Mouse IHH peptide

Trichloroethylene (TCE) had been shown to induce aberrant DNA methylation changes in mouse liver, which could be critical in the development of hepatocellular carcinoma. To understand the effect of methionine, a methyl donor, on TCE-induced mouse liver cancer, we exposed B6C3F1 mice to TCE in the presence or absence of methionine. We found that supplementation with methionine attenuated the TCE-induced hypo-and hyper-methylation status of Cdkn1a and Ihh in mouse liver, respectively. The TCE-induced mRNA expression changes of Cdkn1a, Ihh and Jun were also alleviated by methionine. However, methionine supplementation accelerated the TCE-induced mRNA over-expression of Mki67, and enhanced the TCE-induced mRNA down-regulation of Dnmt3a and Tet2. In summary, our results showed that methionine could attenuate at least part of the TCE-induced DNA methylation changes, but the additional gene expression changes induced by supplementary of methionine does not support the assumption that methionine could prevent TCE-induced liver carcinogenesis.

Objective: To explore the effect of different tensile strain stimulations on the proliferation, inflammatory factor expression and components of the Hedgehog pathway in rat mandibular condylar chondrocytes. Methods: Cultured rat mandibular condylar cartilage cells were used for this study. Different tensile strains were applied to the chondrocytes for 4 h using a Flexcell-4000TM strain unit. The tensile strain amplitudes were 0, 3, and 15%, at a frequency of 0.5 Hz. Cell proliferation was measured using the CCK-8 method. The mRNA expression levels of PCNA, caspase-3, COL II, IL-1 beta, TNF-alpha, Ihh, Ptc, and Smo were quantified via real-time PCR. Results: Compared with the control group, chondrocytes subjected to 3% tensile strain showed higher proliferation rates and had higher mRNA levels of PCNA, COL II, Ihh, Ptc and Smo. At a 15% tensile strain, the mRNA levels of caspase-3, IL-1 beta and TNF-alpha were up-regulated, but the mRNA levels of PCNA and Smo were down-regulated. Compared with those subjected to 3% tensile strain, chondrocytes subjected to 15% tensile strain showed a lower proliferation rate, down-regulated mRNA levels of PCNA, COL II, Ihh and Smo and up-regulated mRNA levels of IL-1 beta and caspase-3. Conclusions: The proliferation of chondrocytes and the expression of inflammatory factors may change with different levels of tensile strain. We show that a 15% tensile strain induces the expression of apoptotic and inflammatory factors, and a 3% tensile strain increases chondrocyte proliferation and cartilage matrix synthesis. Moreover, Hedgehog pathway signaling molecules are sensitive to tensile strain and were found to participate in the regulation of the mechanical stimulation of chondrocytes.