Glia Maturation Factor-β Supports Liver Regeneration by Remodeling Actin Network to Enhance STAT3 Proliferative Signals

Yin, Guang; Zeng, Weisen; Li, Rong; Zeng, Manman; Chen, Ronghua; Liu, Yaxue; Jiang, Ronglong; Wang, Yan

doi:10.1016/j.jcmgh.2022.07.016

Cited by 3 publications

(3 citation statements)

References 49 publications

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“…The increased expression of VCL in saliva could potentially be associated with muscle damage and seizures that usually are presented in the case of meningitis [14]. In this line, in our study, we have also observed an upregulation in the actin-depolymerizing factor (GSN) whose family is involved in the muscle actin filament organization and muscle contraction [17].…”

Section: Changes In Salivary Proteins In Pigs With Meningitissupporting

confidence: 75%

Revealing the Changes in Saliva and Serum Proteins of Pigs with Meningitis Caused by Streptococcus Suis: A Proteomic Approach

López-Martínez

Beletić

Kuleš

et al. 2022

IJMS

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Meningitis due to Streptococcus suis causes high mortality and morbidity on pig farms and has increasing zoonotic potential worldwide. Saliva proteome analysis would potentially be useful in elucidating pathophysiological changes and mining for new biomarkers to diagnose and monitor S. suis infection. The objective of this study was to investigate the changes in the salivary and serum proteome profile of piglets with meningitis. The LC-MS/MS TMT proteomic approach was used to analyze saliva and serum samples from 20 male piglets: 10 with meningitis and 10 healthy. In saliva, 11 proteins had higher and 10 had lower relative abundance in piglets with meningitis. The proteins with the highest relative abundance were metavinculin (VCL) and desmocollin-2 (DSC2). Adenosine deaminase (ADA) was selected for validation using a spectrophotometric assay and demonstrated excellent performance in the differentiation between healthy and pigs with meningitis due to S. suis. In serum, the most protruding changes occurred for one SERPIN and haptoglobin (HP). In saliva and serum, the highest number of proteins with altered abundance were linked, via the enrichment analysis, with platelet and neutrophil pathways. Overall, meningitis caused by S. suis resulted in specific proteome changes in saliva and serum, reflecting different pathophysiological mechanisms, and marking new potential biomarkers for this infection.

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Section: Changes In Salivary Proteins In Pigs With Meningitissupporting

confidence: 75%

Revealing the Changes in Saliva and Serum Proteins of Pigs with Meningitis Caused by Streptococcus Suis: A Proteomic Approach

López-Martínez

Beletić

Kuleš

et al. 2022

IJMS

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“…In the other study, GMF𝛽 knockout mice were found to develop more serious liver damage after partial hepatectomy, which was associated with interleukin (IL)6/Janus kinase/signal transducer and activator of transcription 3 (STAT3) signaling. [5] Since perivascular inflammation plays an essential role in PAH, and GMF𝛽 can induce inflammation by promoting the production of inflammatory cytokines, we hypothesized that GMF𝛽 may be involved in the formation of PAH.…”

Section: Introductionmentioning

confidence: 99%

Preliminary Mechanism of Glial Maturation Factor β on Pulmonary Vascular Remodeling in Pulmonary Arterial Hypertension

Li,

Shi,

Yan

et al. 2024

Advanced Biology

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Recent evidence suggests that glia maturation factor β (GMFβ) is important in the pathogenesis of pulmonary arterial hpertension (PAH), but the underlying mechanism is unknown. To clarify whether GMFβ can be involved in pulmonary vascular remodeling and to explore the role of the IL‐6‐STAT3 pathway in this process, the expression of GMFβ in PAH rats is examined and the expression of downstream molecules including periostin (POSTN) and interleukin‐6 (IL‐6) is measured using real‐time quantitative polymerase chain reaction (RT‐qPCR) and western blot analysis. The location and expression of POSTN is also tested in PAH rats using immunofluorescence. It is proved that GMFβ is upregulated in the lungs of PAH rats. Knockout GMFβ alleviated the MCT‐PAH by reducing right ventricular systolic pressure (RVSP), mean pulmonary arterial pressure (mPAP), and pulmonary vascular remodeling. Moreover, the inflammation of the pulmonary vasculature is ameliorated in PAH rats with GMFβ absent. In addition, the IL‐6‐STAT3 signaling pathway is activated in PAH; knockout GMFβ reduced POSTN and IL‐6 production by inhibiting the IL‐6‐STAT3 signaling pathway. Taken together, these findings suggest that knockout GMFβ ameliorates PAH in rats by inhibiting the IL‐6‐STAT3 signaling pathway.

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“…For instance, pro-inflammatory M1 macrophages have been found to induce harm to neighboring tissues and impede the regeneration of surrounding cells by secreting pro-inflammatory cytokines and chemokines that activate intracellular cell death mechanisms [ 9 ]. On the other hand, they can also produce pro-inflammatory cytokines, including IL-6, TNF-α, and IL-1β, that are critical for supporting liver regeneration [ 10 , 11 ]. M2 macrophages secrete anti-inflammatory cytokines, which can reduce inflammation and promote tissue repair [ 3 ].…”

Section: Introductionmentioning

confidence: 99%

TRIM26 deficiency enhancing liver regeneration through macrophage polarization and β-catenin pathway activation

Li,

Zhong,

et al. 2024

Cell Death Dis

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Liver regeneration is a complex process involving the crosstalk between parenchymal and non-parenchymal cells, especially macrophages. However, the underlying mechanisms remain incompletely understood. Here, we identify the E3 ubiquitin ligase TRIM26 as a crucial regulator of liver regeneration. Following partial hepatectomy or acute liver injury induced by carbon tetrachloride, Trim26 knockout mice exhibit enhanced hepatocyte proliferation compared to wild-type controls, while adeno-associated virus (AAV)-mediated overexpression of Trim26 reverses the promotional effects. Mechanistically, Trim26 deficiency promotes the recruitment of macrophages to the liver and their polarization towards pro-inflammatory M1 phenotype. These M1 macrophages secrete Wnts, including Wnt2, which subsequently stimulate hepatocyte proliferation through the activation of Wnt/β-catenin signaling. In hepatocytes, Trim26 knockdown reduces the ubiquitination and degradation of β-catenin, thereby further enhancing Wnt/β-catenin signaling. Pharmacological inhibition of Wnt/β-catenin pathway by ICG-001 or depletion of macrophages by clodronate liposomes diminishes the pro-regenerative effects of Trim26 deficiency. Moreover, bone marrow transplantation experiments provide evidence that Trim26 knockout in myeloid cells alone can also promote liver regeneration, highlighting the critical role of macrophage Trim26 in this process. Taken together, our study uncovers TRIM26 as a negative regulator of liver regeneration by modulating macrophage polarization and Wnt/β-catenin signaling in hepatocytes, providing a potential therapeutic target for promoting liver regeneration in clinical settings.

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Glia Maturation Factor-β Supports Liver Regeneration by Remodeling Actin Network to Enhance STAT3 Proliferative Signals

Cited by 3 publications

References 49 publications

Revealing the Changes in Saliva and Serum Proteins of Pigs with Meningitis Caused by Streptococcus Suis: A Proteomic Approach

Revealing the Changes in Saliva and Serum Proteins of Pigs with Meningitis Caused by Streptococcus Suis: A Proteomic Approach

Preliminary Mechanism of Glial Maturation Factor β on Pulmonary Vascular Remodeling in Pulmonary Arterial Hypertension

TRIM26 deficiency enhancing liver regeneration through macrophage polarization and β-catenin pathway activation

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