 2013 American Society of Andrology and European Academy of Andrology. Source

Menendez S.,Center for Regenerative Medicine Barcelona | Camus S.,Center for Regenerative Medicine Barcelona | Belmonte J.C.I.,Center for Regenerative Medicine Barcelona | Belmonte J.C.I.,Salk Institute for Biological Studies
Cell Cycle | Year: 2010

The reprogramming of somatic cells to induced pluripotent stem (iPS) cells is one of the major discoveries of recent years. The development and application of patient specific iPS lines could potentially revolutionise cell-based therapy, facilitating the treatment of a wide range of diseases. Despite the numerous technological advancements in the field, an indepth mechanistical understanding of the pathways involved in reprogramming is still lacking. Several groups have recently provided a mechanistical insight into the role of the p53 tumour suppressor pathway in reprogramming. The repercussions of these findings are profound and reveal an unexpected role of p53 as a "guardian of reprogramming", ensuring genomic integrity during reprogramming at the cost of a reduced efficiency of the process. Here we analyse the latest findings in the field and discuss their relevance for future applications of iPS cell technology. © 2010 Landes Bioscience. Source

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