Three-dimensional structure of liver vessels and spatial distribution of hepatic immune cells

Xu, Mengli; Liu, Zheng; Li, Xinlin; Wang, Xinru; Yuan, Xuenan; Han, Chuntan; Zhang, Zhihong

doi:10.1142/s1793545823300069

Cited by 3 publications

(2 citation statements)

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“…27a ). In light of this fact and our previous study on 3D vascular architecture of intact mouse liver lobe 42 , 43 , we successfully segmented out hepatic veins (HVs) including its branch central veins (CVs), portal veins (PVs), and MPs, and created a liver lobe’s 3D structure showing the spatial locations of MPs and blood vessels (Fig. 4a , Supplementary Movie 1 ).…”

Section: Resultsmentioning

confidence: 96%

UFObow: A single-wavelength excitable Brainbow for simultaneous multicolor ex-vivo and in-vivo imaging of mammalian cells

Hu,

Yang,

Liu

et al. 2024

Commun Biol

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Brainbow is a genetic cell-labeling technique that allows random colorization of multiple cells and real-time visualization of cell fate within a tissue, providing valuable insights into understanding complex biological processes. However, fluorescent proteins (FPs) in Brainbow have distinct excitation spectra with peak difference greater than 35 nm, which requires sequential imaging under multiple excitations and thus leads to long acquisition times. In addition, they are not easily used together with other fluorophores due to severe spectral bleed-through. Here, we report the development of a single-wavelength excitable Brainbow, UFObow, incorporating three newly developed blue-excitable FPs. We have demonstrated that UFObow enables not only tracking the growth dynamics of tumor cells in vivo but also mapping spatial distribution of immune cells within a sub-cubic centimeter tissue, revealing cell heterogeneity. This provides a powerful means to explore complex biology in a simultaneous imaging manner at a single-cell resolution in organs or in vivo.

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Section: Resultsmentioning

confidence: 96%

UFObow: A single-wavelength excitable Brainbow for simultaneous multicolor ex-vivo and in-vivo imaging of mammalian cells

Hu,

Yang,

Liu

et al. 2024

Commun Biol

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“…The functions of Mon/Mφs in the liver are closely related to their spatial localization 29 , 30 . The hepatic lobule is the basic structural and functional unit of the liver 35 , 36 . Therefore, studying the arrangement of CX3CR1 GFP cells in the hepatic lobules of the fibrotic liver is valuable.…”

Section: Resultsmentioning

confidence: 99%

Intravital imaging of splenic classical monocytes modifying the hepatic CX3CR1⁺ cells motility to exacerbate liver fibrosis via spleen-liver axis

Han,

Zhai,

Wang

et al. 2024

Theranostics

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CX3CR1 + cells play a crucial role in liver fibrosis progression. However, changes in the migratory behavior and spatial distribution of spleen-derived and hepatic CX3CR1 + cells in the fibrotic liver as well as their influence on the liver fibrosis remain unclear. Methods: The CX3CR1 GFP/+ transgenic mice and CX3CR1-KikGR transgenic mice were used to establish the CCl4-induced liver fibrosis model. Splenectomy, adoptive transfusion of splenocytes, in vivo photoconversion of splenic CX3CR1 + cells and intravital imaging were performed to study the spatial distribution, migration and movement behavior, and regulatory function of CX3CR1 + cells in liver fibrosis. Results: Intravital imaging revealed that the CX3CR1 GFP cells accumulated into the fibrotic liver and tended to accumulate towards the central vein (CV) in the hepatic lobules. Two subtypes of hepatic CX3CR1 + cells existed in the fibrotic liver. The first subtype was the interacting CX3CR1 GFP cells, most of which were observed to distribute in the liver parenchyma and had a higher process velocity; the second subtype was mobile CX3CR1 GFP cells, most of which were present in the hepatic vessels with a faster moving speed. Splenectomy ameliorated liver fibrosis and decreased the number of CX3CR1 + cells in the fibrotic liver. Moreover, splenectomy rearranged CX3CR1 GFP cells to the boundary of the hepatic lobule, reduced the process velocity of interacting CX3CR1 GFP cells and decreased the number and mobility of mobile CX3CR1 GFP cells in the fibrotic liver. Transfusion of spleen-derived classical monocytes increased the process velocity and mobility of hepatic endogenous CX3CR1 GFP cells and facilitated liver fibrosis progression via the production of proinflammatory and profibrotic cytokines. The photoconverted splenic CX3CR1 + KikRed + cells were observed to leave the spleen, accumulate into the fibrotic liver and contact with hepatic CX3CR1 + KikGreen + cells during hepatic fibrosis. Conclusion: The splenic CX3CR1 + monocytes with classical phenotype migrated from the spleen to the fibrotic liver, modifying the migratory behavior of hepatic endogenous CX3CR1 GFP cells and exacerbating liver fibrosis via the secretion of cytokines. This study reveals that splenic CX3CR1 + classical monocytes are a key driver of liver fibrosis via the spleen-liver axis and may be potential candidate targets for the treatment of chronic liver fibrosis.

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Polyploidy-mediated resilience in hepatic aging: molecular mechanisms and functional implication

Addissouky

2024

Egypt Liver Journal

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Background Polyploidization, a process where cells acquire additional chromosome sets, is a unique characteristic of hepatocytes. This process has been increasingly recognized as an adaptive mechanism for maintaining liver function during aging, a period characterized by cellular senescence, DNA damage, and metabolic dysregulation. Purpose This review explores the molecular mechanisms underlying hepatocyte polyploidization and its potential role in promoting resilience against the aging-related decline in liver function. We assess how polyploid hepatocytes contribute to genomic stability, stress resistance, and metabolic adaptation, highlighting their relevance to liver aging. Main body Hepatocyte polyploidization occurs through mechanisms such as cytokinesis failure and endoreplication, leading to binuclear or mononuclear polyploid cells. Polyploid hepatocytes exhibit enhanced DNA repair capacity, which helps mitigate the accumulation of age-related genomic damage. The increased gene dosage in polyploid cells facilitates better stress responses, particularly against oxidative stress and genotoxic insults. Metabolic adaptations, including enhanced xenobiotic metabolism and lipid regulation, further support the liver’s ability to maintain homeostasis during aging. Additionally, polyploid cells demonstrate altered epigenetic landscapes and proteostasis mechanisms, contributing to improved cellular function and reduced susceptibility to senescence. These adaptations collectively enhance liver resilience against age-related metabolic and structural challenges. Conclusion Hepatocyte polyploidization represents a critical protective mechanism in liver aging, promoting cellular adaptations that safeguard against genomic instability, metabolic dysfunction, and oxidative stress. Understanding the molecular pathways driving polyploidization could pave the way for novel therapeutic strategies to combat age-related liver disorders and enhance health span. Graphical Abstract

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Three-dimensional structure of liver vessels and spatial distribution of hepatic immune cells

Cited by 3 publications

References 73 publications

UFObow: A single-wavelength excitable Brainbow for simultaneous multicolor ex-vivo and in-vivo imaging of mammalian cells

UFObow: A single-wavelength excitable Brainbow for simultaneous multicolor ex-vivo and in-vivo imaging of mammalian cells

Intravital imaging of splenic classical monocytes modifying the hepatic CX3CR1⁺ cells motility to exacerbate liver fibrosis via spleen-liver axis

Polyploidy-mediated resilience in hepatic aging: molecular mechanisms and functional implication

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Three-dimensional structure of liver vessels and spatial distribution of hepatic immune cells

Cited by 3 publications

References 73 publications

UFObow: A single-wavelength excitable Brainbow for simultaneous multicolor ex-vivo and in-vivo imaging of mammalian cells

UFObow: A single-wavelength excitable Brainbow for simultaneous multicolor ex-vivo and in-vivo imaging of mammalian cells

Intravital imaging of splenic classical monocytes modifying the hepatic CX3CR1+ cells motility to exacerbate liver fibrosis via spleen-liver axis

Polyploidy-mediated resilience in hepatic aging: molecular mechanisms and functional implication

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Product

Resources

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Intravital imaging of splenic classical monocytes modifying the hepatic CX3CR1⁺ cells motility to exacerbate liver fibrosis via spleen-liver axis