The Anti-inflammatory Effect of GV1001 Mediated by the Downregulation of ENO1-induced Pro-inflammatory Cytokine Production.
- Author:
Jiyea CHOI
1
;
Hyemin KIM
;
Yejin KIM
;
Mirim JANG
;
Jane JEON
;
Young Il HWANG
;
Won Jun SHON
;
Yeong Wook SONG
;
Jae Seung KANG
;
Wang Jae LEE
Author Information
- Publication Type:Original Article
- Keywords: GV1001; ENO1; Inflammation
- MeSH: Arthritis, Rheumatoid; Concanavalin A; Cytokines; Down-Regulation*; Humans; Inflammation; Interleukin-6; Interleukins; Macrophages; Monocytes; NF-kappa B; p38 Mitogen-Activated Protein Kinases; Protein Kinases; Telomerase; Tumor Necrosis Factor-alpha
- From:Immune Network 2015;15(6):291-303
- CountryRepublic of Korea
- Language:English
- Abstract: GV1001 is a peptide derived from the human telomerase reverse transcriptase (hTERT) sequence that is reported to have anti-cancer and anti-inflammatory effects. Enolase1 (ENO1) is a glycolytic enzyme, and stimulation of this enzyme induces high levels of pro-inflammatory cytokines from concanavalin A (Con A)-activated peripheral blood mononuclear cells (PBMCs) and ENO1-expressing monocytes in healthy subjects, as well as from macrophages in rheumatoid arthritis (RA) patients. Therefore, this study investigated whether GV1001 downregulates ENO1-induced pro-inflammatory cytokines as an anti-inflammatory peptide. The results showed that GV1001 does not affect the expression of ENO1 in either Con A-activated PBMCs or RA PBMCs. However, ENO1 stimulation increased the production of pro-inflammatory cytokines such as tumor necrosis factor (TNF)-alpha, interleukin (IL)-1beta, and IL-6, and these cytokines were downregulated by pretreatment with GV1001. Moreover, p38 mitogen-activated protein kinase (MAPK) and nuclear factor (NF)-kappaB were activated when ENO1, on the surface of Con A-activated PBMCs and RA PBMCs, was stimulated, and they were successfully suppressed by pre-treatment with GV1001. These results suggest that GV1001 may be an effective anti-inflammatory peptide that downregulates the production of pro-inflammatory cytokines through the suppression of p38 MAPK and NF-kappaB activation following ENO1 stimulation.
