Research ExplorerPublicationsIL-22 promotes liver regeneration after portal vein ligation

IL-22 promotes liver regeneration after portal vein ligation

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IL-22 promotes liver regeneration after portal vein ligation. / Zhang, Tao; Seeger, Philipp; Simsek, Yashin J; Sabihi, Morsal; Lücke, Jöran; Zazara-Giannou, Dimitra; Shiri, Mustafa; Kempski, Jan Michael; Blankenburg, Tom; Zhao, Lilan; Belios, Ioannis; Machicote, Andres Pablo; Mercanoglu, Baris; Fard-Aghaie, Mohammad; Notz, Sara Johanna; Lykoudis, Panagis M; Kemper, Marius; Ghadban, Tarik; Mann, Oliver; Hackert, Thilo; Izbicki, Jakob; Renne, Thomas; Huber, Samuel; Giannou, Anastasios; Li, Jun.

In: HELIYON, Vol. 10, No. 6, 30.03.2024, p. e27578.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Zhang, T, Seeger, P, Simsek, YJ, Sabihi, M, Lücke, J, Zazara-Giannou, D, Shiri, M, Kempski, JM, Blankenburg, T, Zhao, L, Belios, I, Machicote, AP, Mercanoglu, B, Fard-Aghaie, M, Notz, SJ, Lykoudis, PM, Kemper, M, Ghadban, T, Mann, O, Hackert, T, Izbicki, J, Renne, T, Huber, S, Giannou, A & Li, J 2024, 'IL-22 promotes liver regeneration after portal vein ligation', HELIYON, vol. 10, no. 6, pp. e27578. https://doi.org/10.1016/j.heliyon.2024.e27578

APA

Zhang, T., Seeger, P., Simsek, Y. J., Sabihi, M., Lücke, J., Zazara-Giannou, D., Shiri, M., Kempski, J. M., Blankenburg, T., Zhao, L., Belios, I., Machicote, A. P., Mercanoglu, B., Fard-Aghaie, M., Notz, S. J., Lykoudis, P. M., Kemper, M., Ghadban, T., Mann, O., ... Li, J. (2024). IL-22 promotes liver regeneration after portal vein ligation. HELIYON, 10(6), e27578. https://doi.org/10.1016/j.heliyon.2024.e27578

Vancouver

Zhang T, Seeger P, Simsek YJ, Sabihi M, Lücke J, Zazara-Giannou D et al. IL-22 promotes liver regeneration after portal vein ligation. HELIYON. 2024 Mar 30;10(6):e27578. https://doi.org/10.1016/j.heliyon.2024.e27578

Bibtex

@article{6680af5f1b42429c93d2ddd5d02279d6,
title = "IL-22 promotes liver regeneration after portal vein ligation",
abstract = "BackgroundInsufficient remnant liver volume (RLV) after the resection of hepatic malignancy could lead to liver failure and mortality. Portal vein ligation (PVL) prior to hepatectomy is subsequently introduced to increase the remnant liver volume and improve the outcome of hepatic malignancy. IL-22 has previously been reported to promote liver regeneration, while facilitating tumor development in the liver via Steap4 upregulation. Here we performed PVL in mouse models to study the role of IL-22 in liver regeneration post-PVL.MethodsLiver weight and volume was measured via magnetic resonance imaging (MRI). Immunohistochemistry for Ki67 and hepatocyte growth factor (HGF) was performed. IL-22 was analyzed by flow cytometry and quantitative polymerase chain reaction (qPCR) was used for acquisition of Il-33, Steap4, Fga, Fgb and Cebpd. To analyze signaling pathways, mice with deletion of STAT3 and a neutralizing antibody for IL-22 were used.ResultsThe remnant liver weight and volume increased over time after PVL. Additionally, we found that liver regenerative molecules, including Ki67 and HGF, were significantly increased in remnant liver at day 3 post-PVL, as well as IL-22. Administration of IL-22 neutralizing antibody could reduce Ki67 expression after PVL. The upregulation of IL-22 after PVL was mainly derived from innate cells. IL-22 blockade resulted in lower levels of IL-33 and Steap4 in the remnant liver, which was also the case in mice with deletion of STAT3, the main downstream signaling molecule of IL-22, in hepatocytes.ConclusionIL-22 promotes liver regeneration after PVL. Thus, a combination of IL-22 supplementation and Steap4 blockade could potentially be applied as a novel therapeutic approach to boost liver regeneration without facilitating tumor progression after PVL.",
author = "Tao Zhang and Philipp Seeger and Simsek, {Yashin J} and Morsal Sabihi and J{\"o}ran L{\"u}cke and Dimitra Zazara-Giannou and Mustafa Shiri and Kempski, {Jan Michael} and Tom Blankenburg and Lilan Zhao and Ioannis Belios and Machicote, {Andres Pablo} and Baris Mercanoglu and Mohammad Fard-Aghaie and Notz, {Sara Johanna} and Lykoudis, {Panagis M} and Marius Kemper and Tarik Ghadban and Oliver Mann and Thilo Hackert and Jakob Izbicki and Thomas Renne and Samuel Huber and Anastasios Giannou and Jun Li",
year = "2024",
month = mar,
day = "30",
doi = "10.1016/j.heliyon.2024.e27578",
language = "English",
volume = "10",
pages = "e27578",
journal = "HELIYON",
issn = "2405-8440",
publisher = "Elsevier BV",
number = "6",

}

RIS

TY - JOUR

T1 - IL-22 promotes liver regeneration after portal vein ligation

AU - Zhang, Tao

AU - Seeger, Philipp

AU - Simsek, Yashin J

AU - Sabihi, Morsal

AU - Lücke, Jöran

AU - Zazara-Giannou, Dimitra

AU - Shiri, Mustafa

AU - Kempski, Jan Michael

AU - Blankenburg, Tom

AU - Zhao, Lilan

AU - Belios, Ioannis

AU - Machicote, Andres Pablo

AU - Mercanoglu, Baris

AU - Fard-Aghaie, Mohammad

AU - Notz, Sara Johanna

AU - Lykoudis, Panagis M

AU - Kemper, Marius

AU - Ghadban, Tarik

AU - Mann, Oliver

AU - Hackert, Thilo

AU - Izbicki, Jakob

AU - Renne, Thomas

AU - Huber, Samuel

AU - Giannou, Anastasios

AU - Li, Jun

PY - 2024/3/30

Y1 - 2024/3/30

N2 - BackgroundInsufficient remnant liver volume (RLV) after the resection of hepatic malignancy could lead to liver failure and mortality. Portal vein ligation (PVL) prior to hepatectomy is subsequently introduced to increase the remnant liver volume and improve the outcome of hepatic malignancy. IL-22 has previously been reported to promote liver regeneration, while facilitating tumor development in the liver via Steap4 upregulation. Here we performed PVL in mouse models to study the role of IL-22 in liver regeneration post-PVL.MethodsLiver weight and volume was measured via magnetic resonance imaging (MRI). Immunohistochemistry for Ki67 and hepatocyte growth factor (HGF) was performed. IL-22 was analyzed by flow cytometry and quantitative polymerase chain reaction (qPCR) was used for acquisition of Il-33, Steap4, Fga, Fgb and Cebpd. To analyze signaling pathways, mice with deletion of STAT3 and a neutralizing antibody for IL-22 were used.ResultsThe remnant liver weight and volume increased over time after PVL. Additionally, we found that liver regenerative molecules, including Ki67 and HGF, were significantly increased in remnant liver at day 3 post-PVL, as well as IL-22. Administration of IL-22 neutralizing antibody could reduce Ki67 expression after PVL. The upregulation of IL-22 after PVL was mainly derived from innate cells. IL-22 blockade resulted in lower levels of IL-33 and Steap4 in the remnant liver, which was also the case in mice with deletion of STAT3, the main downstream signaling molecule of IL-22, in hepatocytes.ConclusionIL-22 promotes liver regeneration after PVL. Thus, a combination of IL-22 supplementation and Steap4 blockade could potentially be applied as a novel therapeutic approach to boost liver regeneration without facilitating tumor progression after PVL.

AB - BackgroundInsufficient remnant liver volume (RLV) after the resection of hepatic malignancy could lead to liver failure and mortality. Portal vein ligation (PVL) prior to hepatectomy is subsequently introduced to increase the remnant liver volume and improve the outcome of hepatic malignancy. IL-22 has previously been reported to promote liver regeneration, while facilitating tumor development in the liver via Steap4 upregulation. Here we performed PVL in mouse models to study the role of IL-22 in liver regeneration post-PVL.MethodsLiver weight and volume was measured via magnetic resonance imaging (MRI). Immunohistochemistry for Ki67 and hepatocyte growth factor (HGF) was performed. IL-22 was analyzed by flow cytometry and quantitative polymerase chain reaction (qPCR) was used for acquisition of Il-33, Steap4, Fga, Fgb and Cebpd. To analyze signaling pathways, mice with deletion of STAT3 and a neutralizing antibody for IL-22 were used.ResultsThe remnant liver weight and volume increased over time after PVL. Additionally, we found that liver regenerative molecules, including Ki67 and HGF, were significantly increased in remnant liver at day 3 post-PVL, as well as IL-22. Administration of IL-22 neutralizing antibody could reduce Ki67 expression after PVL. The upregulation of IL-22 after PVL was mainly derived from innate cells. IL-22 blockade resulted in lower levels of IL-33 and Steap4 in the remnant liver, which was also the case in mice with deletion of STAT3, the main downstream signaling molecule of IL-22, in hepatocytes.ConclusionIL-22 promotes liver regeneration after PVL. Thus, a combination of IL-22 supplementation and Steap4 blockade could potentially be applied as a novel therapeutic approach to boost liver regeneration without facilitating tumor progression after PVL.

U2 - 10.1016/j.heliyon.2024.e27578

DO - 10.1016/j.heliyon.2024.e27578

M3 - SCORING: Journal article

C2 - 38533053

VL - 10

SP - e27578

JO - HELIYON

JF - HELIYON

SN - 2405-8440

IS - 6

ER -