Treatment with Streptozotocin (STZ) increases expression of macrophage migration inhibitory factor (MIF) but not metalloproteinase‐13 (MMP‐13) mRNA in the liver of channel catfish

Abstract

Tissue repair during liver damage depends on the recruitment and activation of macrophages. In rodents, the production of MIF is essential for the recruitment of scar‐forming macrophages. In addition, production of MMP‐13 appears to be critical for successful remodeling and hepatic tissue repair. In our previous studies with channel catfish, STZ treatment induced hypoglycemia and an abnormal gross morphology of the liver and gall bladder. This suggests that the liver is the target organ for STZ in channel catfish and causes acute liver damage. This results in hypoglycemia, necrosis and eventually organ failure. However, whether liver damage induced by the STZ treatment results in recruitment and activation of macrophage in the liver of channel catfish has never been examined. Liver samples were collected from juvenile channel catfish 7 days after intraperitoneal administration of 0, 3.6, 36, 180, or 360 mg/kg STZ on day 0 (n=4 fish/treatment). Expression of genes (MMP‐13 and MIF) were measured using quantitative real‐time PCR. Expression of MIF and MMP‐13 changed in response to increases in STZ dosage (p<0.01, and p=0.05, respectively.) Expression of MMP‐13 mRNA decreased in response to an increase in STZ dosage. Expression of MIF mRNA was significantly higher in fish treated with 360 mg/kg body weight compared to control (p<0.05). Decreased expression of MMP‐13 suggests STZ treatment inhibits macrophage‐mediated tissue repair. Given that MIF has been associated with multiple liver diseases, STZ treatment may activate multiple mechanisms other than those associated with fibrosis to induce liver damage in channel catfish.Support or Funding InformationThis study is supported by Kansas Idea Network of Biomedical Research Excellence (P20GM103418).This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.