Document Type: Original Article


1 Immunology and Hematology Departments, Medical School, Rafsanjan University of Medical Sciences, Rafsanjan, Iran

2 Biochemistry Department, Faculty of Life Sciences, Manchester University, Manchester, UK


Background: It is now well established that several environmental stress factors cause activation of p38 MAP kinase and JNK in various cell types to produce chemokines.
Objective: To investigate the expression of CXC chemokines Gro/KC and SDF- 1a in rat's H4 hepatoma cells in response to heat shock, hyperosmolarity and oxidative stress.
Methods: Hepatoma cells were maintained in MEM medium. Cells were subjected to different stresses [(H2O2 0.15% (w/v), manitol and NaCl (160 mM) and heat shock (42 °C for 20 minutes)]. Cells were harvested and RNA was extracted, purified and the CXC chemokine Gro/KC and SDF-1a expression was analysed by RT-PCR. cDNA was separated by gel electrophoresis on a 1% (w/v) agarose gel and visualized under a UV transilluminator.
Results: There was detectable but low expression of both SDF-1a and Gro/KC in H4 hepatoma cells. Heat shock failed to induce expression of SDF-1a and Gro/KC in H4 hepatoma cells of rat. Hyperosmolarity also did not stimulate SDF-1a and Gro/KC expression. In this study we have also shown that oxidative stress did not induce expression of SDF-1a and Gro/KC. Overall, although detection is possible but regulatory responses were not observed in H4 hepatoma cells.
Conclusion: Several known injurious conditions cause recruitment of macrophages, neutrophils and other immune cells to the liver. Immune cells are recruited to the hepatic vasculature following local liver injury and subsequent chemokine production. Our results demonstrated that failure to produce chemokines by hepatoma cells may be a way to escape from mechanism of immune surveillance.