prikaz prve stranice dokumenta CD26 Deficiency Controls Macrophage Polarization Markers and Signal Transducers during Colitis Development and Resolution
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Scientific paper - Original scientific paper
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

Institutional repository: Repository of the University of Rijeka, Faculty of Medicine

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Vukelić, I., Buljević, S., Batičić, L., Barišić, K., Franović, B. & 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, no. 10, 2022. https://doi.org/10.3390/ijms23105506

Vukelić, Iva, Sunčica Buljević, Lara Batičić, Karmela Barišić, Barbara Franović and Dijana Detel. "CD26 Deficiency Controls Macrophage Polarization Markers and Signal Transducers during Colitis Development and Resolution." International Journal of Molecular Sciences 23, no. 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]. 2022 May 14 [cited 2024 November 23];23(10). doi: 10.3390/ijms23105506

I. Vukelić, S. Buljević, L. Batičić, K. Barišić, B. Franović and D. Detel, "CD26 Deficiency Controls Macrophage Polarization Markers and Signal Transducers during Colitis Development and Resolution", International Journal of Molecular Sciences, vol. 23, no. 10, May 2022. [Online]. Available at: https://urn.nsk.hr/urn:nbn:hr:184:440073. [Accessed: 23 November 2024]

Metadata
Title (english)CD26 Deficiency Controls Macrophage Polarization Markers and Signal Transducers during Colitis Development and Resolution
AuthorIva Vukelić
AuthorSunčica Buljević
AuthorLara Batičić
AuthorKarmela Barišić
AuthorBarbara Franović
AuthorDijana Detel
Author's institutionUniversity of Rijeka
Faculty of Medicine
(Department of Chemistry and Biochemistry)
Scientific / art field,
discipline and subdiscipline		BIOMEDICINE AND HEALTHCARE
Basic Medical Sciences
Medical Biochemistry
Abstract (english)
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.
Keywords (english)
Languageenglish
Publication typeScientific paper - Original scientific paper
Publication statusPublished
Peer reviewPeer review - international
Publication versionPublished version
Journal titleInternational Journal of Molecular Sciences
Numberingvol. 23, no. 10, 5506
e-ISSN1422-0067
DOIhttps://doi.org/10.3390/ijms23105506
URN:NBNurn:nbn:hr:184:440073
Publication2022-05-14
ProjectNumber: IP-2019-04-4624
Title (croatian): Gensko, proteinsko i RNA profiliranje kolorektalnog karcinoma primjenom tekuće biopsije
Title (english): Genetic, Protein and RNA Profiling of Colorectal Cancer Using Liquid Biopsy
Acronym: CRCMolProfil
Leader: Karmela Barišić
Jurisdiction: Croatia
Funding stream: IP
ProjectNumber: uniri-biomed-18-114
Title (croatian): Uloga novootkrivenih proteaza u razvoju i progresiji tumora debelog crijeva
Title (english): The role of recently discovered proteases in colorectal cancer development and progression
Leader: Dijana Detel
Jurisdiction: Croatia
Funding stream: Sveučilište u Rijeci
Document URLhttps://www.mdpi.com/1422-0067/23/10/5506
Type of resourceText
Access conditionsOpen access
Terms of useLicence Attribution 4.0 International (CC BY 4.0) icon
Created on2022-06-30 10:57:48