Pregled bibliografske jedinice broj: 1204749
CD26 Deficiency Controls Macrophage Polarization Markers and Signal Transducers during Colitis Development and Resolution
CD26 Deficiency Controls Macrophage Polarization Markers and Signal Transducers during Colitis Development and Resolution // International journal of molecular sciences, 23 (2022), 10; 5506, 16 doi:10.3390/ijms23105506 (međunarodna recenzija, članak, znanstveni)
CROSBI ID: 1204749 Za ispravke kontaktirajte CROSBI podršku putem web obrasca
Naslov
CD26 Deficiency Controls Macrophage Polarization Markers and Signal Transducers during Colitis Development and Resolution
Autori
Vukelic, Iva ; Buljevic, Suncica ; Batičić, Lara ; Barisic, Karmela ; Franovic, Barbara ; Detel, Dijana
Izvornik
International journal of molecular sciences (1422-0067) 23
(2022), 10;
5506, 16
Vrsta, podvrsta i kategorija rada
Radovi u časopisima, članak, znanstveni
Ključne riječi
Ulcerative colitis ; Dipeptidyl peptidase 4 ; CD26 deficiency ; Macrophage polarization ; STAT molecules
Sažetak
Ulcerative colitis (UC) is a multifactorial condition characterized by a destructive immune response that failed to be attenuated by common regulatory mechanisms which reduce inflammation and promote mucosa healing. The inhibition of CD26, a multifunctional glycoprotein that controls the immune response via its dipeptidyl peptidase (DP) 4 enzyme activity, was proven to have beneficial effects in various autoimmune inflammatory diseases. The polarization of macrophages into either pro-inflammatory M1 or anti-inflammatory M2 subclass is a key intersection that mediates the immune-inflammatory process in UC. Hence, we hypothesized that the deficiency of CD26 affects that process in the dextran sulfate sodium (DSS)-induced model of UC. We found that mRNA expression of M2 markers arginase 1 and Fizz were increased, while the expression of M1 marker inducible NO synthase was downregulated in CD26−/− mice. Decreased STAT1 mRNA, as well as upregulated pSTAT6 and pSTAT3, additionally support the demonstrated activation of M2 macrophages under CD26 deficiency. Finally, we investigated DP8 and DP9, proteins with DP4-like activity, and found that CD26 deficiency is not a key factor for the noted upregulation of their expression in UC. In conclusion, we demonstrate that CD26 deficiency regulates macrophage polarization toward the anti-inflammatory M2 phenotype, which is driven by STAT6/STAT3 signalling pathways. This process is additionally enhanced by the reduction of M1 differentiation via the suppression of proinflammatory STAT1. Therefore, further studies should investigate the clinical potential of CD26 inhibitors in the treatment of UC.
Izvorni jezik
Engleski
Znanstvena područja
Temeljne medicinske znanosti
POVEZANOST RADA
Projekti:
--uniri-biomed-18-114 - Uloga novootkrivenih proteaza u razvoju i progresiji tumora debelog crijeva (Detel, Dijana) ( CroRIS)
IP-2019-04-4624 - Gensko, proteinsko i RNA profiliranje kolorektalnog karcinoma primjenom tekuće biopsije (CRCMolProfil) (Barišić, Karmela, HRZZ - 2019-04) ( CroRIS)
Ustanove:
Farmaceutsko-biokemijski fakultet, Zagreb,
Medicinski fakultet, Rijeka
Profili:
Lara Batičić
(autor)
Dijana Detel
(autor)
Karmela Barišić
(autor)
Iva Vukelić
(autor)
Sunčica Buljević
(autor)
Citiraj ovu publikaciju:
Časopis indeksira:
- Current Contents Connect (CCC)
- Web of Science Core Collection (WoSCC)
- Science Citation Index Expanded (SCI-EXP)
- SCI-EXP, SSCI i/ili A&HCI
- Scopus
- MEDLINE