Liver fibrosis can arise from a number of unrelated causes and is characterised by chronic inflammation, excessive collagen deposition and significant loss of hepatocytes. Liver fibrosis can progress to cirrhosis, carcinoma and finally to liver disease. Currently, liver transplantation is the only therapy available for patients with cirrhosis and liver disease. Therefore, it is necessary to develop new innovative therapeutic strategies. Monocytes traffic to inflamed tissue and differentiate into inflammatory macrophages (M1 Macrophages) which can stimulate collagen deposition by hepatic myofibroblasts (pro-fibrotic macrophages). Our recent research showed that placental MSCs can shift the differentiation of M1 macrophages into anti-inflammatory macrophages (M2 Macrophages). These M2 macrophages are known for their ability to resolve inflammation and break down collagen and therefore can reduce fibrosis; so they are known as anti-fibrotic macrophages. However, it remains unclear whether placental MSCs can resolve inflammation and fibrosis in liver. Therefore, in this study, we are using an animal model of liver fibrosis to determine if human placental stem cells can be used as a therapy for liver failure. This study will allow us to develop a therapeutic strategy using human placental MSCs in the treatment of liver failure.
Morphological effects of human placental MSCs on the differentiation of human monocytes into macrophages (A) M1-like macrophages (fried egg-shaped morphology, scale bar 10µm) differentiated from monocytes and (B) elongated, spindle-like morphology (M2-like anti-inflammatory macrophages, scale bar 100µm) differentiated from monocytes in the presence of placental MSCs (Abumaree et al., 2013)