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Filename: controllers/Detail.php
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The protective epithelial barrier in our skin undergoes constant regulation, whereby the balance between differentiation and proliferation of keratinocytes plays a major role. Impaired keratinocyte differentiation and proliferation are key elements in the pathophysiology of several important dermatological diseases, including atopic dermatitis and psoriasis. Ca(2+) influx plays an essential role in this process presumably mediated by different transient receptor potential (TRP) channels. However, investigating their individual role was hampered by the lack of specific stimulators or inhibitors. Because we have recently identified hyperforin as a specific TRPC6 activator, we investigated the contribution of TRPC6 to keratinocyte differentiation and proliferation. Like the endogenous differentiation stimulus high extracellular Ca(2+) concentration ([Ca(2+)](o)), hyperforin triggers differentiation in HaCaT cells and in primary cultures of human keratinocytes by inducing Ca(2+) influx via TRPC6 channels and additional inhibition of proliferation. Knocking down TRPC6 channels prevents the induction of Ca(2+)- and hyperforin-induced differentiation. Importantly, TRPC6 activation is sufficient to induce keratinocyte differentiation similar to the physiological stimulus [Ca(2+)](o). Therefore, TRPC6 activation by hyperforin may represent a new innovative therapeutic strategy in skin disorders characterized by altered keratinocyte differentiation.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2662218 | PMC |
http://dx.doi.org/10.1074/jbc.M801844200 | DOI Listing |
J Oral Biol Craniofac Res
December 2024
Clinical Genetics Lab, Centre for Cellular and Molecular Research, Saveetha Dental College & Hospital, Saveetha Institute of Medical and Technical Sciences [SIMATS], Saveetha University, Chennai, India.
Background: Periodontitis is considered to be one of the major risk factors associated with cancers of the oral cavity. Periodontogenic pathogens such as and are the important pathogens associated with periodontitis. Chronic exposure to bacterial components induces changes in the nearby cells.
View Article and Find Full Text PDFMethods Mol Biol
December 2024
Systems Toxicology Group, FEST Division, CSIR-Indian Institute of Toxicology Research (CSIR-IITR), Lucknow, Uttar Pradesh, India.
Isolation of primary keratinocyte stem cells (KSCs) from neonatal mouse epidermis is essential for studying skin physiology and related disorders. Traditional methods often struggle to balance keratinocyte proliferation and differentiation, and although recent advancements using low-calcium culture conditions have improved these techniques, protocols remain scattered. This study presents a streamlined approach to expand mouse KSCs in low-calcium medium (<0.
View Article and Find Full Text PDFCureus
November 2024
Internal Medicine, Kettering Health Network, Kettering, USA.
Aquagenic syringeal acrokeratoderma (ASA) is a rare dermatological condition characterized by the transient appearance of edematous, white, translucent papules on the palms following water exposure. While the condition is most commonly associated with cystic fibrosis (CF) and predominantly affects young women, this report presents a unique case in a 24-year-old man without a history of cystic fibrosis. The patient reported a 10-month history of painful, pruritic eruptions on the hands following exposure to water.
View Article and Find Full Text PDFBr J Dermatol
December 2024
The Pennsylvania State University College of Medicine, Department of Dermatology, Hershey, PA, USA.
Background: Therapeutic options for mild hidradenitis suppurativa (HS) represent a significant gap in the current treatment landscape, with no FDA approved therapies for early stage HS. Topical JAnus Kinase inhibitors (JAKi) are a compelling option due to the known upregulation of inflammatory JAK signaling in HS lesions and the recent success of systemic JAKi for moderate to severe HS.
Objectives: This is a pilot, single-site, open-label, prospective 24-week clinical trial with topical ruxolitinib (NCT04414514).
J Invest Dermatol
December 2024
Department of Genetics, Yale University School of Medicine, New Haven, CT 06520, USA; Department of Dermatology, Yale University School of Medicine, New Haven, CT 06520, USA; Department of Pathology, Yale University School of Medicine, New Haven, CT 06520, USA. Electronic address:
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