5-HT and Intraplatelet 5-HT: a potential upstream regulator of YAP in liver regeneration

He, Chao; Zhai, Mimi; Shu, Bo; Deng, Chaolin; Li, Li; Liu, Sushun

doi:10.1038/s12276-019-0324-1

Cited by 2 publications

(3 citation statements)

References 8 publications

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“…While depletion of IP 5‐HT is associated with delayed LR after partial hepatectomy 5 downstream effects targeted by 5‐HT remain unclear. Previous experimental results suggested that 5‐HT might affect YAP‐1 signaling during LR 17,43 . In this context, TPH −/− mice show significantly reduced levels of YAP‐1 expression during LR with concomitantly reduced regenerative capacity.…”

Section: Discussionmentioning

confidence: 93%

“…Previous experimental results suggested that 5-HT might affect YAP-1 signaling during LR. 17,43 In this context, TPH −/− mice show significantly reduced levels of YAP-1 expression during LR with concomitantly reduced regenerative capacity. In line with these results, we observed that portal venous 5-HT levels were associated with intrahepatic YAP-1 expression during LR.…”

Section: Discussionmentioning

confidence: 99%

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Tyrosine phosphorylation of YAP‐1 in biliary epithelial cells mediates posthepatectomy liver regeneration and is affected by serotonin

Starlinger

Brunnthaler

Watkins

et al. 2023

J of Cellular Biochemistry

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Experimental data suggested activation of yes-associated protein (YAP-1) as a critical regulator of liver regeneration (LR). Serotonin (5-HT) promotes LR in rodent models and has been proposed to act via YAP-1. How 5-HT affects LR is incompletely understood. A possible mechanism how 5-HT affects human LR was explored. Sixty-one patients were included. Tissue samples prior and 2 h after induction of LR were collected. Circulating levels of 5-HT and osteopontin (OPN) were assessed. YAP-1, its phosphorylation states, cytokeratin 19 (CK-19) and OPN were assessed using immunofluorescence. A mouse model of biliary epithelial cells (BECs) specific deletion of YAP/TAZ was developed. YAP-1 increased as early as 2 h after induction of LR (p = 0.025) predominantly in BECs. BEC specific deletion of YAP/TAZ reduced LR after 70% partial hepatectomy in mice (Ki67%, p < 0.001). SSRI treatment, depleting intra-platelet 5-HT, abolished YAP-1 and OPN induction upon LR. Portal vein 5-HT levels correlated with intrahepatic YAP-1 expression upon LR (R = 0.703, p = 0.035). OPN colocalized with YAP-1 in BECs and its circulating levels increased in the liver vein 2 h after induction of LR (p = 0.017). In the context of LR tyrosine-phosphorylated YAP-1 significantly increased (p = 0.042). Stimulating BECs with 5-HT resulted in increased YAP-1 activation via tyrosine-phosphorylation and subsequently increased OPN expression. BECs YAP-1 appears to be critical for LR in mice and humans.Our evidence suggests that 5-HT, at least in part, exerts its pro-regenerative effects via YAP-1 tyrosine-phosphorylation in BECs and subsequent OPNdependent paracrine immunomodulation.

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Section: Discussionmentioning

confidence: 93%

Section: Discussionmentioning

confidence: 99%

Tyrosine phosphorylation of YAP‐1 in biliary epithelial cells mediates posthepatectomy liver regeneration and is affected by serotonin

Starlinger

Brunnthaler

Watkins

et al. 2023

J of Cellular Biochemistry

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“…Interferon alpha is also involved in the LR process mediated by oval cells after liver injury ( Batusic et al, 2011 ). In addition to protein molecules, sphingosine-1-phosphate, prostaglandin E2, and serotonin are also involved in the regulation of LR ( Ding et al, 2016 ; He et al, 2019 ; Cheng et al, 2021 ). Extracellular vesicles represent another form of mediating communication between cells ( Brandel et al, 2022 ), and due to their accessibility, extracellular vesicles have become an important approach for the diagnosis and treatment of various diseases ( Sun et al, 2023 ).…”

Section: Cell Interaction Dimension Analysis Of Lr: Cytokine Interactionmentioning

confidence: 99%

Unveiling the power of microenvironment in liver regeneration: an in-depth overview

Hu,

Wang,

et al. 2023

Front. Genet.

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The liver serves as a vital regulatory hub for various physiological processes, including sugar, protein, and fat metabolism, coagulation regulation, immune system maintenance, hormone inactivation, urea metabolism, and water-electrolyte acid-base balance control. These functions rely on coordinated communication among different liver cell types, particularly within the liver’s fundamental hepatic lobular structure. In the early stages of liver development, diverse liver cells differentiate from stem cells in a carefully orchestrated manner. Despite its susceptibility to damage, the liver possesses a remarkable regenerative capacity, with the hepatic lobule serving as a secure environment for cell division and proliferation during liver regeneration. This regenerative process depends on a complex microenvironment, involving liver resident cells, circulating cells, secreted cytokines, extracellular matrix, and biological forces. While hepatocytes proliferate under varying injury conditions, their sources may vary. It is well-established that hepatocytes with regenerative potential are distributed throughout the hepatic lobules. However, a comprehensive spatiotemporal model of liver regeneration remains elusive, despite recent advancements in genomics, lineage tracing, and microscopic imaging. This review summarizes the spatial distribution of cell gene expression within the regenerative microenvironment and its impact on liver regeneration patterns. It offers valuable insights into understanding the complex process of liver regeneration.

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5-HT and Intraplatelet 5-HT: a potential upstream regulator of YAP in liver regeneration

Cited by 2 publications

References 8 publications

Tyrosine phosphorylation of YAP‐1 in biliary epithelial cells mediates posthepatectomy liver regeneration and is affected by serotonin

Tyrosine phosphorylation of YAP‐1 in biliary epithelial cells mediates posthepatectomy liver regeneration and is affected by serotonin

Unveiling the power of microenvironment in liver regeneration: an in-depth overview

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