Serial passaging has a profound effect on primary cells. Since serially passaged cells show signs of cellular aging, serial passaging is used as an in vitro model of aging. To relate the effect of in vitro aging more to in vivo aging, we generated human skin equivalents (HSEs). We investigated if HSEs generated with late passage fibroblasts show characteristics of aged skin when compared with HSEs generated with early passage fibroblasts. Late passage fibroblasts had enlarged cell bodies and were more often positive for myofibroblast marker α-smooth muscle actin, senescence associated β-galactosidase and p16 compared with early passage fibroblasts. Skin equivalents generated with late passage fibroblasts had a thinner dermis, which could partly be explained by increased matrix metalloproteinase-1 secretion. In equivalents generated with late passage fibroblasts epidermal expression of keratin 6 was increased, and of keratin 10 slightly decreased. However, epidermal proliferation, epidermal thickness and basement membrane formation were not affected. In conclusion, compared with HSEs generated with early passage fibroblasts, HSEs generated with late passage fibroblasts showed changes in the dermis, but no or minimal changes in the basement membrane and the epidermis.
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http://dx.doi.org/10.1007/s10522-013-9416-9 | DOI Listing |
Matrix Biol
January 2025
Division of Rheumatology/Department of Medicine, Medical University of South Carolina, Charleston, SC 29425. Electronic address:
The role of cells of the hematopoietic lineage in fibrosis is controversial. Here we evaluate the contribution of Col I+/CD45+ cells (fibrocytes) to lung fibrosis. Systemic bleomycin treatment was used to induce fibrosis in a bone marrow transplant and two transgenic mouse models.
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December 2024
Department of Neurology, O'Donnell Brain Institute, University of Texas Southwestern Medical Center, 6000 Harry Hines Boulevard, Dallas, TX 75390, USA.
Friedreich's ataxia (FRDA) is a multisystem, autosomal recessive disorder caused by mutations in the frataxin () gene. As FRDA is considered an FXN deficiency disorder, numerous therapeutic approaches in development or clinical trials aim to supplement FXN or restore endogenous expression. These include gene therapy, protein supplementation, genome editing or upregulation of transcription.
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December 2024
Department of Orthopedic Surgery, E-Da Hospital, I-Shou University, Kaohsiung City 824, Taiwan.
Olfactory ensheathing cell (OEC) transplantation demonstrates promising therapeutic results in neurological disorders, such as spinal cord injury. The emerging cell-free secretome therapy compensates for the limitations of cell transplantation, such as low cell survival rates. However, the therapeutic benefits of the human OEC secretome remain unclear.
View Article and Find Full Text PDFExp Ther Med
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Department of General Surgical Science, Division of Hepatobiliary and Pancreatic Surgery, Gunma University Graduate School of Medicine, Maebashi, Gunma 371-8511, Japan.
The present study aimed to investigate the role of a recombinant protein based on human collagen type I (RCPhC1) as a scaffold in maintaining the human tumor microenvironment within a patient-derived tumor xenograft (PDTX) model. RCPhC1, synthesized under animal component-free conditions, was explored for its potential to support the human-specific stroma associated with tumor growth. PDTX models were established using resected colorectal cancer liver metastasis specimens, and stromal cell populations from humans and mice were compared using three scaffolds: No scaffold (control), Matrigel and recombinant human collagen type I, across two passages.
View Article and Find Full Text PDFInt J Mol Sci
December 2024
Biomedical Engineering Program, Maroun Semaan Faculty of Engineering and Architecture, American University of Beirut, Beirut 1107 2020, Lebanon.
The limited self-repair capacity of cartilage due to its avascular and aneural nature leads to minimal regenerative ability. Autologous chondrocyte transplantation (ACT) is a popular treatment for cartilage defects but faces challenges due to chondrocyte dedifferentiation in later passages, which results in undesirable fibroblastic phenotypes. A promising treatment for cartilage injuries and diseases involves tissue engineering using cells (e.
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