Author/Authors :
Zuo, Sheng Department of Respiration - Shanghai Sixth People’s Hospital East Affiliated to Shanghai University of Medicine & Health Sciences, Shanghai, China , Zhu, Zhen Department of Respiration - Shanghai Sixth People’s Hospital East Affiliated to Shanghai University of Medicine & Health Sciences, Shanghai, China , Liu, Yi Department of Respiration - Shanghai Sixth People’s Hospital East Affiliated to Shanghai University of Medicine & Health Sciences, Shanghai, China , Li, Hong Department of Respiration - Shanghai Sixth People’s Hospital East Affiliated to Shanghai University of Medicine & Health Sciences, Shanghai, China , Song, Shuang Department of Respiration - Shanghai Sixth People’s Hospital East Affiliated to Shanghai University of Medicine & Health Sciences, Shanghai, China , Yin, Shaojun Department of Respiration - Shanghai Sixth People’s Hospital East Affiliated to Shanghai University of Medicine & Health Sciences, Shanghai, China
Abstract :
Aim. The transmembrane chemokine (C-X-C motif ) ligand 16 (CXCL16) plays a vital role in the pathogenesis of organ fibrosis,
including the liver and kidney. However, the detailed biological function of CXCL16 is still not fully understood in the progression
of pulmonary fibrosis (PF). The aim of present study is to examine the function of CXCL16 in PF. Materials and Methods. In this
study, we constructed the PF model on mouse by using bleomycin and analyzed the effect of the mouse recombinant protein
CXCL16 on mouse lung fibroblast L929 (LF) as well. To further examine the connection between CXCL16 and STAT3 in mouse
LF cells, the STAT3 inhibitor AG490 was utilized to inhibit the expression of STAT3. Meanwhile, lipopolysaccharide was used to
enhance the phosphorylation of STAT3 (p-STAT3) in mouse LF cells. Results. Our results indicated that the level of CXCL16/
CXCR6 was significantly upregulated in the mouse PF model. Moreover, the level of p-STAT3 was also promoted. In addition, the
mouse recombinant protein CXCL16 not only contributed to the proliferation of mouse LF cells but also induced the expression of
p-STAT3 in LF cells. However, the effect of CXCL16 was deeply abolished by the STAT3 inhibitor AG490 in LF cells. Meanwhile,
the antibody of CXCL16 deeply reduced the phosphorylation of STAT3 in lipopolysaccharide (LPS) cultured cells. Conclusions.
All these results demonstrated that CXCL16 promoted the phosphorylation of STAT3 and further demonstrated that STAT3 was a
critical component in CXCL16/CXCR6 signaling pathway. -is research not only enhanced the comprehension of CXCL16 but
also indicated its potential value as a target in the treatment for human PF.
