: Autocrine fibroblast growth factor 2 increases the multipotentiality of human adipose-derived mesenchymal stem cells. Stem Cells , 26, 1598—1608.
16. Shroff, G., Agarwal, P., Mishra, A., Sonowal, N., 2015: Human embryonic stem cells in treatment of spinal cord injury: A prospective study. J. Neurol. Res. , 5, 213—220.
17. Slovinská, L., Székiová, E., Blaško, J., Devaux, S., Salzet, M., Čížková, D., 2015: Comparison of dynamic behaviour and maturation of neural multipotentcells derived from different spinal cord developmental stages: an in vitro study
Jolanta Opiela, Daniel Lipiński, Joanna Romanek, Wojciech Juzwa, Michał Bochenek and Piotr Wilczek
Mesenchymal stem cell (MSC) differentiation is regulated intrinsically by transcription factors and extrinsically by the extracellular matrix. We tested whether matrix metalloproteinase-2 (MMP-2) and its inhibitor TIMP-2, MEF2a and TAZ transcription factors are involved in porcine MSC differentiation towards adipocytes and osteocytes. Flow cytometry and immunofluorescence were used to investigate the expression levels of multipotent cell surface markers CD73 and CD105. Real- time PCR was performed to detect the osteogenic- and adipogenic-specific markers, osteocalcin and aP2, respectively, and to estimate the MMP-2, TIMP-2, MEF2a and TAZ transcript expression levels in three groups of cell, i.e., undifferentiated MSCs, adipocytes (A) and osteocytes (O). We showed that at the transcript level, the differentiation of MSCs towards adipocyte fate may involve MMP-2, TIMP-2 and TAZ. We also show that the differentiation of MSCs toward osteocyte fate may involve TIMP-2, MEF2a and TAZ. Our research provides preliminary data on the possible role of the MMP-2, TIMP-2 and TAZ transcripts in adipogenic differentiation and of the TIMP-2, TAZ and MEF2a transcripts in the osteogenic differentiation of porcine MSCs. We report for the first time the possible involvement of MEF2a in the osteogenesis of porcine MSCs. Our work may provide additional evidence for the MMP-independent function of TIMP-2 during osteogenesis.
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18. Jones EA, Kinsey SE, English A, et al. Isolation and characterization of bone marrow multipotential mesenchymal progenitor cells. Arthritis Rheum. 2002; 46:3349-60.
19. Wenisch S, Trinkaus K, Hild A, et al. Immunochemical, ultrastructural and electrophysiological investigations of bonederived stem cells in the course of neuronal differentiation. Bone. 2006; 38:911-21.
20. Yen B, Huang HI, Chien CC, et al. Isolation of multipotentcells from human term placenta. Stem Cells. 2005; 23: 3
Edmund C. Mbegbu, Ikechukwu R. Obidike and Ali A. Fouladi-Nashta
9. Rosner A, Moiseeva E, Rinkevich Y, Lapidot Z, Rinkevich B: Vasa and the germ line lineage in a colonial urochordate. Developmental Biology 2009, 331: 113–128.
10. Gustafson EA, Wessel GM: Vasa genes: Emerging roles in the germ line and in multipotentcells. Bioessays 2010, 32: 626–637.
11. Rouhana L, Shibata N, Nishimura O, Agata K: Different requirements for conserved post-transcriptional regulators in planarian regeneration and stem cell maintenance. Developmental Biology 2010, 341: 429–443.
12. Wagner DE, Ho JJ, Reddien PW
Güleser Saylam, Ömer Bayır, Salih Sinan Gültekin, Ferda Alparslan Pınarlı, Ünsal Han, Mehmet Hakan Korkmaz, Mehmet Eser Sancaktar, İlkan Tatar, Mustafa Fevzi Sargon and Emel Çadallı Tatar
cell administration superior to amifostine, and our findings may provide an alternative option, in absence of frequent side effects.
Stem cells can transform into different cells due to their regenerative capacity. 20 They have recently drawn attraction in regenerative medicine. 21 MSCs are present in mature tissues as multipotentcells, and can differentiate into specific cells that originate from the mesoderm. Mesenchymal cells have self-renewable properties; they can be easily cultured in vitro , and accepted by target tissues. MSCs can be isolated from
Bilal Mujtaba, Ahmed Taher, Matthew J. Fiala, Sameh Nassar, John E. Madewell, Abdelrahman K. Hanafy and Rizwan Aslam
affected tissues. 3 , 14 As a result, the most frequently used prophylactic medications are nonsteroidal anti-inflammatory drugs. 15 However, the underlying mechanisms for HO formation are still not clear. The Literature suggests multiple cellular origins for the formation of HO, pointing to muscle satellite cells 16 , smooth muscle cells 17 , and even endothelial cells. 18 Although the exact cellular origin is debated, it is commonly accepted to be multipotentcells in the local tissue. The requirements necessary for HO formation include having an inducing agent, an