prikaz prve stranice dokumenta LPS‐induced inflammation desensitizes hepatocytes to Fas‐induced apoptosis through Stat3 activation—The effect can be reversed by ruxolitinib
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LPS‐induced inflammation desensitizes hepatocytes to Fas‐induced apoptosis through Stat3 activation—The effect can be reversed by ruxolitinib
Journal of Cellular and Molecular Medicine, 24 (2020), 5; 2981-2992. https://doi.org/10.1111/jcmm.14930
Markotić, Antonio; Flegar, Darja; Grčević, Danka; Šućur, Alan; Lalić, Hrvoje; Turčić, Petra; Kovačić, Nataša; Lukač, Nina; Pravdić, Danijel; Vukojević, Katarina; Čavar, Ivan; Kelava, Tomislav

Institucijski repozitorij: Dr Med - digitalni repozitorij Medicinskog fakulteta Sveučilišta u Zagrebu

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Markotić, A., Flegar, D., Grčević, D., Šućur, A., Lalić, H., Turčić, P. ... Kelava, T. (2020). LPS‐induced inflammation desensitizes hepatocytes to Fas‐induced apoptosis through Stat3 activation—The effect can be reversed by ruxolitinib. Journal of Cellular and Molecular Medicine, 24. (5), 2981-2992. doi: 10.1111/jcmm.14930

Markotić, Antonio, et al. "LPS‐induced inflammation desensitizes hepatocytes to Fas‐induced apoptosis through Stat3 activation—The effect can be reversed by ruxolitinib." Journal of Cellular and Molecular Medicine, vol. 24, br. 5, 2020, str. 2981-2992. https://doi.org/10.1111/jcmm.14930

Markotić, Antonio, Darja Flegar, Danka Grčević, Alan Šućur, Hrvoje Lalić, Petra Turčić, Nataša Kovačić, et al. "LPS‐induced inflammation desensitizes hepatocytes to Fas‐induced apoptosis through Stat3 activation—The effect can be reversed by ruxolitinib." Journal of Cellular and Molecular Medicine 24, br. 5 (2020): 2981-2992. https://doi.org/10.1111/jcmm.14930

Markotić, A., et al. (2020) 'LPS‐induced inflammation desensitizes hepatocytes to Fas‐induced apoptosis through Stat3 activation—The effect can be reversed by ruxolitinib', Journal of Cellular and Molecular Medicine, 24(5), str. 2981-2992. doi: 10.1111/jcmm.14930

Markotić A, Flegar D, Grčević D, Šućur A, Lalić H, Turčić P, i sur.. LPS‐induced inflammation desensitizes hepatocytes to Fas‐induced apoptosis through Stat3 activation—The effect can be reversed by ruxolitinib. Journal of Cellular and Molecular Medicine [Internet]. 03.2020. [pristupljeno 18.12.2024.];24(5):2981-2992. doi: 10.1111/jcmm.14930

A. Markotić, et al., "LPS‐induced inflammation desensitizes hepatocytes to Fas‐induced apoptosis through Stat3 activation—The effect can be reversed by ruxolitinib", Journal of Cellular and Molecular Medicine, vol. 24, br. 5, str. 2981-2992, Ožujak 2020. [Online]. Dostupno na: https://urn.nsk.hr/urn:nbn:hr:105:210422. [Citirano: 18.12.2024.]

Za citiranje koristite ovu mrežnu adresu: https://urn.nsk.hr/urn:nbn:hr:105:210422
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Naslov (engleski)LPS‐induced inflammation desensitizes hepatocytes to Fas‐induced apoptosis through Stat3 activation—The effect can be reversed by ruxolitinib
AutorAntonio Markotić
AutorDarja Flegar
AutorDanka Grčević
AutorAlan Šućur
AutorHrvoje Lalić
AutorPetra Turčić
AutorNataša Kovačić
AutorNina Lukač
AutorDanijel Pravdić
AutorKatarina Vukojević
AutorIvan Čavar
AutorTomislav Kelava
Autorova ustanovaSveučilište u Zagrebu
Medicinski fakultet
Znanstveno / umjetničko
područje, polje i grana		BIOMEDICINA I ZDRAVSTVO
Temeljne medicinske znanosti
Anatomija
Znanstveno / umjetničko
područje, polje i grana		BIOMEDICINA I ZDRAVSTVO
Temeljne medicinske znanosti
Fiziologija čovjeka
Sažetak (hrvatski)
Recent studies have established a concept of tumour necrosis factor-α (TNF-α)/Fas signalling crosstalk, highlighting TNF-α as a critical cytokine in sensitizing hepatocytes to death induced by Fas activation. However, in the exact inflammatory response, besides TNF-α, many other mediators, that might modulate apoptotic response differentially, are released. To resolve the issue, we studied the effects of lipopolysaccharide (LPS), one of the crucial inductors of inflammation in the liver, on apoptotic outcome. We show that LPS-induced inflammation diminishes the sensitivity of hepatocytes to Fas stimulus in vivo at caspase-8 level. Analysis of molecular mechanisms revealed an increased expression of various pro-inflammatory cytokines in non-parenchymal liver cells and hepatocyte-specific increase in Bcl-xL, associated with signal transducer and activator of transcription 3 (Stat3) phosphorylation. Pre-treatment with ruxolitinib, a selective Janus kinase (JAK) 1/2 inhibitor, prevented the LPS-induced Stat3 phosphorylation and restored the sensitivity of hepatocytes to Fas-mediated apoptosis. Furthermore, ruxolitinib pre-treatment diminished the LPS-induced Bcl-xL up-regulation without an inhibitory effect on LPS-induced expression of pro-inflammatory cytokines. In summary, although the reports are showing that the effects of isolated pro-inflammatory mediators, such as TNF-α or neutrophils, are pro-apoptotic, the overall effect of inflammatory milieu on hepatocytes in vivo is Stat3-dependent desensitization to Fas-mediated apoptosis.
Ključne riječi (engleski)
Jezikhrvatski
Vrsta publikacijeZnanstveni rad - Izvorni znanstveni rad
Status objaveObjavljen
Vrsta recenzijeRecenziran
Verzija publikacijeObjavljena verzija rada (izdavačev PDF)
Naslov časopisaJournal of Cellular and Molecular Medicine
Brojčani podacivol. 24, br. 5, str. 2981-2992
p-ISSN1582-1838
e-ISSN1582-4934
DOIhttps://doi.org/10.1111/jcmm.14930
URN:NBNurn:nbn:hr:105:210422
Datum objave publikacije2020-03
URL dokumentahttps://onlinelibrary.wiley.com/doi/abs/10.1111/jcmm.14930
Vrsta resursaTekst
Prava pristupaOtvoreni pristup
Uvjeti korištenjaIkona licence Imenovanje 4.0 međunarodna (CC BY 4.0)
Datum i vrijeme pohrane2021-03-23 13:09:29