Comparative study on effect of mesenchymal stem cells and endothelial progenitor cells on treatment of experimental CCL4-induced liver fibrosis

Abdelgwad, Marwa; Ewaiss, Manal; Sabry, Dina; Khalifa, Warda A; Altaib, Z M; Alhelf, Maha

doi:10.1080/13813455.2020.1752256

Cited by 5 publications

(5 citation statements)

References 34 publications

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“…42 By secreting HGF, umbilical cord MSCs promote liver regeneration, 43 and the transplantation of endothelial progenitor cells positive effects in hepatocyte proliferation mediated by HGF. 44 Also, a study showed that GRP78 overexpression in MSCs enhanced neovascularization by increasing HGF content. 45 In this study, we found that the overexpression of GRP78 increased the HGF content in rBMSCs, which might be a possible reason for GRP78 to improve the therapeutic efficacy of BMSCs, while the deep mechanism is elusive and needs further study.…”

Section: Discussionmentioning

confidence: 99%

“…HGF has been proven to be a good protective factor against hepatotoxicity by isoniazid or rifampicin induced, 41 and HGF was activated when liver injury occurred and inhibited hepatocyte apoptosis 42 . By secreting HGF, umbilical cord MSCs (UCMSCs) promote liver regeneration, 43 and the transplantation of endothelial progenitor cells produces positive effects in hepatocyte proliferation mediated by HGF 44 . Also, a study showed that GRP78 overexpression in MSCs enhanced neovascularization by increasing HGF content 45 .…”

Section: Discussionmentioning

confidence: 99%

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GRP78 improves the therapeutic effect of mesenchymal stem cells on hemorrhagic shock‐induced liver injury: Involvement of the NF–кB and HO‐1/Nrf‐2 pathways

Han,

Jia,

Yao

et al. 2023

The FASEB Journal

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Mesenchymal stem cells (MSCs) are a popular cell source for repairing the liver. Improving the survival rate and colonization time of MSCs may significantly improve the therapeutic outcomes of MSCs. Studies showed that 78‐kDa glucose‐regulated protein (GRP78) expression improves cell viability and migration. This study aims to examine whether GRP78 overexpression improves the efficacy of rat bone marrow‐derived MSCs (rBMSCs) in HS‐induced liver damage. Bone marrow was isolated from the femurs and tibias of rats. rBMSCs were transfected with a GFP‐labeled GRP78 expression vector. Flow cytometry, transwell invasion assay, scratch assay immunoblotting, TUNEL assay, MTT assay, and ELISA were carried out. The results showed that GRP78 overexpression enhanced the migration and invasion of rBMSCs. Moreover, GRP78‐overexpressing rBMSCs relieved liver damage, repressed liver oxidative stress, and inhibited apoptosis. We found that overexpression of GRP78 in rBMSCs inhibited activation of the NLRP3 inflammasome, significantly decreased the levels of inflammatory factors, and decreased the expression of CD68. Notably, GRP78 overexpression activated the Nrf‐2/HO‐1 pathway and inhibited the NF–κB pathway. High expression of GRP78 efficiently enhanced the effect of rBMSC therapy. GRP78 may be a potential target to improve the therapeutic efficacy of BMSCs.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

GRP78 improves the therapeutic effect of mesenchymal stem cells on hemorrhagic shock‐induced liver injury: Involvement of the NF–кB and HO‐1/Nrf‐2 pathways

Han,

Jia,

Yao

et al. 2023

The FASEB Journal

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“…According to previous information, hepatic fibrosis typically begins with hepatocyte injury, which stimulates Kupffer cells and secretes cytokines and growth factors. This caused fibroblast-like cells to multiply and release a lot of connective tissue components [ 61 ]. Another element that promotes the growth of fibroblasts and a component of connective tissue is the oxidative stress caused by CCL 4 [ 62 ].…”

Section: Discussionmentioning

confidence: 99%

A comparative study on the hepatoprotective effect of selenium-nanoparticles and dates flesh extract on carbon tetrachloride induced liver damage in albino rats

Nady Ouais,

Hassan

2023

Anat Cell Biol

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Exposure to environmental pollutants such as carbon tetrachloride (CCL 4 ) causes liver damage. This study aimed to compare the ameliorative activity of the dates flesh extract (DFE) and selenium-nanoparticles (SeNPs) on CCL 4 -induced hepatotoxicity and if DFE could be a useful alternative supplement. Twenty-four male albino rats were enrolled and randomly divided into four equal groups (6 rats in each group): control group received only basal diet with no medications. Group II received CCL 4 in a dose of 0.5 mg/kg intraperitoneal injection twice weekly for four weeks. Group III rats were pretreated with SeNPs in a dose of 2.5 mg/kg once a day orally three times/wk for four weeks alone then combined with the previously described dose of CCL 4 for another four weeks. Group IV rats were pretreated with DFE in a dose of 8 ml of the aqueous extract/kg/d orally for four weeks alone then combined with the previously described dose of CCL 4 for another four weeks. The liver damage was assessed by estimation of plasma concentration of albumin and enzymes activities of alanine aminotransferase and tissue genes expression. Liver oxidation levels were assessed by measuring the tissue concentration of the malondialdehyde, superoxide dismutase, and the total glutathione. Additionally, inflammatory mediators tumour necrosis factor--α and interleukin-6 were estimated. Detecting the liver’s cellular structural damage was done by histopathological and immunohistochemical examination. This study suggests that CCL 4 -induced liver damage in rats can be protected by administration whether the costly SeNPs or the economical DFE.

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“…Hepatocyte growth factor (HGF) secreted by various stem cells plays a critical role in their antifibrotic effects. Umbilical cord mesenchymal stem cells promoted liver repair by secreting HGF in [ 55 ], while menstrual blood-derived mesenchymal stem cells suppressed activated hepatic stellate cells via the paracrine activation of HGF and other mediators in [ 56 ], and the endothelial progenitor cells’ transplantation induced beneficial effects in carbon tetrachloride-induced liver fibrosis by activated HGF-mediated hepatocyte proliferation in [ 57 ]. Moreover, ADSCs’ conditioned media inhibited the proliferation of fibroblasts derived from a human hypertrophic scar in a dose-dependent manner via HGF-like protein in [ 58 ], which supports our hypothesis that ADSCs and HGF have a positive feedback loop and further enhance their protective role in liver fibrosis.…”

Section: Discussionmentioning

confidence: 99%

Adipose-Derived Stem Cells (ADSCs) Supplemented with Hepatocyte Growth Factor (HGF) Attenuate Hepatic Stellate Cell Activation and Liver Fibrosis by Inhibiting the TGF-β/Smad Signaling Pathway in Chemical-Induced Liver Fibrosis Associated with Diabetes

Gharbia

Nazarie²,

Dinescu³

et al. 2022

Cells

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Liver fibrosis can develop on the background of hyperglycemia in diabetes mellitus. However, xenobiotic-related factors may accelerate diabetes-associated liver fibrosis. In this study, we aimed to assess the antfibrotic effect of ADSC and HGF therapy and to establish the cellular and molecular mechanisms through in vitro and in vivo experiments. In vitro, TGF-β1-activated hepatic stellate cells (HSCs) were cocultured with ADSCs or HGF, and the expression of several fibrosis markers was investigated. The antifibrotic effect of the ADSCs, HGF, and ADSCs supplemented with HGF was further assessed in vivo on diabetic mice with liver fibrosis experimentally induced. In vitro results showed the inhibition of HSC proliferation and decrease in fibrogenesis markers. Coadministration of ADSCs and HGF on diabetic mice with liver fibrosis enhanced antifibrotic effects confirmed by the downregulation of Col I, α-SMA, TGF-β1, and Smad2, while Smad7 was upregulated. Moreover, stem cell therapy supplemented with HGF considerably attenuated inflammation and microvesicular steatosis, decreased collagen deposits, and alleviated liver fibrosis. In conclusion, the HGF-based ADSC therapy might be of interest for the treatment of liver fibrosis in diabetic patients, consecutive aggression exerts by different environmental factors.

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Comparative study on effect of mesenchymal stem cells and endothelial progenitor cells on treatment of experimental CCL4-induced liver fibrosis

Cited by 5 publications

References 34 publications

GRP78 improves the therapeutic effect of mesenchymal stem cells on hemorrhagic shock‐induced liver injury: Involvement of the NF–кB and HO‐1/Nrf‐2 pathways

GRP78 improves the therapeutic effect of mesenchymal stem cells on hemorrhagic shock‐induced liver injury: Involvement of the NF–кB and HO‐1/Nrf‐2 pathways

A comparative study on the hepatoprotective effect of selenium-nanoparticles and dates flesh extract on carbon tetrachloride induced liver damage in albino rats

Adipose-Derived Stem Cells (ADSCs) Supplemented with Hepatocyte Growth Factor (HGF) Attenuate Hepatic Stellate Cell Activation and Liver Fibrosis by Inhibiting the TGF-β/Smad Signaling Pathway in Chemical-Induced Liver Fibrosis Associated with Diabetes

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