Photoaged skin contains elastotic materials in the upper reticular dermis, a result of a commonly known as solar elastosis. It is known that the primary transcript of elastin undergoes extensive alternative splicing and that this results in the translation of multiple heterogeneous protein isoforms. In this study, we found that UV irradiation and heat treatment increased the levels of elastin transcript containing exon 26A and its encoded elastin isoform in the epidermis of human skin in vivo and in cultured human keratinocytes in vitro. We also found that the elastin transcript containing exon 26A was upregulated in photoaged forearm skin compared with intrinsically aged buttock skin in the same elderly individuals. We observed that topical retinoic acid treatment to human skin did not increase the expression of exon 26A mRNA, but that tropoelastin mRNA expression was increased by this treatment. These findings suggest that the production of the elastin isoform containing exon 26A peptide is increased by UV exposure and heat treatment in human skin in vivo and that it may play an important role in the development of solar elastosis in photoaged human skin.
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http://dx.doi.org/10.1111/j.1600-0625.2008.00799.x | DOI Listing |
Target Oncol
November 2023
Department of Thoracic Oncology, Univ. Lille, CHU Lille, Boulevard du Professeur Leclercq, 59000, Lille, France.
Background: Chemo-immunotherapy (CIT) is the standard of care for advanced non-small cell lung cancer (NSCLC), but the impact of routinely available histo-molecular biomarkers on its efficacy has not yet been fully assessed.
Objective: The purpose of this multicenter study was to evaluate the clinical activity of CIT according to oncogenic drivers, STK11 and TP53 mutations, and MET overexpression.
Patients And Methods: Patients receiving CIT for advanced NSCLC with available comprehensive molecular profile were included.
Commun Biol
December 2021
Structural Genomics Consortium, University of Toronto, Toronto, ON, M5G 1L7, Canada.
Huntington's disease results from expansion of a glutamine-coding CAG tract in the huntingtin (HTT) gene, producing an aberrantly functioning form of HTT. Both wildtype and disease-state HTT form a hetero-dimer with HAP40 of unknown functional relevance. We demonstrate in vivo and in cell models that HTT and HAP40 cellular abundance are coupled.
View Article and Find Full Text PDFClin Chim Acta
December 2021
Tianjin Pediatric Research Institute, Tianjin Children's Hospital (Tianjin University Children's Hospital), No. 238 Longyan Road, Beichen District, Tianjin 300134, China; Tianjin Key Laboratory of Birth Defects for Prevention and Treatment, No. 238 Longyan Road, Beichen District, Tianjin 300134, China; Department of Neurosurgery, Tianjin Children's Hospital (Tianjin University Children's Hospital), No. 238 Longyan Road, Beichen District, Tianjin 300134, China. Electronic address:
Introduction: Primary hypomagnesemia with secondary hypocalcemia (HSH) is a rare autosomal recessive disease caused by biallelic variants in TRPM6 gene.
Methods: In this study, we reported a Chinese patient diagnosed with HSH in Tianjin Children's Hospital. Detailed clinical examination and laboratory test were performed and whole exome sequencing (WES) was applied to detect the pathogenic gene in the proband.
Dermatol Ther (Heidelb)
December 2021
Department of Research and Innovation, Laboratory of Molecular Biology, Grupo Boticário, Rua Alfredo Pinto, 1500, São José dos Pinhais, Paraná, 83065-150, Brazil.
Introduction: Photoaging is the process by which ultraviolet rays gradually induce clinical and histological changes in the skin through the production and organization of biological molecules, such as elastin, which is critical to skin strength and elasticity. After exposure to radiation, elastin may undergo alternative mRNA splicing, resulting in modified proteins that contribute to the formation of aging characteristics, such as solar elastosis. The present work aimed to study two different forms of elastin under these conditions: normal elastin and elastin that had been altered in exon 26A.
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