ARTİRİK HASARA SPESİFİK UYANDIRILMIŞ SİNOVİAL KÖKENLİ MEZENKİMAL KÖK HÜCRELERİN REJENERASYONUNUN İNCELENMESİ

Proje no. 565 · Durum: Kapanmış · 2016

Özet

Goal: The pathogenesis caused by the extracellular matrix immunoinflammation is fully understood, but the regeneration effect is not sampled in many tissues. Immunological damage occurs in tissues exposed to extracellular matrix proteases due to inflammation and increases in cellular mediators. In this case, the swelling redness and temperature increase occur in these damaged tissues, which causes pain and movement restriction. Hence, molecular alteration of stem cells in such pathogenesis and cellular regeneration of these damages are currently discussed in the literature. Migration of the stem cells to the extracellular matrix where the damage is experienced due to migration from the damaged tissue, which results in the acceleration of the destruction of the tissue due to the occlusion of some tissue repair mechanisms. Stem cells require microenvironmental niches to regenerate. In many studies on regeneration mechanisms, the pathways that work in stem cells are well understood. I concentrated on the JUNB, MEPE, MMP13, MMP2 proteins involved in these pathways. The proteins encoded by these genes function in important functions such as stem cell remodeling, asymmetric cleavage, tissue repair. It has been argued that the effect of tissue inflammation on tissues in tissue has lost its role in stem cell migration. The loss of their ability to regenerate the tissue was thought to be due to the degradation of microenvironmental niches and the decrease in their ability to hold. Materials and Methods: In the assay, imitation of extracellular matrix damage was performed on various tissue stem cells, and expression levels of important proteins of regenerating pathways regulated in pre-defined damage models and pharmacological modulation models were measured. For this purpose, Sinobiyal, Umbilical cord and Adispose tissue stem cells were cultured on 3 plates in 9 plates with 6 wells. Each plate was designed to be IL-1 and IL-1 + canacinumab antagonists with placebo cultures for 24 hours and 48 hours as culture supernatants. Then mRNA was isolated from cultured samples and cDNAs were obtained from isolated mRNAs by Reverse T. PCR and the cDNAs obtained were measured by RealTime PCR on ABI7000 RT-PCR as expression levels Ct value using JUNB, MEPE, MMP13, MMP2 Taqman Ready Probe. The results were evaluated with the ? ?Ct account. And the fold change formula is calculated fold change. Results: According to the evaluations, changes in the expression of genes encoding proteins involved in extracellular matrix damage mimicities and pharmacological modulation in cellular regeneration pathways were observed. In IL-1 damage mimicry, a decrease in gene expression was detected, which would result in the reduction of the proteins involved in the regeneration pathway. Discussion and Conclusion: According to our experimental findings, extracellular matrix inflammation damage is lost in regenerating ability after in-vitro pretreatment cultures in which cells and tissues regenerate are separated from the niches that the cells are holding, including inflammatory reactions and suspen- sion that they will not function. In addition, the JEPA protein initiates regeneration of single cell damage while the MEPE protein, which is exogenously expressed in stem cells in damage to root cells and surrounding tissue cells by inflammatory damage, increases in expression level and functions as an increasing signal in the whole tissue.

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