ArticleCellular and molecular gastroenterology and hepatology2022
Glia Maturation Factor-β Supports Liver Regeneration by Remodeling Actin Network to Enhance STAT3 Proliferative Signals.
Article in Cellular and molecular gastroenterology and hepatology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 11 citations in OpenAlex.
- Hepassocin prevents age-related liver senescence and facilitates liver regeneration by activating AMPK.Signal transduction and targeted therapy · 2026Article
- GMFB promotes lung adenocarcinoma progression by activating the MAPK/ERK signaling pathway.Molecular and cellular biochemistry · 2026Article
- Lipid metabolism orchestrates liver regeneration: an integrated metabolic network.Journal of translational medicine · 2025Review
- Glial maturation factor-β deficiency prevents oestrogen deficiency-induced bone loss by remodelling the actin network to suppress adipogenesis of bone marrow mesenchymal stem cells.Cell death & disease · 2024Article
- TRIM26 deficiency enhancing liver regeneration through macrophage polarization and β-catenin pathway activation.Cell death & disease · 2024Article
- Revealing the Changes in Saliva and Serum Proteins of Pigs with Meningitis Caused by Streptococcus Suis: A Proteomic Approach.International journal of molecular sciences · 2022Article
Corrections and comments
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Authors and funding
8 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND &
aimsGlia maturation factor-β (GMFB) is a bona fide member of the actin depolymerizing factor homology family. Recently, emerging evidence suggested its implication in liver diseases, but data on its role in liver remain limited.
methodsAssessment of GMFB in liver histology, impact on liver regeneration and hepatocyte proliferation, and the underlying molecular pathways were conducted using mouse models with acute liver injury.
resultsGMFB is widely distributed in normal liver. Its expression increases within 24 hours after partial hepatectomy (PHx). Adult Gmfb knockout mice and wild-type littermates are similar in gross appearance, body weight, liver function, and histology. However, compared with wild-type control, Gmfb knockout mice post-PHx develop more serious liver damage and steatosis and have delayed liver regeneration; the dominant change in liver transcriptome at 24 hours after PHx is the significantly suppressed acute inflammation pathways; the top down-regulated gene sets relate to interleukin (IL)6/Janus kinase/signal transducer and activator of transcription 3 (STAT3) signaling. Another mouse model intoxicated with carbon tetrachloride replicated these findings. Furthermore, Gmfb knockout and wild-type groups have the similar numbers of Kupffer cells, but Gmfb knockout Kupffer cells once stimulated produce less IL6, tumor necrosis factor, and IL1β. In hepatocytes treated with IL6, GMFB associates positively with cell proliferation and STAT3/cyclin D1 activation, but without any direct interaction with STAT3. In Gmfb knockout hepatocytes, cytoskeleton-related gene expression was changed significantly, with an abnormal-appearing morphology of actin networks. In hepatocyte modeling, actin-filament turnover, STAT3 activation, and metabolite excretion show a strong reliance on the status of actin-filament organization.
conclusionsGMFB plays a significant role in liver regeneration by promoting acute inflammatory response in Kupffer cells and by intracellularly coordinating the responsive hepatocyte proliferation.
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