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Replicative senescence of periodontal fibroblasts induces the changes in gene expression pattern
Yi, Tac Ghee,Jun, JI-Hae,Min, Byung-Moo,Kim, Moonkyu,Kim, Gwan-shik,Baek, Jeong-Hwa 대한구강생물학회 2007 International Journal of Oral Biology Vol.32 No.1
Tooth loss in elderly is mainly caused by alveolar bone loss via severe periodontitis. Although the severity of periodontitis is known to be affected by age, the aging process or the genetic changes during the aging of periodontal tissue cells are not well characterized. In this study, we investigated the effect of in vitro aging on the change of gene expression pattern in periodontal fibroblasts. Gingival fibroblasts (GF) and periodontal ligament fibroblasts (PDL) were obtained from two young patients and replicative senescence was induced by sequential subcultivation. When more than 90% cells were positively stained with senescence-associated β-galactosidase, those cells were regarded as aged cells. In aged GF and PDL, the level of phosphorylated retinoblastoma (RB) and p16^(INK4A) protein was significantly decreased and increased, respectively. However, the protein level of p53 and p21, well known senescence-inducing genes, did not increase in aged GF and PDL. Although p27^(kip1) and p15^(INK4B) another cyclin-dependent kinase inhibitors, were reported to be involved in replicative senescence of human cells, they were decreased in aged GF and PDL. Because senescent cells showed flattened and enlarged cell shape and are known to have increased focal adhesion, we examined the protein level of several integrins. Aged GF and PDL showed increased protein level of integrin α2, αv, and β1. When the gene expression profiles of actively proliferating young cells and aged cells were compared by cDNA microarray of 3,063 genes and were confirmed by reverse transcription polymerase chain reaction, 7 genes and 15 genes were significantly and commonly increased and decreased, respectively, in aged GF and PDL. Among them, included are the genes that were known to be involved in the regulation of cell cycle, gene transcription, or integrin signaling. The change of gene expression pattern in GF and PDL was minimally similar to that of oral keratinocyte. These results suggest that p16^(INK4A)/RB might be involved in replicative senescence of periodontal fibroblasts and the change of gene expression profile during aging process is cell type specific.
Park, Jin Seok,Yi, Tac-Ghee,Park, Jong-Min,Han, Young Min,Kim, Jun-Hyung,Shin, Dong-Hee,Tak, Seon Ji,Lee, Kyuheon,Lee, Youn Sook,Jeon, Myung-Shin,Hahm, Ki-Baik,Song, Sun U,Park, Seok Hee the Society for Free Radical Research Japan 2015 Journal of clinical biochemistry and nutrition Vol.57 No.3
<P>Mouse bone marrow-derived clonal mesenchymal stem cells (mcMSCs), which were originated from a single cell by a subfractionation culturing method, are recognized as new paradigm for stem cell therapy featured with its homogenous cell population. Next to proven therapeutic effects against pancreatitis, in the current study we demonstrated that mcMSCs showed significant therapeutic effects in dextran sulfate sodium (DSS)-induced experimental colitis model supported with anti-inflammatory and restorative activities. mcMSCs significantly reduced the disease activity index (DAI) score, including weight loss, stool consistency, and intestinal bleeding and significantly increased survival rates. The pathological scores were also significantly improved with mcMSC. We have demonstrated that especial mucosal regeneration activity accompanied with significantly lowered level of apoptosis as beneficiary actions of mcMSCs in UC models. The levels of inflammatory cytokines including TNF-α, IFN-γ, IL-1β, IL-6, and IL-17 were all significantly concurrent with significantly repressed NF-κB activation compared to the control group and significantly decreased infiltrations of responsible macrophage and neutrophil. Conclusively, our findings provide the rationale that mcMSCs are applicable as a potential source of cell-based therapy in inflammatory bowel diseases, especially contributing either to prevent relapse or to accelerate healing as solution to unmet medical needs in IBD therapy.</P>
Msx2 mediates the inhibitory action of TNF-${\alpha}$ on osteoblast differentiation
Lee, Hye-Lim,Yi, Tac-Ghee,Woo, Kyung-Mi,Ryoo, Hyun-Mo,Kim, Gwan-Shik,Baek, Jeong-Hwa Korean Society for Biochemistry and Molecular Bion 2010 Experimental and molecular medicine Vol.42 No.6
TNF-${\alpha}$, a proinflammatory cytokine, inhibits osteoblast differentiation under diverse inflammatory conditions; however, the underlying mechanisms in terms of the TNF-${\alpha}$ signaling pathway remain unclear. In this study, we examined the role of Msx2 in TNF-${\alpha}$-mediated inhibition of alkaline phosphatase (ALP) expression and the signaling pathways involved. TNF-${\alpha}$ down-regulated ALP expression induced by bone morphogenetic protein 2 (BMP2) in C2C12 and Runx2$^{-/-}$ calvarial cells. Over-expression of Msx2 suppressed BMP2-induced ALP expression. Furthermore, TNF-${\alpha}$ induced Msx2 expression, and the knockdown of Msx2 by small interfering RNAs rescued ALP expression, which was inhibited by TNF-${\alpha}$. TNF-${\alpha}$ activated the NF-${\kappa}$B and the JNK pathways. Inhibition of NF-${\kappa}$B or JNK activation reduced the inhibitory effect of TNF-${\alpha}$ on ALP expression, whereas TNF-${\alpha}$-induced Msx2 expression was only suppressed by the inhibition of the NF-${\kappa}$B pathway. Taken together, these results indicate that Msx2 mediates the inhibitory action of TNF-${\alpha}$ on BMP2-regulated osteoblast differentiation and that the TNF-${\alpha}$-activated NF-${\kappa}$B pathway is responsible for Msx2 induction.