Hepatic fibrosis and cirrhosis is the common end-point of chronic liver injury. Fibrosis is mediated by activated hepatic stellate cells that express fibrillar collagens, control the balance of extracellular matrix remodeling enzymes, and stimulate the inflammatory immune response. Relaxin is an anti-fibrotic hormone that has been shown to abrogate the effects of activated hepatic stellate cells and promote a wound healing microenvironment. During liver fibrosis, activated hepatic stellate cells are recruited from a population of mesenchymal progenitor cells in the bone marrow that are known to migrate to areas of inflammation and injury. Because of their inherent therapeutic benefits and targeting capabilities, these mesenchymal stem cells (MSCs) are a promising gene delivery vector. In this thesis work, we present an animal model of liver fibrosis induced with long-term administration of oral thioacetamide that is both persistent and authentic to human disease for the use of testing potential therapeutics. We have engineered and characterized MSCs that can secrete a bioactive relaxin peptide, and we have successfully delivered MSCs to the liver. We present an attempt to reverse liver fibrosis in a TAA model using mesenchymal stem cell-mediated gene delivery of relaxin.