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1.  Relaxin Reduces Fibrosis in Models of Progressive and Established Hepatic Fibrosis 
The effect of relaxin administration before (prevention) or after (treatment) the establishment of hepatic fibrosis in a mouse model was examined. In the prevention study, relaxin reduced collagen and smooth muscle actin (SMA) content, and significantly reduced serum levels of the liver enzymes ALT and AST. In the treatment study, relaxin for 1 week reduced collagen and SMA, but not liver enzyme levels. Relaxin for 2 weeks had no significant effect. In conclusion, the data suggest that relaxin treatment before fibrosis can reduce collagen and improve liver function, but that there is little effect of short-term relaxin treatment after fibrosis is established.
doi:10.1111/j.1749-6632.2008.03783.x
PMCID: PMC2716062  PMID: 19416217
Hepatic fibrosis; liver; collagen; relaxin
2.  Degradation of Relaxin Family Peptides by Insulin-degrading Enzyme 
Insulin-degrading enzyme (IDE) is a ubiquitously expressed metalloproteinase responsible for the intracellular degradation of insulin. IDE also interacts with other members of the insulin superfamily, including relaxin, but no studies have been reported regarding the interaction of other relaxin-like peptides with IDE. In this study, we determined that relaxin, relaxin-3 and InsL3 all competitively inhibited the degradation of insulin by IDE to different degrees, and all inhibited covalent cross-linking of insulin to IDE. Each of the peptides was degraded by IDE to various degrees (insulin>relaxin>InsL3=relaxin-3). In summary, relaxin, InsL3 and relaxin-3 all bound to IDE, competed with the binding and degradation of insulin, and were all substrates for the proteolytic activity of IDE. Therefore, it is possible that in addition to insulin, IDE may be important for the cellular proteolysis of relaxin, InsL3 and relaxin-3.
doi:10.1111/j.1749-6632.2008.03782.x
PMCID: PMC2708001  PMID: 19416156
Insulin-degrading enzyme; insulysin; relaxin; relaxin-3; InsL3; Relaxin-like factor

Results 1-2 (2)