Pregled bibliografske jedinice broj: 1090216
Mechanisms of extracellular Hsp70 induced inflammatory effects in 16HBE cells
Mechanisms of extracellular Hsp70 induced inflammatory effects in 16HBE cells // 22nd European Respiratory Society International Congress (ERS 2020)
online, 2020. str. 1-1 (poster, međunarodna recenzija, sažetak, znanstveni)
CROSBI ID: 1090216 Za ispravke kontaktirajte CROSBI podršku putem web obrasca
Naslov
Mechanisms of extracellular Hsp70 induced inflammatory effects in 16HBE cells
Autori
Hulina-Tomašković, Andrea ; Somborac-Bačura, Anita ; Hlapčić, Iva ; Grdić Rajković, Marija ; Rumora, Lada
Vrsta, podvrsta i kategorija rada
Sažeci sa skupova, sažetak, znanstveni
Skup
22nd European Respiratory Society International Congress (ERS 2020)
Mjesto i datum
Online, 05.09.2020. - 09.09.2020
Vrsta sudjelovanja
Poster
Vrsta recenzije
Međunarodna recenzija
Ključne riječi
16HBE cells ; extracellular Hsp70 ; MAPK, NF-kappaB ; cytokines
Sažetak
Extracellular heat shock protein (eHsp) 70 is a damage-associated molecular pattern that could participate in inflammatory response in bronchial epithelial cells. We hypothesized that the inflammatory response to eHsp70 as well as its effects on cell survival are mediated via mitogen-activated protein kinase (MAPK) and NF-κB signalling pathways in 16HBE bronchial epithelial cell line. We aimed to investigate these mechanisms using the specific NF-κB and MAPK inhibitors. 16HBE cells were pre-treated with specific inhibitors (BAY11-7082 for NF-κB, PD98059 for ERK, SP600125 for JNK, and SB202190 for p38) for 1 h before adding recombinant human (rh) Hsp70 (3 μg/ml) for 24 h. IL-1α, IL-6 and TNF-α concentrations were determined in cell supernatants using ELISA method, while cell viability was assessed by MTS assay. IL-1α secretion was decreased after pre-treatment with ERK, JNK and p38 inhibitors compared to rhHsp70 alone. IL-6 and TNF-α secretion was decreased with all inhibitors. Inhibition of NF-κB and p38 pathways almost completely attenuated secretion of TNF-α and IL-6. rhHsp70 alone did not affect cell viability ; however, inhibition of JNK and p38 pathways significantly lowered it in 16HBE cells. In conclusion, the results support our hypothesis that the NF-κB signalling is an important factor in inflammation, while MAPK signalling pathways are involved in both inflammatory processes and cell survival in 16HBE cells. This could have a potential role in new therapeutic drug discoveries.
Izvorni jezik
Engleski
Znanstvena područja
Temeljne medicinske znanosti, Farmacija
POVEZANOST RADA
Projekti:
IP-2014-09-1247 - Uloga stresnog proteina Hsp70 u imunosno-upalnom odgovoru kod kronične opstrukcijske plućne bolesti (Hsp70COPD) (HRZZ - 2014-09) ( CroRIS)
Ustanove:
Farmaceutsko-biokemijski fakultet, Zagreb
Profili:
Iva Hlapčić
(autor)
Marija Grdić Rajković
(autor)
Andrea Hulina Tomašković
(autor)
Lada Rumora
(autor)
Anita Somborac Bačura
(autor)