A5021914381- Liver physiology and pathology
- Liver Disease Diagnosis and Treatment
- Organ Transplantation Techniques and Outcomes
- Telomeres, Telomerase, and Senescence
- MicroRNA in disease regulation
- Extracellular vesicles in disease
- Digestive system and related health
- Genetics, Aging, and Longevity in Model Organisms
- Phagocytosis and Immune Regulation
- Endoplasmic Reticulum Stress and Disease
- Salivary Gland Disorders and Functions
- Cardiovascular Disease and Adiposity
- Liver Disease and Transplantation
- Mesenchymal stem cell research
- Head and Neck Cancer Studies
- Adipose Tissue and Metabolism
- Hedgehog Signaling Pathway Studies
University Medical Center Groningen
2020-2024
University of Groningen
2020-2024
Autonomous University of Aguascalientes
2018-2021
Upon liver injury, hepatic stellate cells (HSCs) transdifferentiate to migratory, proliferative and extracellular matrix-producing myofibroblasts (e.g., activated HSCs; aHSCs) causing fibrosis. HSC activation is associated with increased glycolysis glutaminolysis. Here, we compared the contribution of glycolysis, glutaminolysis mitochondrial oxidative phosphorylation (OXPHOS) in rat human activation. Basal levels (extracellular acidification rate ~3-fold higher) particularly respiration...
Liver sinusoidal endothelial cells (LSECs) play a crucial role in maintaining liver microcirculation and exchange of nutrients the are thought to be involved pathogenesis metabolic dysfunction-associated steatotic disease (MASLD). The activation hepatic stellate (HSCs) Kupffer (KCs) has been considered responsible for onset fibrosis aggravation injury. However, paracrine regulatory effects LSECs development MASLD, particular LSEC-derived extracellular vesicles (EVs) remains unclear....
Liver fibrosis is the response of liver to chronic inflammation. The communication between resident macrophages (Kupffer cells [KCs]) and hepatic stellate (HSCs) has been mainly viewed as one-directional: from KCs HSCs with promoting fibrogenesis. However, recent studies indicated that may function a hub intercellular communications. Therefore, aim present study was investigate role on inflammatory phenotype KCs. Primary rat were isolated male Wistar rats. HSCs-derived conditioned medium...
Activation of hepatic stellate cells (HSC) is a key event in the initiation liver fibrosis. Activated HSCs proliferate and secrete excessive amounts extracellular matrix (ECM), disturbing architecture function, leading to fibrosis eventually cirrhosis. Collagen most abundant constituent ECM proline amino acid collagen. Arginine precursor biosynthetic pathway proline. exclusive substrate both nitric oxide synthase (NOS) arginase. NOS an M1 (proinflammatory) marker macrophage polarization...
Activated hepatic stellate cells (aHSCs) are the main effector during liver fibrogenesis. α-1 adrenergic antagonist doxazosin (DX) was shown to be anti-fibrotic in an vivo model of fibrosis (LF), but mechanism remains elucidated. Recent studies suggest that reversion LF can achieved by inducing cellular senescence characterized irreversible cell-cycle arrest and acquisition senescence-associated secretory phenotype (SASP).To elucidate effect DX determine whether it induces senescence.Primary...
Regulation of the mechanisms fibrosis is an important goal in treatment liver cirrhosis. One mechanism participation hepatic stellate cells fibrogenesis when activated by catecholamines. Consequently, α / β adrenoblockers are proposed as alternative for chronic lesions such and/or cirrhosis and possible regeneration. We herein analyzed effect doxazosin carvedilol treatments during regeneration tissue a hamster model Tissue samples were examined H&E PAS to evaluate damage with Sirius red...
Activation of hepatic stellate cells (HSC) leads to initiation and progression fibrosis. HSC senescence is inversely correlated with proliferation activation. Therefore, induction may be a strategy treat Coumarin-derivatives like esculetin have been suggested inhibit fibrogenic cells. in this study we aimed investigate the effect on activation senescence. Primary rat were used all experiments. Real-time cell analyzer BrdU incorporation assay determine proliferation. Gene expression...
Irradiation of the salivary glands during head and neck cancer treatment induces cellular senescence in response to DNA damage contributes radiation-induced hyposalivation by affecting gland stem/progenitor cell (SGSC) niche. Cellular senescence, such as that induced radiation, is a state cell-cycle arrest, accompanied an altered pro-inflammatory secretome known senescence-associated secretory phenotype (SASP) with potential detrimental effects on surrounding microenvironment. We...
The prevalence of metabolic dysfunction-associated fatty liver disease (MAFLD) is increasing rapidly worldwide due to the obesity epidemic. Advanced stages MAFLD, such as non-alcoholic steatohepatitis (NASH) with advanced fibrosis or cirrhosis are affecting global health. Extracellular vesicles (EVs) released by all cell types and important in cell-to-cell communication maintaining homeostasis, but they also play a role pathogenesis various diseases. EVs contain biological information...
Abstract Liver fibrosis results from excessive proliferation of, and collagen production by hepatic stellate cells (HSCs) that is caused chronic liver injury. No drugs are available to cure fibrosis. Hydroxyurea an anti‐proliferative drug used in benign malignant disorders. Here, we studied the effect of hydroxyurea on primary HSCs its anti‐fibrotic CCl 4 mouse model Primary rat were cultured absence or presence (0.1–1.0 mmol/L). vehicle was administered C57BL/6/J mice for weeks, with...