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Article ; Online: Extracellular vesicles derived from liver sinusoidal endothelial cells inhibit the activation of hepatic stellate cells and Kupffer cells in vitro.

Wang, Junyu / Wu, Zongmei / Xia, Mengmeng / Salas, Sandra Serna / Ospina, Johanna Arroyave / Buist-Homan, Manon / Harmsen, Martin C / Moshage, Han

Biochimica et biophysica acta. Molecular basis of disease

2024 Volume 1870, Issue 3, Page(s) 167020

Abstract: Liver sinusoidal endothelial cells (LSECs) play a crucial role in maintaining liver microcirculation and exchange of nutrients in the liver and are thought to be involved in the pathogenesis of metabolic dysfunction-associated steatotic liver disease ( ... ...

Abstract	Liver sinusoidal endothelial cells (LSECs) play a crucial role in maintaining liver microcirculation and exchange of nutrients in the liver and are thought to be involved in the pathogenesis of metabolic dysfunction-associated steatotic liver disease (MASLD). The activation of hepatic stellate cells (HSCs) and Kupffer cells (KCs) has been considered to be responsible for the onset of liver fibrosis and the aggravation of liver injury. However, the paracrine regulatory effects of LSECs in the development of MASLD, in particular the role of LSEC-derived extracellular vesicles (EVs) remains unclear. Therefore, the aim of the present study was to investigate the influence of LSEC-derived EVs on HSCs and KCs. Primary rat LSECs, HSCs and KCs were isolated from male Wistar rats. LSEC-derived EVs were isolated from conditioned medium by ultracentrifugation and analyzed by nanoparticle tracking analysis, and expression of specific markers. LSEC-derived EVs reduced the expression of activation markers in activated HSCs but did not affect quiescent HSCs. Also, LSEC-derived EVs suppressed proliferation of activated HSCs activation, as assessed by Xcelligence and BrdU assay. LSEC-derived EVs also increased the expression of inflammatory genes in HSCs that normally are lowly expression during their activation. In contrast, EVs decreased the expression of inflammatory genes in activated KCs. In summary, our results suggest that LSEC-derived EVs may attenuate the fibrogenic phenotype of activated HSCs and the inflammatory phenotype of KCs. Our results show promise for LSEC-derived EVs as therapeutic moieties to treat MASLD. In addition, these EVs might prove of diagnostic value.
MeSH term(s)	Rats ; Animals ; Male ; Kupffer Cells/metabolism ; Hepatic Stellate Cells/metabolism ; Endothelial Cells/metabolism ; Rats, Wistar ; Liver/metabolism ; Extracellular Vesicles
Language	English
Publishing date	2024-01-19
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	60-7
ISSN	1879-260X ; 1879-2596 ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650 ; 0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
ISSN (online)	1879-260X ; 1879-2596 ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650
ISSN	0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
DOI	10.1016/j.bbadis.2024.167020
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Article ; Online: Responses of retinal and brain microvasculature to streptozotocin induced diabetes revealed by global expression profiling.

Li, Youhai / Faiz, Alen / Moshage, Han / Schilling, Lothar / Kamps, Jan Aam

Diabetes & vascular disease research

2023 Volume 20, Issue 1, Page(s) 14791641221147533

Abstract: This study aims to determine the effects of diabetes in the retinal and brain microvasculature through gene expression profiling. Twelve male Wistar rats were randomly divided into two groups: streptozotocin-induced diabetic rats and time-matched ... ...

Abstract	This study aims to determine the effects of diabetes in the retinal and brain microvasculature through gene expression profiling. Twelve male Wistar rats were randomly divided into two groups: streptozotocin-induced diabetic rats and time-matched nondiabetic rats. The retinal microvessels (RMVs) and brain microvessels (BMVs) were mechanically isolated from individual rats. Differentially expressed genes (DEGs) in diabetic and nondiabetic microvessels were identified by cDNA microarrays analysis. In RMVs, we identified 43 DEGs, of which 20 were upregulated while 23 were downregulated by diabetes. In BMVs, 35 genes DEGs were identified, of which 22 were upregulated and 13 were downregulated by diabetes. Altered expression of the Nars, Gars, Mars, Iars, Yars, Bcl2, Nqo1, NR4A3, Gpd1, Stc1, Tsc22d3, Tnfrsf21 mRNA as observed in the microarray analyses, was confirmed by quantitative RT-PCR. The aminoacyl-tRNA synthetases (aaRSs) pathway in RMVs was significantly overrepresented as compared to BMVs. Our study demonstrates for the first time that in the brain microvasculature multiple compensatory mechanisms exists, serving to protect brain tissue from diabetic insults, whereas these mechanisms are not activated in the retinal microvasculature. This provides new insights as to why brain microvasculature is less susceptible to diabetes.
MeSH term(s)	Animals ; Male ; Rats ; Brain ; Diabetes Mellitus, Experimental/genetics ; Diabetes Mellitus, Experimental/metabolism ; Diabetic Retinopathy/genetics ; Diabetic Retinopathy/metabolism ; Microvessels/metabolism ; Rats, Wistar ; Retinal Vessels/metabolism ; Streptozocin
Chemical Substances	Streptozocin (5W494URQ81)
Language	English
Publishing date	2023-01-17
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2250793-0
ISSN	1752-8984 ; 1479-1641
ISSN (online)	1752-8984
ISSN	1479-1641
DOI	10.1177/14791641221147533
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Article: The Coumarin-Derivative Esculetin Protects against Lipotoxicity in Primary Rat Hepatocytes via Attenuating JNK-Mediated Oxidative Stress and Attenuates Free Fatty Acid-Induced Lipid Accumulation.

Xia, Mengmeng / Wu, Zongmei / Wang, Junyu / Buist-Homan, Manon / Moshage, Han

Antioxidants (Basel, Switzerland)

2023 Volume 12, Issue 11

Abstract: Coumarin derivates have been proposed as a potential treatment for metabolic-dysfunction-associated fatty liver disease (MAFLD). However, the mechanisms underlying their beneficial effects remain unclear. In the present study, we explored the potential ... ...

Abstract	Coumarin derivates have been proposed as a potential treatment for metabolic-dysfunction-associated fatty liver disease (MAFLD). However, the mechanisms underlying their beneficial effects remain unclear. In the present study, we explored the potential of the coumarin derivate esculetin in MAFLD, focusing on hepatocyte lipotoxicity and lipid accumulation. Primary cultures of rat hepatocytes were exposed to palmitic acid (PA) and palmitic acid plus oleic acid (OA/PA) as models of lipotoxicity and lipid accumulation, respectively. Esculetin significantly reduced oxidative stress in PA-treated hepatocytes, as shown by decreased total reactive oxygen species (ROS) and mitochondrial superoxide production and elevated expression of antioxidant genes, including Nrf2 and Gpx1. In addition, esculetin protects against PA-induced necrosis. Esculetin also improved lipid metabolism in primary hepatocytes exposed to nonlipotoxic OA/PA by decreasing the expression of the lipogenesis-related gene Srebp1c and increasing the expression of the fatty acid β-oxidation-related gene Ppar-α. Moreover, esculetin attenuated lipid accumulation in OA/PA-treated hepatocytes. The protective effects of esculetin against lipotoxicity and lipid accumulation were shown to be dependent on the inhibition of JNK and the activation of AMPK, respectively. We conclude that esculetin is a promising compound to target lipotoxicity and lipid accumulation in the treatment of MAFLD.
Language	English
Publishing date	2023-10-27
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2704216-9
ISSN	2076-3921
ISSN	2076-3921
DOI	10.3390/antiox12111922
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Article ; Online: Protective effects of caffeine against palmitate-induced lipid toxicity in primary rat hepatocytes is associated with modulation of adenosine receptor A1 signaling.

Arroyave-Ospina, Johanna C / Buist-Homan, Manon / Schmidt, Martina / Moshage, Han

Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie

2023 Volume 165, Page(s) 114884

Abstract: Background: Epidemiological evidence has shown an association between coffee consumption and reduced risk for chronic liver diseases, including metabolic-dysfunction-associated liver disease (MALFD). Lipotoxicity is a key cause of hepatocyte injury ... ...

Abstract	Background: Epidemiological evidence has shown an association between coffee consumption and reduced risk for chronic liver diseases, including metabolic-dysfunction-associated liver disease (MALFD). Lipotoxicity is a key cause of hepatocyte injury during MAFLD. The coffee component caffeine is known to modulate adenosine receptor signaling via the antagonism of adenosine receptors. The involvement of these receptors in the prevention of hepatic lipotoxicity has not yet been explored. The aim of this study was to explore whether caffeine protects against palmitate-induced lipotoxicity by modulating adenosine receptor signaling. Methods: Primary hepatocytes were isolated from male rats. Hepatocytes were treated with palmitate with or without caffeine or 1,7DMX. Lipotoxicity was verified using Sytox viability staining and mitochondrial JC-10 staining. PKA activation was verified by Western blotting. Selective (ant)agonists of A1AR (DPCPX and CPA, respectively) and A2AR (istradefyline and regadenoson, respectively), the AMPK inhibitor compound C, and the Protein Kinase A (PKA) inhibitor Rp8CTP were used. Lipid accumulation was verified by ORO and BODIPY 453/50 staining. Results: Caffeine and its metabolite 1,7DMX prevented palmitate-induced toxicity in hepatocytes. The A1AR antagonist DPCPX also prevented lipotoxicity, whereas both the inhibition of PKA and the A1AR agonist CPA (partially) abolished the protective effect. Caffeine and DPCPX increased lipid droplet formation only in palmitate-treated hepatocytes and decreased mitochondrial ROS production. Conclusions: The protective effect of caffeine against palmitate lipotoxicity was shown to be dependent on A1AR receptor and PKA activation. Antagonism of A1AR also protects against lipotoxicity. Targeting A1AR receptor may be a potential therapeutic intervention with which to treat MAFLD.
MeSH term(s)	Rats ; Male ; Animals ; Caffeine/pharmacology ; Coffee ; Palmitates/pharmacology ; Hepatocytes ; Receptor, Adenosine A1/metabolism
Chemical Substances	Caffeine (3G6A5W338E) ; Coffee ; Palmitates ; Receptor, Adenosine A1
Language	English
Publishing date	2023-07-07
Publishing country	France
Document type	Journal Article
ZDB-ID	392415-4
ISSN	1950-6007 ; 0753-3322 ; 0300-0893
ISSN (online)	1950-6007
ISSN	0753-3322 ; 0300-0893
DOI	10.1016/j.biopha.2023.114884
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Article ; Online: Studying Hepatic Stellate Cell Senescence.

Serna-Salas, Sandra A / Soto-Gámez, Abel A / Wu, Zongmei / Klaver, Myrthe / Moshage, Han

Methods in molecular biology (Clifton, N.J.)

2023 Volume 2669, Page(s) 79–109

Abstract: Hepatic stellate cells (HSCs) are the key effector cells in liver fibrosis. They are the main producers of excessive amounts of extracellular matrix components during fibrogenesis and therefore a potential target for the treatment of liver fibrosis. ... ...

Abstract	Hepatic stellate cells (HSCs) are the key effector cells in liver fibrosis. They are the main producers of excessive amounts of extracellular matrix components during fibrogenesis and therefore a potential target for the treatment of liver fibrosis. Induction of senescence in HSCs may be a promising strategy to slow down, stop, or even reverse fibrogenesis. Senescence is a complex and heterogeneous process linked to fibrosis and cancer, but the exact mechanism and relevant markers can be cell-type dependent. Therefore, many markers of senescence have been proposed, and many methods to detect senescence have been developed. In this chapter, we review relevant methods and biomarkers to detect cellular senescence in hepatic stellate cells.
MeSH term(s)	Humans ; Hepatic Stellate Cells ; Kupffer Cells ; Cellular Senescence ; Liver Cirrhosis ; Research ; Liver
Language	English
Publishing date	2023-05-29
Publishing country	United States
Document type	Review ; Journal Article
ISSN	1940-6029
ISSN (online)	1940-6029
DOI	10.1007/978-1-0716-3207-9_6
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Article: Role of Oxidative Stress in the Pathogenesis of Non-Alcoholic Fatty Liver Disease: Implications for Prevention and Therapy.

Arroyave-Ospina, Johanna C / Wu, Zongmei / Geng, Yana / Moshage, Han

Antioxidants (Basel, Switzerland)

2021 Volume 10, Issue 2

Abstract: Oxidative stress (OxS) is considered a major factor in the pathophysiology of inflammatory chronic liver diseases, including non-alcoholic liver disease (NAFLD). Chronic impairment of lipid metabolism is closely related to alterations of the oxidant/ ... ...

Abstract	Oxidative stress (OxS) is considered a major factor in the pathophysiology of inflammatory chronic liver diseases, including non-alcoholic liver disease (NAFLD). Chronic impairment of lipid metabolism is closely related to alterations of the oxidant/antioxidant balance, which affect metabolism-related organelles, leading to cellular lipotoxicity, lipid peroxidation, chronic endoplasmic reticulum (ER) stress, and mitochondrial dysfunction. Increased OxS also triggers hepatocytes stress pathways, leading to inflammation and fibrogenesis, contributing to the progression of non-alcoholic steatohepatitis (NASH). The antioxidant response, regulated by the Nrf2/ARE pathway, is a key component in this process and counteracts oxidative stress-induced damage, contributing to the restoration of normal lipid metabolism. Therefore, modulation of the antioxidant response emerges as an interesting target to prevent NAFLD development and progression. This review highlights the link between disturbed lipid metabolism and oxidative stress in the context of NAFLD. In addition, emerging potential therapies based on antioxidant effects and their likely molecular targets are discussed.
Language	English
Publishing date	2021-01-26
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2704216-9
ISSN	2076-3921
ISSN	2076-3921
DOI	10.3390/antiox10020174
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Article ; Online: Scopoletin and umbelliferone protect hepatocytes against palmitate- and bile acid-induced cell death by reducing endoplasmic reticulum stress and oxidative stress.

Wu, Zongmei / Geng, Yana / Buist-Homan, Manon / Moshage, Han

Toxicology and applied pharmacology

2021 Volume 436, Page(s) 115858

Abstract: Background: The number of patients with non-alcoholic fatty liver disease (NAFLD) is rapidly increasing due to the growing epidemic of obesity. Non-alcoholic steatohepatitis (NASH), the inflammatory stage of NAFLD, is characterized by lipid accumulation ...

Abstract	Background: The number of patients with non-alcoholic fatty liver disease (NAFLD) is rapidly increasing due to the growing epidemic of obesity. Non-alcoholic steatohepatitis (NASH), the inflammatory stage of NAFLD, is characterized by lipid accumulation in hepatocytes, chronic inflammation and hepatocyte cell death. Scopoletin and umbelliferone are coumarin-like molecules and have antioxidant, anti-cancer and anti-inflammatory effects. Cytoprotective effects of these compounds have not been described in hepatocytes and the mechanisms of the beneficial effects of scopoletin and umbelliferone are unknown. Aim: To investigate whether scopoletin and/or umbelliferone protect hepatocytes against palmitate-induced cell death. For comparison, we also tested the cytoprotective effect of scopoletin and umbelliferone against bile acid-induced cell death. Methods: Primary rat hepatocytes were exposed to palmitate (1 mmol/L) or the hydrophobic bile acid glycochenodeoxycholic acid (GCDCA; 50 μmol/L). Apoptosis was assessed by caspase-3 activity assay, necrosis by Sytox green assay, mRNA levels by qPCR, protein levels by Western blot and production of reactive oxygen species (ROS) by fluorescence assay. Results: Both scopoletin and umbelliferone protected against palmitate and GCDCA-induced cell death. Both palmitate and GCDCA induced the expression of ER stress markers. Scopoletin and umbelliferone decreased palmitate- and GCDCA-induced expression of ER stress markers, phosphorylation of the cell death signaling intermediate JNK as well as ROS production. Conclusion: Scopoletin and umbelliferone protect against palmitate and bile acid-induced cell death of hepatocytes by inhibition of ER stress and ROS generation and decreasing phosphorylation of JNK. Scopoletin and umbelliferone may hold promise as a therapeutic modality for the treatment of NAFLD.
MeSH term(s)	Animals ; Antioxidants/metabolism ; Apoptosis/drug effects ; Bile Acids and Salts/pharmacology ; Cell Death/drug effects ; Cell Line, Tumor ; Endoplasmic Reticulum Stress/drug effects ; Glycochenodeoxycholic Acid/pharmacology ; Hep G2 Cells ; Hepatocytes/drug effects ; Hepatocytes/metabolism ; Humans ; Male ; Necrosis/metabolism ; Non-alcoholic Fatty Liver Disease/drug therapy ; Non-alcoholic Fatty Liver Disease/metabolism ; Oxidative Stress/drug effects ; Palmitates/pharmacology ; Rats ; Rats, Wistar ; Reactive Oxygen Species/metabolism ; Scopoletin/pharmacology ; Signal Transduction/drug effects ; Umbelliferones/pharmacology
Chemical Substances	Antioxidants ; Bile Acids and Salts ; Palmitates ; Reactive Oxygen Species ; Umbelliferones ; Glycochenodeoxycholic Acid (640-79-9) ; Scopoletin (KLF1HS0SXJ)
Language	English
Publishing date	2021-12-31
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	204477-8
ISSN	1096-0333 ; 0041-008X
ISSN (online)	1096-0333
ISSN	0041-008X
DOI	10.1016/j.taap.2021.115858
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Article: Modulation of Oxidative Stress-Induced Senescence during Non-Alcoholic Fatty Liver Disease.

Pedroza-Diaz, Johanna / Arroyave-Ospina, Johanna C / Serna Salas, Sandra / Moshage, Han

Antioxidants (Basel, Switzerland)

2022 Volume 11, Issue 5

Abstract: Non-alcoholic fatty liver disease is characterized by disturbed lipid metabolism and increased oxidative stress. These conditions lead to the activation of different cellular response mechanisms, including senescence. Cellular senescence constitutes an ... ...

Abstract	Non-alcoholic fatty liver disease is characterized by disturbed lipid metabolism and increased oxidative stress. These conditions lead to the activation of different cellular response mechanisms, including senescence. Cellular senescence constitutes an important response to injury in the liver. Recent findings show that chronic oxidative stress can induce senescence, and this might be a driving mechanism for NAFLD progression, aggravating the disturbance of lipid metabolism, organelle dysfunction, pro-inflammatory response and hepatocellular damage. In this context, the modulation of cellular senescence can be beneficial to ameliorate oxidative stress-related damage during NAFLD progression. This review focuses on the role of oxidative stress and senescence in the mechanisms leading to NAFLD and discusses the possibilities to modulate senescence as a therapeutic strategy in the treatment of NAFLD.
Language	English
Publishing date	2022-05-16
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2704216-9
ISSN	2076-3921
ISSN	2076-3921
DOI	10.3390/antiox11050975
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Article ; Online: Arginase 1 expression is increased during hepatic stellate cell activation and facilitates collagen synthesis.

Zhang, Mengfan / Wu, Zongmei / Salas, Sandra Serna / Aguilar, Magnolia Martinez / Trillos-Almanza, Maria C / Buist-Homan, Manon / Moshage, Han

Journal of cellular biochemistry

2023 Volume 124, Issue 6, Page(s) 808–817

Abstract: Activation of hepatic stellate cells (HSC) is a key event in the initiation of liver fibrosis. Activated HSCs proliferate and secrete excessive amounts of extracellular matrix (ECM), disturbing liver architecture and function, leading to fibrosis and ... ...

Abstract	Activation of hepatic stellate cells (HSC) is a key event in the initiation of liver fibrosis. Activated HSCs proliferate and secrete excessive amounts of extracellular matrix (ECM), disturbing liver architecture and function, leading to fibrosis and eventually cirrhosis. Collagen is the most abundant constituent of ECM and proline is the most abundant amino acid of collagen. Arginine is the precursor in the biosynthetic pathway of proline. Arginine is the exclusive substrate of both nitric oxide synthase (NOS) and arginase. NOS is an M1 (proinflammatory) marker of macrophage polarization whereas arginase-1 (Arg1) is an M2 (profibrogenic) marker of macrophage polarization. Differential expression of NOS and Arg1 has not been studied in HSCs yet. To identify the expression profile of arginine catabolic enzymes during HSC activation and to investigate their role in HSC activation, primary rat HSCs were cultured-activated for 7 days and expression of iNOS and Arg1 were investigated. Nor-NOHA was used as a specific and reversible arginase inhibitor. During HSC activation, iNOS expression decreased whereas Arg1 expression increased. Inhibition of Arg1 in activated HSCs efficiently inhibited collagen production but not cell proliferation. HSC activation is accompanied by a switch of arginine catabolism from iNOS to Arg1. Inhibition of Arg1 decreases collagen synthesis. Therefore, we conclude that Arg1 can be a therapeutic target for the inhibition of liver fibrogenesis.
MeSH term(s)	Rats ; Animals ; Hepatic Stellate Cells/metabolism ; Arginase/genetics ; Arginase/metabolism ; Liver Cirrhosis/metabolism ; Collagen/metabolism ; Arginine
Chemical Substances	Arginase (EC 3.5.3.1) ; Collagen (9007-34-5) ; Arginine (94ZLA3W45F)
Language	English
Publishing date	2023-04-12
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	392402-6
ISSN	1097-4644 ; 0730-2312
ISSN (online)	1097-4644
ISSN	0730-2312
DOI	10.1002/jcb.30403
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Article ; Online: Hydroxyurea attenuates hepatic stellate cell proliferation in vitro and liver fibrogenesis in vivo.

Haijer, Floris / Koets-Shajari, Shiva / Heegsma, Janette / Serna-Salas, Sandra / Blokzijl, Tjasso / Buist-Homan, Manon / Moshage, Han / Faber, Klaas Nico

FASEB journal : official publication of the Federation of American Societies for Experimental Biology

2023 Volume 37, Issue 9, Page(s) e23124

Abstract: Liver fibrosis results from excessive proliferation of, and collagen production by hepatic stellate cells (HSCs) that is caused by chronic liver injury. No drugs are available to cure liver fibrosis. Hydroxyurea is an anti-proliferative drug that is used ...

Abstract	Liver fibrosis results from excessive proliferation of, and collagen production by hepatic stellate cells (HSCs) that is caused by chronic liver injury. No drugs are available to cure liver fibrosis. Hydroxyurea is an anti-proliferative drug that is used in benign and malignant disorders. Here, we studied the effect of hydroxyurea on primary HSCs and its anti-fibrotic effect in the CCl
MeSH term(s)	Mice ; Rats ; Animals ; Hydroxyurea/adverse effects ; Hepatic Stellate Cells/metabolism ; Mice, Inbred C57BL ; Liver/metabolism ; Liver Cirrhosis/chemically induced ; Liver Cirrhosis/drug therapy ; Liver Cirrhosis/metabolism ; Necrosis/pathology ; Collagen/metabolism ; Cell Proliferation ; RNA, Messenger/genetics ; Carbon Tetrachloride/toxicity
Chemical Substances	Hydroxyurea (X6Q56QN5QC) ; Collagen (9007-34-5) ; RNA, Messenger ; Carbon Tetrachloride (CL2T97X0V0)
Language	English
Publishing date	2023-08-08
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	639186-2
ISSN	1530-6860 ; 0892-6638
ISSN (online)	1530-6860
ISSN	0892-6638
DOI	10.1096/fj.202300920R
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