prikaz prve stranice dokumenta CD26 Deficiency Controls Macrophage Polarization Markers and Signal Transducers during Colitis Development and Resolution
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CD26 Deficiency Controls Macrophage Polarization Markers and Signal Transducers during Colitis Development and Resolution
International Journal of Molecular Sciences, 23 (2022), 10; 5506. https://doi.org/10.3390/ijms23105506
Vukelić, Iva; Buljević, Sunčica; Batičić, Lara; Barišić, Karmela; Franović, Barbara; Detel, Dijana

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Vukelić, I., Buljević, S., Batičić, L., Barišić, K., Franović, B. i Detel, D. (2022). CD26 Deficiency Controls Macrophage Polarization Markers and Signal Transducers during Colitis Development and Resolution. International Journal of Molecular Sciences, 23. (10). doi: 10.3390/ijms23105506

Vukelić, Iva, et al. "CD26 Deficiency Controls Macrophage Polarization Markers and Signal Transducers during Colitis Development and Resolution." International Journal of Molecular Sciences, vol. 23, br. 10, 2022. https://doi.org/10.3390/ijms23105506

Vukelić, Iva, Sunčica Buljević, Lara Batičić, Karmela Barišić, Barbara Franović i Dijana Detel. "CD26 Deficiency Controls Macrophage Polarization Markers and Signal Transducers during Colitis Development and Resolution." International Journal of Molecular Sciences 23, br. 10 (2022). https://doi.org/10.3390/ijms23105506

Vukelić, I., et al. (2022) 'CD26 Deficiency Controls Macrophage Polarization Markers and Signal Transducers during Colitis Development and Resolution', International Journal of Molecular Sciences, 23(10). doi: 10.3390/ijms23105506

Vukelić I, Buljević S, Batičić L, Barišić K, Franović B, Detel D. CD26 Deficiency Controls Macrophage Polarization Markers and Signal Transducers during Colitis Development and Resolution. International Journal of Molecular Sciences [Internet]. 14.05.2022. [pristupljeno 22.01.2025.];23(10). doi: 10.3390/ijms23105506

I. Vukelić, S. Buljević, L. Batičić, K. Barišić, B. Franović i D. Detel, "CD26 Deficiency Controls Macrophage Polarization Markers and Signal Transducers during Colitis Development and Resolution", International Journal of Molecular Sciences, vol. 23, br. 10, Svibanj 2022. [Online]. Dostupno na: https://urn.nsk.hr/urn:nbn:hr:184:440073. [Citirano: 22.01.2025.]

Za citiranje koristite ovu mrežnu adresu: https://urn.nsk.hr/urn:nbn:hr:184:440073
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Naslov (engleski)CD26 Deficiency Controls Macrophage Polarization Markers and Signal Transducers during Colitis Development and Resolution
AutorIva Vukelić
AutorSunčica Buljević
AutorLara Batičić
AutorKarmela Barišić
AutorBarbara Franović
AutorDijana Detel
Autorova ustanovaSveučilište u Rijeci
Medicinski fakultet
(Katedra za medicinsku kemiju, biokemiju i kliničku kemiju)
Znanstveno / umjetničko
područje, polje i grana		BIOMEDICINA I ZDRAVSTVO
Temeljne medicinske znanosti
Medicinska biokemija
Sažetak (engleski)
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 signaling 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.
Ključne riječi (engleski)
Jezikengleski
Vrsta publikacijeZnanstveni rad - Izvorni znanstveni rad
Status objaveObjavljen
Vrsta recenzijeRecenziran - međunarodna recenzija
Verzija publikacijeObjavljena verzija rada (izdavačev PDF)
Naslov časopisaInternational Journal of Molecular Sciences
Brojčani podacivol. 23, br. 10, 5506
e-ISSN1422-0067
DOIhttps://doi.org/10.3390/ijms23105506
URN:NBNurn:nbn:hr:184:440073
Datum objave publikacije2022-05-14
ProjektŠifra: IP-2019-04-4624
Naziv (hrvatski): Gensko, proteinsko i RNA profiliranje kolorektalnog karcinoma primjenom tekuće biopsije
Naziv (engleski): Genetic, Protein and RNA Profiling of Colorectal Cancer Using Liquid Biopsy
Kratica: CRCMolProfil
Voditelj: Karmela Barišić
Pravna nadležnost: Hrvatska
Financijer: HRZZ
Linija financiranja: IP
ProjektŠifra: uniri-biomed-18-114
Naziv (hrvatski): Uloga novootkrivenih proteaza u razvoju i progresiji tumora debelog crijeva
Naziv (engleski): The role of recently discovered proteases in colorectal cancer development and progression
Voditelj: Dijana Detel
Pravna nadležnost: Hrvatska
Financijer: NadSve
Linija financiranja: Sveučilište u Rijeci
URL dokumentahttps://www.mdpi.com/1422-0067/23/10/5506
Vrsta resursaTekst
Prava pristupaOtvoreni pristup
Uvjeti korištenjaIkona licence Imenovanje 4.0 međunarodna (CC BY 4.0)
Datum i vrijeme pohrane2022-06-30 10:57:48