Our lab focuses on the study of microRNAs and other small non-coding RNAs at the liver-intestine axis that may regulate the pathogenesis of metabolic diseases and specific cancers.
High-throughput sequencing technology has helped unveil the complexity of the mammalian microRNA repertoire. We've identified isoforms of canonical microRNAs (referred to as isomiRs) that may have different functions from their canonical counterparts.
Interactions between gut bacteria and diet influence the functions of the diverse cell types in the intestinal epithelium. We're studying how gut microRNAs help maintain intestinal homeostasis.
We have recently discovered that small RNAs derived from tRNAs are associated with chronic hepatitis C and associated hepatocellular carcinoma.
Enhancers are regulatory elements that interact with promoters to regulate transcription. We've shown that enhancers are also mark pre-microRNA regions in a tissue-specific manner.
We are studying microRNAs in the livers of five different animal models of insulin resistance. Only a few out of the couple hundred microRNAs expressed in the liver are similarly altered across these models.
Small RNA-sequencing is the method of choice for cataloging and quantifying microRNAs. Work from our lab and others has revealed significantly different detection bias across different library preparation methods.
Locked-nucleic acid technology (LNA) facilitates potent inhibition of microRNAs in animal models. We've used LNAs to demonstrate that inhibition of a specific microRNA, miR-29, has a dramatic cholesterol-lowering benefit.
microRNAs have emerged as potentially important regulators of metabolic pathways relevant to diabetes. Our studies show that miR-29 is dysregulated in animal models of insulin resistance and diabetes and may be a candidate therapeutic target.