In vitro proliferation and differentiation of hepatic oval cells and their potential capacity for intrahepatic transplantation

Li, Zhiman; Chen, J.; Li, L.; Ran, Jianghua; Liu, J.; Gao, T.X.; Guo, Bingyu; Li, X.H.; Liu, Z.H.; Liu, G.J.; Gao, Yanchao; Zhang, X.L.

doi:10.1590/1414-431x20132620

Cited by 5 publications

(4 citation statements)

References 23 publications

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“…Hepatic progenitor cells, also termed oval cells, proliferate and differentiate into hepatocytes and biliary epithelial cells following stimulation, including viral infection and cytotoxic drugs. It has been suggested that hepatic oval cells facilitate liver regeneration following orthotopic liver transplantation ( 19 ). Previous studies have demonstrated that WB-F344 oval cells are important in the repair and regeneration of injured liver ( 3 , 20 ).…”

Section: Discussionmentioning

confidence: 99%

Tanshinone IIA promotes the proliferation of WB-F344 hepatic oval cells via Wnt/β-catenin signaling

Jia

et al. 2015

Molecular Medicine Reports

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Tanshinone IIA (TSA) is a widely used traditional Chinese medicine, which has been demonstrated to protect damaged liver cells and is currently administered in the treatment of liver fibrosis. Liver precursor cells, also termed oval cells, are key in the repair of liver tissues following injury. However, whether TSA improves the function of liver cells and protects the liver from injury by enhancing the growth and proliferation of hepatic oval cells remains to be elucidated. In the present study, low to moderate concentrations of TSA were observed to stimulate proliferation, did not induce apoptosis in WB-F344 rat hepatic oval cells and the increased expression levels of β-catenin. WB-F344 cells were treated with various concentrations of TSA (0–80 µg/ml) for 24, 48, 72 and 96 h. Cell proliferation was measured using a Cell Counting kit-8 (CCK-8) assay, a 5-ethynyl-2′-deoxyuridine assay and a carboxyfluorescein diacetate succinimidyl ester (CFSE) assay. The CCK-8 assay demonstrated that treatment of WB-F344 cells with 20–40 µg/ml TSA for up to 72 h significantly increased proliferation. Similar results were observed in the subsequent EdU and CFSE assays. Furthermore, a terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling assay demonstrated that 20–40 µg/ml TSA treatment for up to 96 h did not induce apoptosis of the WB-F344 cells. Notably, the results of western blot, immunofluorescence and reverse transcription-quantitative polymerase chain reaction analyses demonstrated that treatment of the WB-F344 cells with 20–40 µg/ml TSA for up to 72 h significantly increased the expression levels of β-catenin. These data indicated that TSA at concentrations between 20 and 40 µg/ml may induce WB-F344 cell proliferation by activating the canonical Wnt signaling pathway. The results of the present study suggest that TSA may be a useful natural agent to enhance repair and regeneration of the injured liver, and improve liver regeneration following orthotopic liver transplantation.

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Section: Discussionmentioning

confidence: 99%

Tanshinone IIA promotes the proliferation of WB-F344 hepatic oval cells via Wnt/β-catenin signaling

Jia

et al. 2015

Molecular Medicine Reports

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“…Oval cell transplantation after liver transplantation might be useful for liver regeneration. A study by Li et al (2013) isolated oval cells, of which 99.8% were positive for c-kit. After primary culture, oval cells were injected into the rats who underwent liver transplantation.…”

Section: Clinical Implications Of C-kit In Livermentioning

confidence: 99%

“…After primary culture, oval cells were injected into the rats who underwent liver transplantation. Data shows that compared to controls, oval cell transplantation significantly improved the liver function, prolonged median survival time and reduced acute allograft rejection ( Li et al, 2013 ).…”

Section: Clinical Implications Of C-kit In Livermentioning

confidence: 99%

C-Kit, a Double-Edged Sword in Liver Regeneration and Diseases

et al. 2021

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Previous studies have reported an important role of c-kit in embryogenesis and adulthood. Activation of the SCF/KIT signal transduction pathway is customarily linked to cell proliferation, migration and survival thus influence hematopoiesis, pigmentation, and spermatogenesis. The role of c-kit in the liver is controversial, it is however argued that it is a double-edged sword in liver regeneration and diseases. First, liver c-kit+ cells, including oval cells, bile epithelial cells, and part of hepatocytes, participate in liver tissue repair by regenerating target cells according to the type of liver injury. At the same time, c-kit+ mast cells, act as immature progenitors in circulation, playing a critical role in liver fibrosis. Furthermore, c-kit is also a proto-oncogene. Notably, c-kit overexpression regulates gastrointestinal stromal tumors. Various studies have explored on c-kit and hepatocellular carcinoma, nevertheless, the intricate roles of c-kit in the liver are largely understudied. Herein, we extensively summarize previous studies geared toward providing hints for future clinical and basic research.

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“…In fact, as the tissue development proceeds, the ratio of hepatoblast/hepatocytes is decreased until the time in which the regeneration is further followed only by hepatocyte proliferation (Butler et al, 2018; Wang et al, 2020). Similarly, in the regeneration process after partial hepatectomy of mice liver, if no delay in hepatocyte proliferation occurs, a rough simultaneous specification of hepatic resident progenitors and cell cycle activity of parenchymal hepatocytes proceeds, whereas if the hepatocytes proliferation impaired or delayed, the hepatoblast specification precedes, and they invade the adjacent tissue as they proliferate (Li et al, 2013). Based on cell activity characterizations after partial hepatectomy, it has been documented that in a short time, hepatocytes start to proliferate giving a peak in 24 h after hepatectomy.…”

Section: Regeneration Time Framementioning

confidence: 99%

Signaling molecules orchestrating liver regenerative medicine

Zakeri

Mirdamadi

Kalhori

et al. 2020

J Tissue Eng Regen Med

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The liver is in charge of more than 500 functions in the human body, which any damage and failure to the liver can significantly compromise human life. Numerous studies are being carried out in regenerative medicine, as a potential driving force, toward alleviating the need for liver donors and fabrication of a 3D‐engineered transplantable hepatic tissue. Liver tissue engineering brings three main factors of cells, extracellular matrix (ECM), and signaling molecules together, while each of these three factors tries to mimic the physiological state of the tissue to direct tissue regeneration. Signaling molecules play a crucial role in directing tissue fabrication in liver tissue engineering. When mimicking the natural in vivo process of regeneration, it is tightly associated with three main phases of differentiation, proliferation (progression), and tissue maturation through vascularization while directing each of these phases is highly regulated by the specific signaling molecules. The understanding of how these signaling molecules guide the dynamic behavior of regeneration would be a tool for further tailoring of bioengineered systems to help the liver regeneration with many cellular, molecular, and tissue‐level functions. Hence, the signaling molecules come to aid all these phases for further improvements toward the clinical use of liver tissue engineering as the goal.

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In vitro proliferation and differentiation of hepatic oval cells and their potential capacity for intrahepatic transplantation

Cited by 5 publications

References 23 publications

Tanshinone IIA promotes the proliferation of WB-F344 hepatic oval cells via Wnt/β-catenin signaling

Tanshinone IIA promotes the proliferation of WB-F344 hepatic oval cells via Wnt/β-catenin signaling

C-Kit, a Double-Edged Sword in Liver Regeneration and Diseases

Signaling molecules orchestrating liver regenerative medicine

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