Articles tagged with Fibroblasts
Researchers at Baylor College of Medicine found that Gata4 can reduce post-heart attack fibrosis, leading to improved cardiac function in small animal models. The study's results suggest a novel role for Gata4 in heart regeneration and may lead to new treatments for heart failure.
Researchers from the University of Pennsylvania School of Medicine identified a process where cancer cells instruct normal cells to act like viruses, enabling tumors to spread and resist treatment. This 'virus mimic' is detected in the blood of cancer patients and could explain why some breast cancers are more aggressive than others.
Researchers at Vanderbilt University have developed a monoclonal antibody known as SYN0012 that blocks the production of cadherin-11, a protein responsible for calcifying heart valves. The drug shows promise in keeping heart valve leaflets supple and preventing the progression of aortic valve stenosis.
Researchers at Stanford University School of Medicine identified a pathway that drives fibrosis in many organs, including scleroderma and idiopathic pulmonary fibrosis. Blocking the CD-47 signal reverses lung fibrosis in mice.
Researchers discovered ordered arrangement of myosin-II filaments in actin cables of non-muscle cells, enabling slow contractility and movement through connective tissue. This organisation allows for dynamic assembly and disassembly of protein cables, providing the necessary strength to interact with the microenvironment.
A comprehensive review article explores cytokine regulation of fibroblast behavior and extracellular matrix in the lung, shedding light on chronic inflammation. The study highlights the role of metabolic changes, age, and epigenetic mechanisms in affecting fibroblast activity and immune system cell populations.
Researchers discovered two distinct fibroblast subtypes in the dense tumor-enveloping stroma of pancreatic ductal adenocarcinoma, which may be precisely targeted to improve treatment response. The first subtype produces high levels of alpha smooth muscle actin and is adjacent to neoplastic tumor cells.
Scientists discovered that fibroblasts, a type of connective tissue cell, increase HIV infection in immune cells through trans-infection and make them more prone to infection. Epithelial cells, on the other hand, secrete high levels of antiviral proteins that inhibit infection.
Researchers at UCLA discovered that cardiac fibroblasts, which give rise to scar tissue after injury, can also produce bone-like cells. By blocking an enzyme involved in bone mineralization, they prevented calcification in mice, offering a potential new approach for treating abnormal calcium deposits in the heart.
Researchers discovered that activation of the aryl hydrocarbon receptor pathway blocks collagen production and myofibroblast proliferation in thyroid eye disease. The study suggests AHR ligands may be a novel target for treatment, offering hope for targeted therapies.
Researchers discovered that genetic variations in ATAD3A are associated with rare neurological syndromes, including global developmental delay and visual, neurological, and heart problems. A study using Drosophila melanogaster revealed that mutations in the gene cause an aberrant phenotype in mitochondria.
UAB researchers found that removing transcriptional bookmarks can improve reprogramming of human fibroblasts to create induced pluripotent stem cells. This process may increase the yield and quality of iPS cells, essential for patient-specific cell-replacement therapies.
Researchers created a human heart tissue model using induced pluripotent stem cells to study hypertrophic cardiomyopathy, an excessive thickening of the heart associated with rare genetic disorders. The model revealed a previously unknown role for fibroblasts in triggering cardiomyocyte hypertrophy, offering new therapeutic possibilities.
Researchers at IBS find PLEKHG3 plays a crucial role in cell polarity and migration, allowing fibroblasts to move faster. The discovery can benefit fields like cancer, immunology, and neurological research.
Researchers identified a gene driving scarring in conjunctival tissue, linked to mucous membrane pemphigoid, a common cause of blinding conjunctivitis. Disulfiram treatment effectively reduced inflammation and prevented scarring in mouse models and human cells.
A review paper published in Nature Reviews Drug Discovery suggests targeting non-muscle cells in the heart responsible for cardiac scarring could lead to new treatments for heart disease. Scientists aim to utilize natural reparative processes of fibroblasts to modify scar tissue properties.
Researchers at Boston University School of Medicine have discovered a reliable marker (PDGFRβ) to detect carcinoma-associated fibroblasts in oral cancer tissues. This finding could lead to the development of more effective cancer therapies by combining anti-PDGFRβ treatment with existing tumor treatments.
Brown University bioengineers have developed a synthetic bed that works as well as traditional mouse cells without contamination risk. The innovation allows for the cultivation of human embryonic stem cells more safely and could lead to advances in stem cell therapies.
Researchers at Vanderbilt University have discovered that cancer-associated fibroblasts (CAFs) rearrange the extracellular matrix into parallel fibers of fibronectin, creating a road for migrating cancer cells to follow. This allows CAFs to exert traction forces on the ECM, enabling cancer cells to move in a single direction.
Scientists have discovered a signaling axis consisting of three proteins that regulates cell repulsion. This process is essential for preventing cells from sticking together and could play a role in cancer metastasis. The study's findings provide new insights into the molecular mechanisms behind cell migration.
Researchers at the University of Pennsylvania School of Medicine have discovered a way to directly reprogram skin fibroblasts into functional melanocytes, the body's pigment-producing cells. This technique has significant implications for developing new cell-based treatments for skin diseases and screening strategies for melanoma.
Researchers found that cancer cells and fibroblasts collaborate to invade the basement membrane, a process that begins long before the actual movement of cancer cells. CAFs secrete more proteases and matrix proteins than normal fibroblasts, which helps them remodel the basement membrane.
Researchers have successfully created induced neurons that model Alzheimer's disease by starting with fibroblasts taken from skin biopsies. The differentiated cells express normal neuronal markers and proteins associated with the neurodegenerative disorder, including amyloid beta and tau.
Researchers established induced pluripotent stem (iPS) cells from Werner syndrome fibroblasts, which can be used for drug discovery and gene therapy. The iPS cells have recovered telomeric abnormalities and similar expression levels of aging-related genes as normal iPS cells.
Researchers at Houston Methodist develop a new approach to regrow damaged blood vessels using trans-differentiated fibroblasts, improving blood flow and oxygenation. The technique shows promise for treating cardiovascular damage and injuries with minimal risk of chromosome damage.
Researchers at UNC School of Medicine have discovered a new way to generate more blood vessels following a heart attack by turning fibroblasts into endothelial cells. Increasing the level of p53 in scar-forming cells significantly reduces scarring and improves heart function after heart attack.
Researchers found that cardiac fibroblasts are unique cells with organ-specific functions and can be used in replacement therapies for congenital heart disease and heart failure. They have specific genes that tell them to become heart cells, making them a promising alternative to heart transplants.
Scientists at King's College London have discovered two distinct types of fibroblasts in the skin, one responsible for hair growth and the other for repairing wounds. Increasing these cells may lead to new treatments for scarring and aging-related skin issues.
Researchers at Kyoto University successfully induced direct conversion of human dermal fibroblasts into induced chondrogenic cells, displaying the gene pattern of chondrocytes. Transplanted cells generated hyaline cartilage tissue in immunodeficient mice without forming tumors.
Researchers found that basic fibroblast growth factor and heparin promote differentiation of MSCs into motor neurons, increasing acetylcholine levels. This technology may prevent and treat muscular atrophy caused by peripheral nerve injury.
Researchers found that basic fibroblast growth factor protects the spinal cord by reducing calcitonin gene-related peptide and acetylcholinesterase expression in damaged motor neurons. This suggests a potential therapeutic application for treating spinal cord injuries.
Researchers at Gladstone Institutes develop method to reprogram human fibroblasts into beating heart cells using a cocktail of five genes. The transformation has the potential to regenerate damaged heart muscle and could revolutionize treatment for heart attacks.
Researchers have developed a new gene therapy approach to convert fibroblasts from human fetal heart cells and skin into heart muscle cells. This technique may potentially treat heart disease by regenerating a healthy heart within the damaged one.
Scientists at Cincinnati Children's Hospital Medical Center identify a molecular pathway critical to body repair processes after injury, leading to potential new anti-fibrotic or anti-inflammatory agents. The discovery could provide a targeted intervention point in fibrotic diseases, including heart failure and muscular dystrophy.
A new study confirms the existence of a shared pathway between Lou Gehrig's disease and spinal muscular atrophy, linking the two diseases through their impact on motor neuron function. The study suggests that this shared pathway may lead to common treatment options for both conditions.
Researchers at Newcastle University have found that brain cells follow the same molecular pathway as senescent fibroblasts, leading to cell damage and age-related diseases. This discovery opens new possibilities for understanding and treating conditions like dementia and motor neuron disease.
Cardiac injury leads to rapid morphological changes, including enlargement and fibrous growth tissue formation. Advanced stages of remodeling have begun by day seven following injury. This research provides insights into the coordinated events of cardiac pathology and possible intervention targets.
Researchers at Washington University in St. Louis have received $2 million to develop artificial tissue models for testing new drugs that target myofibroblasts, which contribute to heart disease. The study aims to understand how these cells alter the electrical and mechanical properties of heart tissue.
Researchers at the Stowers Institute for Medical Research found that the Arp2/3 complex is essential for forming lamellipodia, which are crucial for cell migration. The study used genetic disruption to investigate the function of Arp2/3 in fibroblast cell motility.
Scientists have made breakthroughs in reprogramming scar tissue from myocardial infarction (MI) into viable heart muscle cells using viral vectors. The new approach has shown promising results in adult mice and offers a potential solution to the major problem of cardiac regeneration after MI.
Researchers at Moffitt Cancer Center found that fibroblasts play a significant role in melanoma tumor growth and progression. The study also revealed that fibroblasts contribute to drug resistance and the 'flare' response, where tumors exhibit enhanced metabolism after targeted therapy is stopped.
Researchers found that combining tamoxifen with dasatinib reverses chemo-resistance caused by cancer-associated fibroblasts. The combination normalized glucose intake and reduced mitochondrial oxidative stress, leading to nearly 80% cell death.
Cigarette smoke exposure fundamentally alters airway tissue in people with chronic obstructive pulmonary disease (COPD), leading to self-perpetuating fibrotic changes. The study reveals that cigarette smoke induces the production of pro-fibrotic cytokines and activates the NF-κB pathway, contributing to COPD persistence.
Researchers found that interleukin-13 stimulates invasion of airway cells called fibroblasts in asthma patients, leading to increased thickness in airway walls and loss of lung function. The protein acts in combination with other mediators, including TGF-β1 and MMPs, to cause cellular changes that contribute to airway remodeling.
A Tel Aviv University researcher has found that fibroblasts, a type of connective tissue cell, can be coerced into supporting inflammation and tumor growth. This discovery opens new avenues for drug research and may help manage inflammation to reduce cancer growth.
Researchers at UC San Diego School of Medicine present a new explanation for how fibrotic cells form in the human liver, upending long-held assumptions about EMT and FSP1. The study reveals endogenous stellate cells are the primary culprit in liver fibrosis, and FSP1 is an unreliable marker.
Fibroblasts, a type of connective tissue cell, have been found to be metabolically active during quiescence, producing proteins that help replenish other cells. This discovery could lead to new strategies for attacking tumors and improving overall health.
Researchers have devised a three-ingredient molecular cocktail that transforms fibroblasts into beating heart cells, potentially solving the issue of cardiac muscle regeneration in heart disease. The cocktail, tested on mice, shows promise in producing new cardiac muscle cells more efficiently than induced pluripotent stem cells.
Researchers at Gladstone Institutes found a way to make beating heart cells from body's own cells, helping to regenerate damaged hearts. The new method directly reprograms structural cells called fibroblasts into cardiomyocytes without needing stem cell state.
Researchers from the University of Illinois at Chicago have discovered a cellular response that breaks down and inhibits excess scar tissue in wound healing. Fibroblasts recruited to the wound site enter a state of reproductive dormancy called senescence, which accelerates collagen breakdown and limits scar tissue formation.
Researchers found that inflammasome activation increases muscle damage in muscular dystrophy, while galectin-7 expression levels are associated with metastasis in breast cancer. These findings provide new insights into disease mechanisms and potential therapeutic targets.
Researchers used organotypic skin cultures to study PPAR-beta/delta's role in skin cell communication. They found that PPAR-beta/delta regulates crosstalk between skin layers, controlling proliferation rates and preventing excessive growth.
Researchers at the Gladstone Institutes have identified a complex signaling process that governs heart cell expansion and division. The study shows that cardiac fibroblasts send signals to cardiomyocytes to divide or grow, which could lead to regenerative therapies after heart attacks.
A University of Iowa study found that smoking decreases a key protein in lung cells, leading to cell aging and damage. The team suggests targeting Werner's syndrome protein for developing treatments for smoking-related diseases like emphysema.
Researchers found that Snail1 promotes tissue invasion and angiogenesis in cancer cells by stimulating fibroblast function. Fibroblasts without Snail1 are less able to degrade the extracellular matrix and form invadopodia, key structures for cell invasion.
Researchers at Salk Institute boost reprogramming efficiency by over 100fold and cut time in half. They successfully generate patient-specific stem cells from a single human hair, providing a practical alternative to embryonic stem cells.
A paper on stress urinary incontinence treatment has been retracted from publication after an investigation found critical deficiencies in patient consent and document authenticity. Senior author Georg Bartsch denied involvement, but the study's flaws have raised concerns about research integrity.
Researchers at the University of California, San Diego, have discovered a novel way to prevent cardiac fibrosis by targeting the Epac molecule. By increasing Epac expression, they were able to block the ability of agents to promote fibrosis in cardiac fibroblasts.
Fibroblasts, key cells in wound healing, transform into powerful contractile cells through a mechanical process. This new understanding could help prevent fibrosis and improve tissue engineering by controlling the rigidity of cell cultures.
Researchers at Massachusetts General Hospital have discovered a crucial molecular pathway underlying idiopathic pulmonary fibrosis (IPF), a deadly lung disease. The study found that lysoposphatidic acid (LPA) and its receptor LPA1 play a key role in attracting fibroblasts, leading to scarring of lung tissue.