Articles tagged with Schwann Cells
Researchers at Johannes Gutenberg University Mainz have discovered that histone deacetylase 8 (HDCA8) inhibits the conversion of Schwann cells into their repair phenotype, slowing down peripheral nervous system recovery. Removing HDAC8 accelerates regeneration and restores sensory function.
Researchers at Doshisha University reveal that 25-hydroxycholesterol causes a specific type of cell death called ferroptosis, which could contribute to various diseases. The study identifies two key mechanisms by which 25-OHC induces ferroptosis, including inhibition of cellular pathways and disruption of antioxidant systems.
Researchers discovered that PMP22 duplication disrupts lipid metabolism and plasma membrane organization in developing Schwann cells, leading to myelin degradation and nerve damage. Targeting dysregulated lipid pathways may reverse some detrimental effects of CMT1A.
Researchers have developed a new approach to treating cutaneous neurofibromas, a common skin tumor associated with neurofibromatosis type 1. By targeting the cAMP and Ras/MAPK pathways, this combination therapy may provide an enduring halt in the expansion of these tumors.
Researchers have discovered that Schwann cells, previously thought to be solely responsible for protecting nerve fibers, also detect sensory stimuli such as touch, heat, and cold. The findings open new avenues for understanding and treating pain and impaired touch perception.
Researchers discovered that fat tissue supports nerve repair by stimulating Schwann cells with leptin. This activation optimizes metabolism, allowing the restoration of original nerve function.
Researchers at Salk Institute uncover a mechanism for repairing damaged nerves during peripheral neuropathy, with protein Mitf playing a key role. The findings have the potential to inspire novel therapeutics that bolster repair function and heal peripheral neuropathy.
Researchers have successfully used AAV1.NT-3 gene therapy to improve muscle physiology and prevent age-related sarcopenia in mice. The treatment resulted in restored muscle mass, strength, and neural connections, offering a potential new option for managing this debilitating condition.
Schwann cells in nerve healing take over immune cell functions to prevent excessive tissue damage and promote regeneration. Similarly, they may stop chronic inflammation in childhood nerve tumors, making them benign. Schwann cells can also regulate T-cell activity, potentially curbing cancer growth.
Researchers identified CUDC907 as a dual phosphoinositide-3 kinase/histone deacetylase inhibitor that promotes apoptosis in NF2 schwannoma cells. The compound reduced viability and induced cell cycle arrest in human merlin deficient Schwann cell models.
Researchers have discovered that Schwann Cell Precursors are the origin of tuberous sclerosis complex tumours in the kidney. Lab-grown 'mini-kidneys' were used to create a genetic profile similar to TSC tumours, revealing the diversity in tumour size and cellular makeup within patients.
A study published in Nature Communications reveals that Schwann cells in the peripheral nervous system generate pain signals during migraines. Blocking these signaling pathways using nanoparticles offers promise for novel migraine treatments.
Researchers have discovered that HIV drugs may be effective in treating low-grade brain tumours, specifically meningioma and acoustic neuroma. High levels of HERV-K proteins were found to stimulate the growth of these tumours, and targeted drugs have been identified to reduce their growth.
A diet rich in palmitic acid makes tumor cells more aggressive and increases their metastatic capacity, a process that is responsible for 90% of cancer deaths. Exposure to palmitic acid leads to permanent epigenetic modifications in tumor cells, allowing them to conserve metastatic capacity even after the fatty acid is removed.
A new study by University of Pennsylvania researchers uses human gingiva-derived mesenchymal stem cells to guide nerve growth and regeneration, achieving similar results as traditional autograft procedures. The approach has potential for treating larger nerve gaps, including those resulting from oral cancer surgery.
A joint research group found a previously unknown cell type in the adrenal glands that might be the origin of neuroblastoma tumour cells. This discovery could provide a basis for effective treatments.
Scientists have discovered a natural signal molecule that stops the uncontrolled growth of malignant tumors and promotes the healing of injured nerve fibers. The molecule, EGFL8, is produced by Schwann cells in benign neuroblastomas and stimulates tumor cell maturation, leading to better survival rates for patients.
Researchers have identified a new class of glial cells in the cornea, known as Schwann cells, with unique genetic properties that could help improve wound healing and nerve regeneration after surgeries and corneal transplants. The study's findings may also provide insights into conditions like dry eye and LASIK-related side effects.
A study published in STEM CELLS revealed that fibulin 5 plays a crucial role in the development of Schwann cells, which produce the myelin sheath surrounding neuronal axons. The research suggests that fibulin 5 may be used to treat Charcot-Marie-Tooth disease and other demyelinating disorders.
Researchers at the University at Buffalo have discovered that hematopoietic stem cell transplantation improves Krabbe disease outcomes through a mechanism independent of cross-correction. The study found that macrophages expressing GALC enzyme aid in myelin debris degradation, leading to better patient outcomes.
NYU Dentistry researcher Yi Ye has received a $2.2 million NIH grant to investigate how oral cancer cells invade nerves and cause pain. Her study aims to understand the role of Schwann cells in this process and identify potential targets for treating oral cancer-related pain.
A complex interaction within Schwann cells has been discovered, which plays a vital role in the correct maturation of these cells. This interaction ensures that DNA is packaged correctly and marked accordingly, leading to proper transport of genetic information.
Injured axons trigger Schwann cells to build specialized actin spheres, breaking down and removing damaged fragments to start regeneration. Oligodendrocytes can also generate actin structures with induced VEGFR1 expression, promoting central nervous system healing.
Researchers have discovered that Schwann cells can spread myelin across multiple axons, overturning the traditional understanding of these cells' function. This finding could lead to new gene-therapy techniques to repair damaged myelin in peripheral nervous system disorders like Charcot-Marie-Tooth disease.
The IADR/AADR Journal of Dental Research has announced the winner of its Cover of the Year Award, 2018 for a study on Schwann cell phenotypes in aging human dental pulp. The award recognizes an aesthetically pleasing and scientifically novel image that enhances the impact of the article.
Researchers have discovered that nerve fibers and associated Schwann cells are the origin of severely disfiguring neurofibromas in NF1 patients. The study found micro-lesions containing these nerve fibers and cells proliferate to form the bulk of the disfiguring neurofibromas.
Researchers found that a blood-clotting protein called thrombin can degrade nerves, but nerve-supporting glial cells like Schwann cells block its effects. This discovery could have implications for diseases such as ALS, MS, and Alzheimer's.
Macrophages play a vital role in controlling the processes of nerve repair following damage by secreting repulsive cues. The interaction between Slit3 and Robo1 allows for the migration of Schwann cells and regrowing nerve projections, enabling successful regeneration and recovery of nerve function.
Researchers at ETH Zurich have discovered that Schwann cells produce fatty acids through an enzyme called FASN, which is essential for myelin layer formation and maintenance. This breakthrough has implications for understanding the development of rare childhood diseases and potential treatments.
Scientists have identified genetic processes that enable nerve-supporting cells to transform into specialized versions that facilitate nerve regeneration. This knowledge may lead to new drug therapies for peripheral neuropathies, a set of conditions causing numbness, muscle weakness, and sensitivity.
Researchers found an anti-sense RNA that regulates myelin genes and promotes demyelination after nerve injury. This discovery could lead to a new therapy by manipulating AS-RNA expression to restore complete nerve function.
Researchers at Cincinnati Children's Hospital Medical Center found that genetic dysfunction disrupts the balanced production of Schwann cells in peripheral nerves. This imbalance leads to nerve insulation defects and can cause conditions like neuropathy and nerve sheath tumors.
A Phase I clinical trial demonstrates the safety of transplanting autologous Schwann cells into a spinal cord lesion, showing no negative effects after 1 year. The study successfully determined safety and feasibility for performing peripheral nerve harvests within 5-30 days followed by intra-spinal transplantation within 4-7 weeks.
The University of Miami's Miami project successfully completes a Phase I clinical trial of schwann cell transplantation to treat spinal cord injuries. The trial demonstrates the safety and feasibility of transplanting autologous human Schwann cells to repair damaged spinal cords.
Researchers have discovered that Merlin plays a vital role in nerve repair after injury, opening up new potential therapies for trauma and diabetes-related damage. The study found that deficient Merlin levels contribute to poor nerve repair, but also identified a crucial pathway for repair using Schwann cells.
Researchers have clarified the beneficial function of a brain protein associated with prion diseases, revealing its role in maintaining nerve cell insulation. The study found that properly folded proteins play a crucial role in keeping axons insulated, enabling rapid nerve signal propagation.
Scientists have identified how prion proteins dock onto Schwann cells to maintain nerve integrity. The discovery resolves a 30-year-old question and holds promise for future treatments of Creutzfeld-Jakob disease and peripheral neuropathy.
Researchers at the University of Newcastle have developed a method to generate large and pure populations of human Schwann cells using small molecules, which support nerves and play a crucial role in nerve repair. These cells exhibit characteristics similar to those found in the body and can interact with nerves in vitro.
Researchers discovered that Schwann cells digest damaged myelin internally through autophagy, clearing 40-50% of the myelin within 5-7 days. This mechanism enables significant nerve repair in the peripheral nervous system, contrasting with the CNS where oligodendrocytes fail to clear myelin.
Researchers found salicylates reduce vestibular schwannoma cell viability and proliferation without affecting healthy nerve cells. The study's results suggest salicylates as promising pharmacotherapies against vestibular schwannomas, which can cause hearing loss and tinnitus.
Researchers discovered that disrupting a tumor suppressor gene disrupts the formation of the protective insulating sheath on peripheral nerves, leading to muscle wasting and neuropathy. The study suggests that normal molecular function of Lkb1 is essential for proper myelination.
Researchers identified over 4000 genes with differing expression profiles between VS cells and normal Schwann cells, including the aberrant PI3K/AKT/mTOR signaling pathway. Testing compounds BEZ235 and PKI-587 reduced tumor cell viability and increased cell death.
Researchers found that rapamycin at a concentration of 1.53 nmol/L significantly promoted Schwann cell migration, whileFK506 had limited efficacy due to its nephrotoxicity and hypertension risks. Rapamycin also upregulated growth-associated protein 43 expression in Schwann cells.
Researchers have found that the growth factor neuregulin-1 can restore balance to impaired Schwann cells in genetically modified rats with Charcot-Marie-Tooth disease. This imbalance leads to insufficient myelination and nerve damage, resulting in symptoms such as numbness and weakness.
Researchers developed a chemically extracted acellular allogeneic nerve graft that combines with ciliary neurotrophic factor (CNTF) to promote sciatic nerve repair. The study found this method to be superior to bridging alone, but inferior to autologous nerve anastomosis.
Quercetin reverses high glucose-induced inhibition of neural cell proliferation and reduces apoptosis through autophagy induction. Autophagic and proliferative activities are rescued in Schwann cells under high glucose conditions after quercetin intervention.
Researchers found that microRNA miR-21 regulates the differentiation of neural crest stem cells (NCSCs) from human hair follicles into Schwann cells. By binding to the 3'-UTR of SOX2 mRNA, miR-21 down-regulates SOX protein expression, increasing SC differentiation capacity.
A new study reveals that parasympathetic neurons originate from immature glial cells in mouse embryos, forming a previously unknown developmental pathway. This discovery may lead to new medical treatments for congenital disorders of the nervous system.
Researchers have successfully expanded cord blood stem cells using histone deacetylase inhibitors, resulting in enhanced proliferation and hematopoietic reconstitution. The findings suggest a potential clinical benefit for children with hematological malignancies or genetic defects.
Researchers found that human periodontal ligament stem cells exhibit similar therapeutic effects to autologous Schwann cells in repairing peripheral nerve injuries. The study suggests a potential value for the use of human periodontal ligament stem cells in the repair of mental nerve injury.
Researchers found that co-transplanting Schwann cells and olfactory ensheathing cells, combined with daily treadmill training, promotes functional recovery in rats with spinal cord injuries. The study reveals a synergistic benefit of the combined therapy on axonal regeneration and motor function improvement.
Researchers at Plymouth University Peninsula Schools of Medicine and Dentistry have discovered how the loss of a tumour suppressing protein leads to abnormal cell division in the brain and nervous system. The study's findings may lead to new drug-based therapies to reduce or negate the need for multiple surgeries or radiotherapies.
A key protein in Schwann cells is essential for normal interactions between nerve cells and Schwann cells, regulating the steps that lead to nerve regeneration. Deficiency of this protein may lead to chronic neuropathic pain, motivating the development of a small molecule drug to mimic its function.
Researchers discovered that crippled mitochondria in Schwann cells lead to a toxic substance build-up, causing nerve damage and symptoms like numbness and pain. This finding may lead to new therapeutic strategies to treat peripheral neuropathies, including drugs that block toxin buildup.
Researchers at Max Planck Institute of Experimental Medicine found that peripheral glial cells produce neuregulin1 to support nerve repair and myelin regeneration. Neuregulin1 is essential for the maturation of Schwann cells and the regeneration of damaged nerves.
Researchers at the University of Edinburgh discovered that bacteria can change the properties of supporting cells within the nerve system, called Schwann cells, to mimic stem cells. This process enables bacteria to spread throughout the body and potentially aid research into degenerative conditions.
A new study reveals that leprosy bacteria reprogram adult Schwann cells into stem cell-like cells and convert them to muscle-like cells, spreading infection. This finding could lead to the development of new therapeutic strategies and regenerative medicine tools.
Researchers from the University of Sheffield have developed a new technique to grow Schwann cells, vital for nerve repair, in less than half the time and at lower cost. The method could be a vital step for use in patients with severe nerve damage.
Researchers at the University of Rochester Medical Center have discovered that dorsal root ganglion neurons can create thick, healthy nerves without provoking an immune response. This breakthrough could lead to better treatment options for the over 350,000 patients with serious nerve injuries in the US each year.
A $1.4 million NIH grant will investigate a method to heal peripheral nerve damage by stimulating the growth of Schwann cells and axons, potentially restoring function in patients with severe injuries. Researchers aim to develop effective tools for nerve repair using electrical stimulation technologies.