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First, MSC may acquire epithelial characteristics by reprogrammation.
In order to better understand the role of MSC in GIT epithelium physiopathology, this study aimed to evaluate the mechanisms by which human bone marrow-derived MSC cultured with epithelial cells may acquire epithelial characteristics in vitro.
In conclusion, our results indicate that fusion could be the predominant mechanism by which human MSC may acquire epithelial characteristics when in close contact with epithelial cells from gastrointestinal origin.
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In this study, we demonstrated for the first time that MSC can acquire epithelial characteristics through a fusion mechanism with gastric and intestinal epithelial cells.
Moreover, mesenchymal-to-epithelial transition (MET), as the reverse process of EMT, indicates the transformation of mesenchymal cells to acquire epithelial traits.
Although CLA possesses apoptotic effect in both normal and cancerous stromal cells (data not shown), cancerous ERα negative breast epithelial cells may acquire independent self-regulation from the surrounding stromal compartment.
Indeed, as a consequence of the increased stiffness in the tumour microenvironment, epithelial cells may acquire a mesenchymal phenotype by losing the cell-cell junctions and cell polarity [ 58].
Thus, initial data combining careful histopathological analysis and use of defined cell lineage markers, suggested that PDAC epithelial cells may acquire a phagocyte-like phenotype characterized by the ectopic expression of CD68 and the ability to cannibalize, a feature that has previously remained unexplored.
Later, it was established that polarized epithelial cells from the renal proximal tubules may acquire Tf-bound iron via the endocytic receptor cubilin, which operates in conjunction with its co-receptor megalin [ 57].
Moreover, within a tumour, cells may acquire stem cell properties through epithelial mesenchymal transition (see Figure 1).
Current evidences suggest that AECs may acquire overdrive activation in the initial step of fibrosis by several mechanisms, including abnormal recapitulation of the developmental pathway, defects of the molecules essential for epithelial integrity, and acceleration of aging-related properties.
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