IL-17 and FGF signaling involved in mouse mesenchymal stem cell proliferation

• Published in: Cell and tissue research Vol. 346; no. 3; pp. 305 - 316
• Main Authors: Mojsilović, Slavko, Krstić, Aleksandra, Ilić, Vesna, Okić-Đorđević, Ivana, Kocić, Jelena, Trivanović, Drenka, Santibañez, Juan Francisko, Jovčić, Gordana, Bugarski, Diana
• Format: Journal Article
• Language: English
• Published: Berlin/Heidelberg Springer-Verlag 01-12-2011; Springer; Springer Nature B.V
• Subjects: Animals; Biomedical and Life Sciences; Biomedicine; Bone marrow; Cell Growth Processes - drug effects; Cell Growth Processes - physiology; Cells, Cultured; Fibroblast growth factors; Fibroblast Growth Factors - metabolism; Fibroblast Growth Factors - pharmacology; Gene therapy; Human Genetics; Interleukin-17 - metabolism; Interleukin-17 - pharmacology; Interleukins; Kinases; Male; Mesenchymal Stromal Cells - cytology; Mesenchymal Stromal Cells - drug effects; Mesenchymal Stromal Cells - metabolism; Mice; Mice, Inbred A; Mice, Inbred BALB C; Mice, Inbred C57BL; Mice, Inbred CBA; Mitogens; Molecular biology; Molecular Medicine; Phosphotransferases; Proteomics; Recombinant Proteins - pharmacology; Regular Article; Rodents; Signal Transduction; Stem cells; Tissue engineering; Signaling; Mouse; bFGF; IL-17; Mesenchymal stem cells
• ISSN: 0302-766X; 1432-0878
• DOI: 10.1007/s00441-011-1284-5

The mouse is a suitable experimental model to study the biology of mesenchymal stem cells (MSCs), as well as to be used in biocompatibility studies and tissue engineering models. However, the isolation and purification of murine MSCs is far more challenging than their counterparts from other species. In this study, we isolated, expanded and characterized mouse MSCs from bone marrow (BM-MSCs). Additionally, we analyzed the effects of two regulatory molecules, interleukin 17 (IL-17) and basic fibroblast growth factor (bFGF), on BM-MSCs growth and elucidated the signaling pathways involved. The results revealed that IL-17 increased the frequency of colony-forming units fibroblast (CFU-F) as well as the BM-MSCs proliferation in a dose-dependent manner, while bFGF supplementation had no significant effect on CFU-F frequency but induced an increase in cell proliferation. Their combined usage did not produce additive effects on BM-MSCs proliferation and even induced reduction in the number of CFU-F. Also, the involvement of both p38 and extracellular signal-regulated kinase (ERK) mitogen-activated protein kinases (MAPKs) signaling in proliferative activity of IL-17 and bFGF on murine BM-MSCs and, moreover, the increased co-activation of a common signaling molecule, p38 MAPK, were demonstrated. Together, the data presented highlighted the role of IL-17 and bFGF in murine BM-MSCs proliferation and pointed to the complexity and specificity of the signaling networks leading to MSCs proliferation in response to different regulatory molecules.