Liver fibrosis occurs during chronic injury and represents, in large part, an 
exaggerated matrigenic output by hepatic stellate cells (HSCs) which become 
activated as a result of injury-induced signaling pathways in parenchymal and 
inflammatory cells (hepatocytes, macrophages, etc.). The molecular components in 
these pathways (e.g., CCN proteins) are modulated by transcription factors as 
well as by factors such as microRNAs (miRs) that act posttranscriptionally. MiRs 
are small (~23 nt) noncoding RNAs that regulate gene expression by specifically 
interacting with the 3' untranslated region (UTR) of target gene mRNA to repress 
translation or enhance mRNA cleavage. As well as acting in their cells of 
production, miRs (and other cellular constituents such as mRNAs and proteins) 
can be liberated from their cells of origin in nanovesicular membrane exosomes, 
which traverse the intercellular spaces, and can be delivered to neighboring 
cells into which they release their molecular payload, causing alterations in 
gene expression in the target cells. Here we summarize some of the experimental 
approaches for studying miR action and exosomal trafficking between hepatic 
cells. Insights into the mechanisms involved will yield new information about 
how hepatic fibrosis is regulated and, further, may identify new points of 
therapeutic intervention.