Articles tagged with Hepatocytes
A study published in Cell found that cells in a three-dimensional environment divide chromosomes correctly, while those in a two-dimensional environment make mistakes. This discovery could help explain why chromosome errors are common in cancerous cells.
Researchers have developed genetically humanized mice that can be persistently infected with Hepatitis Delta Virus (HDV), a common cause of liver fibrosis and cancer. The mice were able to rid themselves of the virus before showing any liver damage, making them an ideal model for testing new treatments.
Scientists at the University of Edinburgh have developed a lab-based system for studying Non-Alcoholic Fatty Liver Disease (NAFLD), the most common cause of liver disease in the developed world. The new tool enables researchers to investigate biological mechanisms and develop effective treatments.
A new study reveals that a malaria parasite manipulates liver cells to survive and reproduce, building strength before invading red blood cells. Disrupting this process by targeting the aquaporin-3 protein may lead to new treatments for malaria before symptoms appear.
Scientists from Cincinnati Children's and UCSF have discovered a mechanism behind an unusual form of tissue regeneration in mice with Alagille syndrome, a rare liver disease. This discovery may lead to a viable treatment for human disease by instructing other types of liver cells to switch identities.
Hemophilia B can be treated for life with a single injection containing disease-free liver cells that produce the missing clotting factor. The finding uses stem-cell strategies and CRISPR/Cas9 gene editing to repair mutations in the patient's FIX gene, allowing normal blood clotting.
Research by BfR scientists reveals that inflammatory processes disrupt liver enzyme function, impairing detoxification capabilities. Fatty liver cells treated with inflammation-promoting substances showed reduced ability to break down foreign substances.
Stanford researchers discover that telomerase-expressing liver cells can rapidly regenerate the liver during normal turnover or tissue damage. These rare cells are evenly distributed throughout the liver's lobules and play a crucial role in enabling the organ to replace damaged cells, potentially leading to cancer.
Researchers discovered that polyploid liver cells can protect the liver against cancer by carrying extra copies of tumor suppressor genes. This finding challenges the notion that polyploidy is a pro-cancer state and suggests it could be an adaptive response within normal liver cells.
Salk researchers have identified how the liver rapidly responds to food by storing pre-RNA molecules involved in glucose and fat metabolism. This finding could help better understand metabolism and some forms of diabetes.
Joseph Kaserman, MD, receives $225,000 award to study risk of liver disease in Alpha-1 carriers using induced pluripotent stem cells and CRISPR technology. The research aims to find new treatments for Alpha-1 related liver disease and address concerns of carrier individuals.
Researchers discovered that a biological clock protein can alleviate symptoms and increase survival rates in fulminant hepatitis by regulating inflammation. The study found that injecting a molecule potentiating the action of this protein reduced the inflammatory response and improved outcomes.
A recent study by KAIST medical scientists reveals that regulatory T cells undergo inflammatory changes in patients with viral hepatitis, leading to the secretion of inflammatory cytokines called TNF. This discovery could pave the way for the development of new clinical treatments for severe viral hepatitis.
Scientists have successfully developed a biologically accurate mass-production platform for bioengineering human liver tissues suitable for therapeutic transplant into people. The new process allows researchers to generate single batches of up to 20,000 genetically matched, three-dimensional and highly functional liver micro-buds.
A new study found that microRNA-34a contributes to liver fibrosis in ALD. Inhibiting this miR-34a reduces liver injury and fibrosis in ALD patients.
Portuguese researchers have identified a crucial defence mechanism used by the malaria parasite to survive inside its host's liver cells. The protein UIS3 binds to LC3, forming a protective shield against autophagy, allowing the parasite to evade the host's cellular defence mechanism.
Researchers have made a breakthrough in treating alpha-1 antitrypsin deficiency by using a new gene editing technique. The approach combines RNA interference and gene augmentation to repopulate diseased livers with healthy cells, preventing damage and promoting regeneration.
A new study published in Nature Communications identifies the cells and genes necessary to make liver ducts in zebrafish, which could lead to the development of new treatments for Alagille syndrome. The research team discovered that Jagged signals come from an unexpected cell type, endoderm-derived cells within the liver itself, stimul...
Researchers at Charité found that retinol saturase plays a role in adaptive processes in liver cells, increasing with body weight and reducing negative metabolic effects associated with excess glucose exposure. The enzyme's inactivation may offer a new approach to treating metabolic liver disease and its related issues.
Researchers discovered that caspase-8 triggers programmed cell death in diseased liver cells, leading to genetic instability and tumor development. This mechanism is remarkably universal across various liver diseases.
A little-studied gene SLC13A5 may explain how liver cancer cells obtain energy to proliferate. Suppressing SLC13A5 in human hepatocellular carcinoma cell lines resulted in slower growth and division of cancer cells.
A team of scientists has developed a way to produce 3D data showing the cardiac conduction system, enabling more accurate computer models of the heartbeat. This breakthrough will improve our understanding of troublesome heart rhythms like atrial fibrillation and help surgeons design operations with less risk of damaging precious tissue.
Researchers at Tokyo Medical and Dental University have identified a molecule called YAP that determines whether liver cells proliferate or are eliminated, depending on the presence or absence of injury. This balance is crucial for maintaining organ structure and function.
Researchers at Princeton University have successfully tested a cell-culture system that allows for the long-term study of hepatitis B virus (HBV) infections. This breakthrough may aid in the development of antiviral drugs to cure chronic HBV, which can cause severe liver disease and cancer.
Researchers have developed a way to engineer liver tissue by organizing tiny subunits that contain three types of cells embedded into a biodegradable scaffold. The engineered livers expanded 50-fold after implantation in mice with damaged livers and performed normal liver functions.
Researchers have found that liver cells can eliminate excess bile from blocked ducts through a mechanism involving the internal structure of the cell, which allows bile to be packaged inside vesicles for transport. This discovery could potentially improve the prognosis for infants with rare liver disease.
Three distinct parasite strains show varying ability to infect human liver cells, with some causing more severe symptoms. Future antimalarial vaccine trials should use multiple strains to accurately predict efficacy.
Researchers bioengineered human liver tissues that exhibit previously unknown genetic-molecular crosstalk controlling developmental processes. The study reveals key communication between signaling proteins and receptors that instruct the development of liver tissues.
Researchers used embryonic stem cells to study the effects of maternal smoking on liver tissue, revealing a potent cocktail of chemicals harms foetal organs. The study found that cigarette chemicals damage the liver differently in male and female foetuses.
Transplanted fetal rat liver cells multiply and give rise to new cells in injured adult liver. This breakthrough has implications for treating liver failure without organ transplants.
A Massachusetts General Hospital research team found that oral doses of intestinal alkaline phosphatase prevented the development of fatty liver in mouse models of binge drinking and chronic alcohol consumption. The study also provided evidence of an expanded role of the liver's stellate cells in alcoholic liver disease.
A study by Houston Methodist researchers found that the surface protein OX40, which helps keep T-cells alive, can trigger the death of liver immune cells. This leads to a chain reaction causing liver inflammation and disease. The research suggests a potential new avenue for intervention, such as OX40 inhibitors or blockers.
Research reveals liver progenitor cells become activated and expand due to oncogenic signals from malignant hepatocytes. Progenitor cells can lead to benign or aggressive tumours, contributing to tumour heterogeneity.
Researchers identified R-LA induced cellular changes, inhibiting glucose production from non-carbohydrate sources. This study suggests a potential therapeutic approach for liver cancer treatment.
Researchers used gene expression analysis to map the functions of liver cells, revealing nine distinct types each specializing in its own tasks. This discovery may help clarify common liver disorders and provide insights into human health.
Researchers found that cardiac glycosides, a class of heart failure drugs, can reduce LDL cholesterol levels in patients who don't respond to statins. The study used liver-like cells generated from patient stem cells and showed significant reductions in ApoB levels, indicating potential for a new treatment option.
A new form of pegylated interferon, TRK-560, has been shown to reduce hepatitis B virus infections more effectively than conventional agents. The novel compound's attachment of PEG reduces neutralizing antibodies and prevents protein cutting enzymes from cleaving it.
A new study links protein c-Fos to liver carcinogenesis, highlighting the importance of maintaining healthy cholesterol levels in preventing liver cancer. The research suggests that statins may also prevent deleterious changes in hepatocytes caused by hypercholesterolemia and reduce inflammation.
Researchers found that a 65% decrease in liver volume and 46% reduction in hepatocyte size occurred in mice on a low protein diet. The liver's ability to regenerate itself was demonstrated after reintroducing a normal protein diet, with an 85% increase in liver volume.
Researchers have successfully reprogrammed liver cells to behave like precursor cells that give rise to the pancreas, paving the way for potential cell therapies for type I diabetes. By altering a single gene, the team induced an identity crisis in liver cells, which then developed into cells with pancreatic properties.
Researchers discovered that paracetamol damages liver cells by disrupting tight junctions, leading to cell death and organ dysfunction. The study aims to develop alternative methods for testing paracetamol toxicity and identify potential targets for new drugs.
Researchers found that food withdrawal leads to the accumulation of p53 protein in liver cells, playing a crucial role in metabolic adaptation to starvation. This discovery may pave the way for new treatments for patients with metabolic or cancer-related disorders.
Researchers at Mayo Clinic have identified a key protein, Rab10, that helps hungry liver cells locate and break down fat for energy. This discovery could lead to new treatments for fatty liver disease.
Researchers discovered that hepatitis C virus induces liver cells to produce microRNAs that inhibit interferon production, blunting the body's antiviral defenses. This finding helps explain why interferon treatments fail in many patients, increasing the risk of liver cancer and treatment resistance.
Scientists at EPFL and Nestéle Institute of Health Sciences identified 5000 proteins affected by the diurnal cycle in mouse liver cells. The study used cutting-edge proteomics to monitor protein accumulation over a 24-hour cycle, revealing key cellular functions such as DNA repair and ribosome biogenesis were also affected.
Researchers have discovered vigilin, a 'lock keeper' protein in liver cells that regulates fat release and influences transport proteins. The study found a strong correlation between vigilin levels and fatty liver percentage.
A research team at Children's Hospital Los Angeles has successfully generated functional human tissue-engineered liver from adult stem and progenitor cells. The tissue-engineered liver exhibited normal structural components, including hepatocytes, bile ducts, and blood vessels, and demonstrated in vivo secretory function.
A research team has devised a new method to enhance genome-wide association studies for liver disease using purified liver cells made from induced pluripotent stem cells. The approach, developed by the Medical University of South Carolina, allows for more accurate identification of genetic mutations causing liver diseases.
Researchers at the University of Pennsylvania School of Medicine have discovered that deleting a specific protein, HNF6, leads to an increase in lipid-producing genes and liver damage. This study highlights the co-dependence of two cell nucleus proteins, HNF6 and Rev-erb-alpha, which regulate liver lipid metabolism.
Researchers created a liver on a chip that accurately replicates the metabolic variations found throughout the organ. The microfluidic device allows for fine control over liver cell metabolism, enabling the study of the effects of toxins and new drugs on the liver.
Researchers developed an in vitro model system for NAFLD using human pluripotent stem cell-derived immature hepatocyte-like cells. The study replicated key steps of the disease, including lipid storage and PPARalpha regulation.
Researchers have identified a small peptide from a bacterium that efficiently binds excess copper from liver cells, offering a potential treatment for Wilson disease. The molecule, methanobactin, was shown to reverse acute stages of the disease and prevent organ failure.
Researchers develop new method to generate large pool of gene-corrected cells, which can repopulate in vivo and treat various disorders
A new approach repairs liver disease by converting fibrosis-causing cells into functional hepatocytes, reducing damage and improving liver function. The technique targets liver fibrosis, a primary driver of liver disease, and may be more efficient than cell transplants.
Researchers found that transplanting liver cells into an extra-hepatic site, such as the intra-mesentery, can help protect against post-operative liver failure and aid in survival of the remaining liver. The study showed improved overall mortality due to acute liver failure in the transplantation group.
A recent study discovered that macrophages in abdominal cavities surrounding organs like the liver and heart can initiate immediate and rapid repair after damage. The study found that these immune cells patrol within the cavity and adhere to damaged areas for quick healing, suggesting a new approach to tissue repair.
Researchers found that a protein called TRIM21 was preventing the body's antioxidant response system from working effectively, leading to serious illness. Inhibiting this protein may lead to effective treatments for liver and heart disease.
Researchers discovered how hepatitis B virus (HBV) counterattacks the host's defense system by destroying a protective protein complex. This finding suggests new avenues for developing innovative therapeutic agents targeting the X protein.
Researchers have found a modified protein that can reverse liver fibrosis and cirrhosis in lab rats. The protein, TRAIL, was coated with a polymer to extend its half-life, allowing it to effectively kill activated hepatic stellate cells and reduce signs of fibrosis.
Researchers have successfully treated a genetic disorder using a viral vector to deliver genome-editing components, correcting the disease-causing mutation. The treatment improved survival in newborn mice but showed poor results in adult animals, highlighting the need for further adjustments to the gene-editing system.