Liver regeneration following partial hepatectomy is improved by enhancing the HGF/Met axis and Akt and Erk pathways after low-power laser irradiation in rats

Araújo, Tiago Gomes; Oliveira, Alexandre G.; Tobar, Natália; Saad, Mário J.A.; Moreira, Luciana Regina; Reis, Edmyr Rosa dos; Nicola, Ester Maria Danielli; Jorge, G.L.; Tártaro, R.R.; Boin, I.F.S.F.; Teixeira, Antônio Roberto Franchi

doi:10.1007/s10103-013-1264-y

Cited by 20 publications

(28 citation statements)

References 43 publications

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“…Araújo and co-workers observed that, after 632.8 nm PBM, hepatectomized animals showed an increase in the expression of HGF followed by increased phosphorylation of Met and its downstream signaling molecules Akt and ERK. This indicates that PBM could enhance liver regeneration after hepatectomy [97]. …”

Section: Molecular Mechanisms Of Pbmmentioning

confidence: 99%

Proposed Mechanisms of Photobiomodulation or Low-Level Light Therapy

Freitas

Hamblin

2016

IEEE J. Select. Topics Quantum Electron.

908

713

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Photobiomodulation (PBM) also known as low-level laser (or light) therapy (LLLT), has been known for almost 50 years but still has not gained widespread acceptance, largely due to uncertainty about the molecular, cellular, and tissular mechanisms of action. However, in recent years, much knowledge has been gained in this area, which will be summarized in this review. One of the most important chromophores is cytochrome c oxidase (unit IV in the mitochondrial respiratory chain), which contains both heme and copper centers and absorbs light into the near-infra-red region. The leading hypothesis is that the photons dissociate inhibitory nitric oxide from the enzyme, leading to an increase in electron transport, mitochondrial membrane potential and ATP production. Another hypothesis concerns light-sensitive ion channels that can be activated allowing calcium to enter the cell. After the initial photon absorption events, numerous signaling pathways are activated via reactive oxygen species, cyclic AMP, NO and Ca2+, leading to activation of transcription factors. These transcription factors can lead to increased expression of genes related to protein synthesis, cell migration and proliferation, anti-inflammatory signaling, anti-apoptotic proteins, antioxidant enzymes. Stem cells and progenitor cells appear to be particularly susceptible to LLLT.

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Section: Molecular Mechanisms Of Pbmmentioning

confidence: 99%

Proposed Mechanisms of Photobiomodulation or Low-Level Light Therapy

Freitas

Hamblin

2016

IEEE J. Select. Topics Quantum Electron.

908

713

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“…Low-power laser irradiation (LPLI) is suggested to be an effective minimally invasive palliative treatment option for patients with small liver tumors [119,120] . Interestingly in this context was that LPLI was shown to improve liver regenerative capacity of a small liver remnant after hepatectomy through activation of the HGF-MAPK/PI3K pathway [121] .…”

Section: Trendsmentioning

confidence: 99%

Effect of liver regeneration on malignant hepatic tumors

Shi

Line

2014

WJG

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Liver regeneration after major surgery may activate occult micrometastases and facilitate tumor growth, leading to liver tumor recurrence. Molecular changes during liver regeneration can provide a microenvironment that stimulates intrahepatic tumor propagation through alterations in cellular signaling pathways, where activation and proliferation of mature hepatocytes, hepatic progenitor cells, non-parenchymal liver cells might favor both liver regeneration and tumor growth. This review highlights recent advances of tumor growth and development in the regenerating liver, possible mechanisms and clinical implications. Key words: Hepatocellular carcinoma; Colorectal cancer; Recurrence; Liver regeneration; Hepatic progenitor cell; Epithelial to mesenchymal transition Core tip: The liver has a unique capacity for regeneration after cellular damage or partial removal of tissue, and modern liver surgery relies on this property. Liver regeneration is a complex process involving a large array of growth factors, cytokines and cells to restore hepatic mass and function. Experimental and clinical data indicate that the regeneration signals facilitate the growth of both primary and secondary liver tumors and can alter their malignant potential. This is an important mechanism underlying recurrence after liver surgery. New therapeutic strategies founded on better insight into the relationship between liver regeneration and tumor biology are needed.Shi JH, Line PD. Effect of liver regeneration on malignant hepatic tumors.

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“…As demonstrated, lack of FGF15/19 resulted in decreased FGFR4 and cyclin A in non-steatotic livers undergoing CD and I/R injury associated with LT. The important role for ERK1/2 in LT and experimental models of liver regeneration in non-steatotic livers has been previously demonstrated [45,[68][69][70][71][72][73]. Thus, it could be bearing in mind the possibility that failure in cell proliferation induced by FGF15 inhibition could be related to a reduced activation of ERK1/2.…”

Section: Discussionmentioning

confidence: 92%

The Effect of Fibroblast Growth Factor 15 Signaling in Non-Steatotic and Steatotic Liver Transplantation from Cardiocirculatory Death

León

Jiménez‐Castro

Cornide‐Petronio

et al. 2019

Cells

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We elucidate the relevance of fibroblast growth factor 15 (FGF15) in liver transplantation (LT) using rats with both steatotic and non-steatotic organs from donors after cardiocirculatory death (DCD). Compared to LT from non-DCDs, the induction of cardiocirculatory death (CD) increases hepatic damage, proliferation, and intestinal and circulatory FGF15. This is associated with high levels of FGF15, bilirubin and bile acids (BAs), and overexpression of the enzyme involved in the alternative BA synthesis pathway, CYP27A1, in non-steatotic livers. Furthermore, CD activates the proliferative pathway, Hippo/YAP, in these types of liver. Blocking FGF15 action in LT from DCDs does not affect CYP27A1 but causes an overexpression of CYP7A, an enzyme from the classic BA synthesis pathway, and this is related to further accumulation of BAs and exacerbated damage. FGF15 inhibition also impairs proliferation without changing Hippo/YAP. In spite of worse damage, steatosis prevents a proliferative response in livers from DCDs. In steatotic grafts, CD does not modify CYP7A1, CYP27A1, BA, or the Hippo/YAP pathway, and FGF15 is not involved in damage or proliferation. Thus, endogenous FGF15 protects against BA accumulation and damage and promotes regeneration independently of the Hippo/YAP pathway, in non-steatotic LT from DCDs. Herein we show a minor role of FGF15 in steatotic LT from DCDs.

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Liver regeneration following partial hepatectomy is improved by enhancing the HGF/Met axis and Akt and Erk pathways after low-power laser irradiation in rats

Cited by 20 publications

References 43 publications

Proposed Mechanisms of Photobiomodulation or Low-Level Light Therapy

Proposed Mechanisms of Photobiomodulation or Low-Level Light Therapy

Effect of liver regeneration on malignant hepatic tumors

The Effect of Fibroblast Growth Factor 15 Signaling in Non-Steatotic and Steatotic Liver Transplantation from Cardiocirculatory Death

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