Version 1
: Received: 7 April 2022 / Approved: 8 April 2022 / Online: 8 April 2022 (14:04:17 CEST)
How to cite:
Wu, C.W.; zhang, M.; Hu, W.; Tian, T. Endotoxins Induced ECM-Receptor Interaction Pathway Signal Effect on the Function of MUC2 in Caco2/HT29 Co-Culture Cells. Preprints2022, 2022040082. https://doi.org/10.20944/preprints202204.0082.v1.
Wu, C.W.; zhang, M.; Hu, W.; Tian, T. Endotoxins Induced ECM-Receptor Interaction Pathway Signal Effect on the Function of MUC2 in Caco2/HT29 Co-Culture Cells. Preprints 2022, 2022040082. https://doi.org/10.20944/preprints202204.0082.v1.
Cite as:
Wu, C.W.; zhang, M.; Hu, W.; Tian, T. Endotoxins Induced ECM-Receptor Interaction Pathway Signal Effect on the Function of MUC2 in Caco2/HT29 Co-Culture Cells. Preprints2022, 2022040082. https://doi.org/10.20944/preprints202204.0082.v1.
Wu, C.W.; zhang, M.; Hu, W.; Tian, T. Endotoxins Induced ECM-Receptor Interaction Pathway Signal Effect on the Function of MUC2 in Caco2/HT29 Co-Culture Cells. Preprints 2022, 2022040082. https://doi.org/10.20944/preprints202204.0082.v1.
Abstract
Endotoxins are toxic substances that widely exist in the environment and can enter the intestine with food and other substances. Intestinal epithelial cells are protected by a mucus layer that contains MUC2 as its main structural component. However, a detailed understanding of the mechanisms involved in the function of the mucus barrier in endotoxin penetration is lacking. Here, we established the most suitable proportion of Caco-2/HT-29 co-culture cells as a powerful tool to evaluate the intestinal mucus layer. Our findings significantly advance current knowledge as focal adhesion and ECM-receptor interaction were identified as the two most significantly implicated pathways in MUC2 small interfering RNA (siRNA)-transfected Caco-2/HT-29 co-culture cells after 24 h of LPS stimulation. When the mucus layer was not intact, LPS was found to damage the tight junctions of Caco-2/HT29 co-cultured cells. Furthermore, LPS was demonstrated to inhibit the integrin-mediated focal adhesion structure and damage the matrix network structure of the extracellular and actin microfilament skeletons. Ultimately, LPS inhibited the interactive communication between the extracellular matrix and the cytoskeleton for 24 h in the siMUC2 group compared with the LPS(+) and LPS(-) groups. Overall, we recognized the potential of MUC2 as a tool for barrier function in several intestinal bacterial diseases.
Copyright:
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
