Abstract:
Inflammatory Bowel Disease (IBD) is comprises of two different phenotypes Ulcerative Colitis (UC) and Crohn’s Disease (CD), both have many conjoint genetic and mechanistic features while having distinctive clinical manifestations. Intestinal epithelial barrier serves as a first line of defense for incoming toxins and plays a crucial role in maintaining the intestinal homeostasis. Any transformation in the integrity of intestinal barrier can lead to multiple maladies as well as IBD. Tight Junctions are crucial part of intestinal barrier, which help in regulating cellular polarity and adhesion of intestinal wall. These tight junction proteins are found to be regulated by certain microRNAs. Identification and analysis of the interaction network of candidate miRNAs and their target gene products would increase our understanding of how to maintain the integrity of intestinal barrier, generating a comprehensive model of cellular signaling pathways associated with IBD will unravel the key components whose imbalance may lead to disease onset. This study attempts to identify the crucial players in the interactome, which regulate important targets and may lead to disease outcomes. In addition, to elucidate how over-expression of certain microRNAs lead to dysfunction of signaling pathways leading to IBD. Antagomir therapy show potential to restore deregulated signaling pathways, which play vital role in homeostasis regulation. Furthermore, we observed how Antagomir application could revert the disease condition by bringing down the up-regulated microRNA. We applied Antagomir therapy to target key microRNAs involved in IBD progression and gauge their impact in recovery.
