Articles tagged with Keratinocytes
Researchers developed a novel mouse model that accurately mirrors the progression and dynamic shift between disease states of lupus. The model demonstrates a direct link between skin defects and systemic disease, with dynamic features including remission and relapse cycles.
Researchers discovered that a gene called ZNF750, active in skin cells, is essential for supporting Langerhans cells and building the body's first line of immune defense. The study found that ZNF750 controls the production of IL-34, a molecule released by skin cells that acts as a survival signal for Langerhans cells.
Researchers at the University of Arizona Comprehensive Cancer Center are investigating novel immune-based approaches to prevent keratinocytic skin cancers. They aim to identify early immune signals that can activate the body's own immune defenses to prevent cancer before it starts.
AcCELLerate has partnered with ATCC to provide customized Master, Working, and assay-ready instaCELL banks for research clients. Researchers will gain access to high-quality, authenticated cell lines with increased assay reproducibility.
A study published in Chinese Medical Journal identified tumor-promoting keratinocytes linked to HPV infection and poor prognosis. These cells were found to interact with immune cells, promoting tumor proliferation and differentiation.
Researchers identify PIEZO2-expressing fibroblasts as key drivers of keloid formation and recurrence. These cells sense mechanical pressure, leading to excessive collagen production and scarring. The study's findings hold significant implications for future diagnosis and treatment options.
A groundbreaking study from Okayama University reveals that keratinocytes, not fibroblasts, are responsible for dermal collagen formation in humans and other vertebrates. Keratinocytes produce collagen fibers in a structured arrangement before fibroblasts modify them.
Researchers at the University of Iowa Health Care have identified a cellular route used by Ebola virus to traverse skin layers and emerge onto the skin surface. The study suggests that the skin's surface may be one route of person-to-person transmission, with human skin specimens actively supporting EBOV infection.
Researchers discovered that Prostaglandin E2 drives skin cells to age and enables some of these cells to become pre-cancerous, leading to increased cancer risk. The study found that blocking PGE2 reduced the chances of aged cells becoming precancerous.
Researchers discovered interleukin-38 forms condensates in keratinocytes, driving programmed keratinocyte death and epidermal renewal. The study offers a new perspective on human epidermis and sheds light on skin diseases like psoriasis and atopic dermatitis.
Researchers used genomic technology to study Marjolin's ulcer, a rare and highly aggressive skin cancer that grows on chronic burn wounds. The study reveals insights into how keratinocytes switch their function to become cancerous, creating a fertile environment for tumor cells to grow and spread.
A team of researchers led by Associate Professor Ken Natsuga found that cell-cell adhesion governs pattern formation in keratinocytes. Starvation also plays a crucial role in the formation of these patterns, which are influenced by cell proliferation and differentiation.
Scientists from Tokyo Medical and Dental University successfully generate autologous skin grafts by introducing mutations into mouse embryos, which then form sheets of epidermis containing hair follicles. These grafted skin patches survive up to 3 months and mimic mature epidermis structure.
Researchers investigated the biological repercussions of UV-C radiation exposure from readily available domestic lamps and found that even brief exposure can lead to irreversible alterations in skin cells and retinal cells. The study highlights the need to prioritize safe utilization of these lamps to prevent potential harm.
A study published in eLife found that nerve fibers in the human skin are ensheathed by keratinocytes, which may play a role in communicating information about external stimuli to the central nervous system. This discovery could lead to new avenues for treating patients with small fiber neuropathy.
Researchers found a significant increase in extracellular vesicles released by aged keratinocytes, which were also enriched with specific microRNAs. These EVs impaired young keratinocyte proliferation and organogenesis, mimicking aged skin defects.
A recent study published in the Journal of Investigative Dermatology has revealed that hemoglobin is present in the epidermis, the outermost layer of our skin. This discovery adds a new facet to understanding the skin's defense mechanisms against aging and cancer.
Defective exosomes in diabetic patients drive inflammation and impair wound healing. Researchers identified alterations in exosome cargo and release that compromise wound healing in diabetes. New exosome-focused therapies may promote healing of chronic wounds.
A new study revealed that people in the UK have facial skin with more DNA damaged from the sun than those in Singapore, leading to a higher risk of developing keratinocyte skin cancers. This is despite lower UV light exposure levels in the UK.
Research finds that skin keratinocytes regulate temperature sensation by controlling the amount of TRPV3 proteins, reducing their activity when bound to TMEM79. This discovery resolves controversy over skin keratinocytes' involvement in temperature detection.
Researchers discovered a novel peptide, T14, that is detectable in human keratinocytes and inversely related to age, with higher levels found in chronically photosensitive individuals. The study suggests that monitoring T14 levels may offer insights into the link between degenerative diseases and epidermal cell profiles.
A Phase I/II study found tofacitinib effective in improving skin and organ issues in systemic sclerosis patients. The drug was well-tolerated, with minimal impact on T-cells, suggesting potential repurposing for treatment.
Researchers explored how differences in skin composition affect susceptibility to diseases like psoriasis and atopic dermatitis. The study found that body site determines skin structure and function, with specific lipids and proteins playing a crucial role in disease diagnosis.
Researchers discovered that dermal contact with nicotine concentrations found in thirdhand smoke and electronic cigarette spills can impair wound healing, increase susceptibility to skin infections, and cause oxidative stress in skin cells. The study suggests that even a short exposure of 24 hours is sufficient to cause skin damage.
Researchers studied naked mole-rats' skin using single-cell RNA-seq to understand its remarkable stability against aging. They found no changes in epidermal gene expression with age and a unique keratinocyte differentiation trajectory that remained intact.
Researchers found that normal-appearing lupus skin contains the same inflammatory signals as skin with rashes, suggesting a primed state for inflammation. The study's findings provide new insights into how UV light triggers rashes in lupus patients and highlight the potential for precision medicine in treating the disease.
A study reveals how CSDE1 coordinates skin cell senescence, slowing down cellular function without causing death. This leads to the formation of a firewall against cancer, suppressing tumor growth.
Researchers at UCI found that PIEZO1, an ion channel mechanosensor, regulates keratinocyte migration and wound healing speed. In mice lacking PIEZO1, wounds heal faster than those with increased PIEZO1 function.
Non-melanoma basal and squamous cell skin cancers saw a 30% rise in Ontario over 15 years, mostly among people under age 35. The annual mortality rates increased by almost 5-fold, with males experiencing higher rates than females.
A UCI-led study identifies a new molecular pathway that promotes wound healing in the skin by relaxing cell-cell adhesions between migrating keratinocytes. This finding may improve understanding of wound healing biology and lead to new therapies for non-healing wounds like diabetic ulcers.
Researchers from Tokyo Medical and Dental University have developed an AI system called DeepACT that quickly identifies healthy stem cells with the same accuracy as humans. This technology speeds up the process of evaluating stem cell quality, which is crucial for skin grafts and other applications.
Researchers develop non-invasive tool to assess oral keratinocyte quality, correlating cell motion speed with regenerative capacity and proliferation potential. The cells/colony motion index makes a reliable quality control tool for engineered cells used in regenerative medicine.
Chronic graft-versus-host disease (cGVHD) causes skin thickening due to the production of TGFβ1 by apoptotic keratinocytes stimulated by interferon-γ, according to researchers at the University of Tsukuba.
Biomechanical engineers at Tohoku University developed a formula to describe permeability of rubbed skin. The study found that mechanical rubbing causes gaps in the skin's barrier function and can potentially allow transdermal virus infection. Further research is needed to determine the risk of skin damage from face masks.
Research at Kobe University reveals that protein secretions by skin cells, keratinocytes, regulate the differentiation of subsurface skin fat cells into white or brown adipose tissue. The study found that suppressing growth factor proteins BMP2 and FGF21 can decrease white fat cell numbers and increase brown fat cells.
Researchers at Duke-NUS Medical School and Singapore General Hospital develop a fully human system to cultivate skin cells for grafting, eliminating the need for animal-derived products. This breakthrough method uses specific laminin proteins to support the growth of human keratinocytes in the laboratory.
Researchers identified ginsenoside Rb1 as a potential therapeutic approach to enhance keratinocyte migration in wound healing. The study found that Rb1 increases the production of sphingosine-1-phosphate, a signaling factor that stimulates wound repair through greater keratinocyte migration.
Researchers develop novel cell culture strategy to investigate early stages of HPV infection, revealing key genetic information about viral life cycle. The approach enables high infection rates in keratinocytes, allowing for the study of HPV's role in cancer development.
A Kyoto University team has demystified the process of melanin transport to epidermis using video cameras and chicken tissue. Melanin pigments protect skin from DNA damage by surrounding keratinocyte nuclei, a discovery that could lead to effective dermatological treatments.
New research clarifies why wounds heal more slowly with age by examining molecular changes in aging mouse skin. The results show that disruptions in communication between skin cells and immune cells slow down the healing process.
Necroptosis is a crucial physiological process that regulates cell death and tissue function. Researchers have now found that RIPK1 inhibits another inducer of necroptosis, ZBP1, which triggers inflammation when mutated. This study provides new insights into the regulation of necroptosis and its role in chronic inflammatory diseases.
Researchers found that IL-17A stimulates skin cells to express genes maintaining an inflammatory microenvironment, leading to psoriasis. The study identified NFKBIZ gene as playing a significant role in the IL-17A pathway.
A study found that FOXO1, a protein promoting tissue repair, acts as an inhibitor of wound healing in diabetes patients. High glucose levels slow keratinocyte migration, while insulin speeds up the process. The research suggests inhibiting FOXO1 could speed healing in diabetic patients.
Researchers at Penn Dental Medicine have identified Foxo1 as a critical molecule that impairs wound healing in diabetics. The study found that deleting Foxo1 in keratinocytes improved wound healing in diabetic mice, suggesting a potential target for therapies to boost healing.
Researchers at CNIO have identified a key regulator of keratinocyte differentiation, Fra-2, which plays a crucial role in the formation of human skin. The study reveals that activation of Fra-2 induces premature differentiation and may hold promise for treating skin diseases.
Researchers found that aspirin inhibits wound healing by reducing the production of 12-HHT, a molecule promoting epithelial layer restoration. A synthetic BLT2 agonist accelerated wound healing in diabetic mice, suggesting potential treatments for chronic wounds.
A team of researchers has developed the first lab-grown epidermis with a functional permeability barrier, enabling the testing of drugs and cosmetics without animal subjects. The new epidermis, grown from human pluripotent stem cells, can be scaled up for commercial use and tailored to study specific skin conditions.
Researchers at Scripps Research Institute discovered a critical role of dendritic epidermal T cells in producing interleukin-17A to promote wound healing. The study found that these skin-resident immune cells function as 'first responders' to skin injuries by producing IL-17A, which wards off infection and promotes wound healing.
Researchers found that UVB exposure activates keratinocyte hyaluronan synthesis through Has3 enzyme, indicating a potential adaptation mechanism to radiation damage. This activation may also be targeted for regulation in tissue malignancy and pre-cancerous alterations.
A new study published in Immunity reveals that preventing necroptosis in keratinocytes is crucial for preventing skin inflammation. The research found that sensitization of keratinocytes to RIP3-mediated cell death triggers skin inflammation, which could be linked to various chronic or acute skin conditions.
Researchers developed a method to generate patient-specific heart cells from hair follicles, enabling disease modeling and drug screening. This approach offers an alternative to existing methods using skin fibroblasts or bone marrow cells, which require surgical intervention.
Researchers have discovered a surprising molecular pathway in skin cells that produces nitric oxide, a versatile signaling molecule involved in wound-healing and temperature-sensation. This alternative process could lead to better drugs for treating wounds.
A new study reveals that certain types of chronic pain may be caused by signals from the skin itself, rather than damage to nerves within the skin. Skin cells generate increased amounts of a lesser-known 'beta' isoform of CGRP, which may be sending pain signals to remaining sensory nerve fibers in the skin.
A Japanese research group discovered that TRPV4 ion channel plays a crucial role in maintaining the skin's barrier function by regulating cell-cell junctions. Removal of TRPV4 from keratinocytes led to leaky junctions and weak skin barriers, highlighting its importance in preventing dehydration.
Researchers have successfully generated human epidermis from human embryonic stem cells, providing a potential unlimited resource for temporary skin replacement in patients with large burns. The skin substitute was shown to be functional and structurally consistent with human skin after just 12 weeks of grafting onto mice.
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 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.
Researchers found that keratinocytes can control melanocyte pigmentation by producing chemical signals, leading to new possibilities for bioengineered skin grafts and cosmetics. This discovery has significant implications for individuals with medical conditions requiring skin transplants or pigment diseases.
A study published in The FASEB Journal has identified specific physiological properties that regulate melanocyte function, offering hope for new treatments of pigmentation disorders. Keratinocytes are found to influence pigment production and help regulate skin coloration.
A study published in JCI Journals reveals that vitamin D3 production is induced by skin wounds, leading to increased expression of antimicrobial peptides and microbial recognition receptors. This mechanism helps protect the skin from harmful microbes and enhances immune response.