Background: Fibroblast growth factors (FGFs) are important regulators of cell proliferation, migration, and differentiation during wound healing. FGF-binding protein (FGF-BP) plays a critical role in activating FGFs by releasing them from the extracellular matrix. Although previous studies have demonstrated a pivotal role for FGF-BP in wound healing and angiogenesis, little is known about the biologic effects of FGF-BP on skin stem cells that contribute to wound healing.
Objective: To investigate the effects of FGF-BP on the growth and migration of skin-derived precursors (SKPs).
Methods: FGF-BP was titrated to determine the optimal concentration that maximally stimulated cell proliferation. Cellular phenotype and telomerase activity were compared in the presence and absence of FGF-BP. The effect of FGF-BP on cell migration was observed by intravenously transplanting SKPs to adult mice.
Results: Cell proliferation was maximally stimulated by FGF-BP at a concentration of 10 ng/mL without changing the intrinsic characteristics of SKPs. Low levels of telomerase activity were detected, and FGF-BP decreased the rate at which telomerase activity was downregulated. In vivo, FGF-BP remarkably enhanced the migration of SKPs to skin lesion sites.
Conclusion: FGF-BP exerts a positive effect on the growth and migration of SKPs, suggesting a potential role for SKPs in wound healing.
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http://dx.doi.org/10.2310/7750.2011.10049 | DOI Listing |
Sci Rep
December 2024
Department of Orthopaedic Surgery, Keio University School of Medicine, 35 Shinanomachi, Shinjuku-Ku, Tokyo, 160-8582, Japan.
Chronic complete spinal cord injury (SCI) is difficult to treat because of scar formation and cavitary lesions. While human iPS cell-derived neural stem/progenitor cell (hNS/PC) therapy shows promise, its efficacy is limited without the structural support needed to address cavitary lesions. Our study investigated a combined approach involving surgical scar resection, decellularized extracellular matrix (dECM) hydrogel as a scaffold, and hNS/PC transplantation.
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December 2024
Department of Urology Surgery, The First Affiliation Hospital of China Medical University, Shenyang, 110000, Liaoning, China.
To evaluate the predictive utility of N6-methyladenosine (m6A)-associated long non-coding RNAs (lncRNAs) for the prognosis and immunotherapy response in papillary renal cell carcinoma (pRCC). Transcriptomic data of pRCC samples were extracted from the TCGA database. The m6A-related lncRNAs were identified by Pearson correlation analysis.
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December 2024
Department of Gynaecology, The Affiliated Wuxi People's Hospital of Nanjing Medical University/Wuxi Medical Center, Nanjing Medical University/Wuxi People's Hospital, 299 Qingyang Road, Wuxi, 214023, Jiangsu, China.
Long non-coding RNAs (lncRNAs) have emerged as crucial regulators in cancer progression. We found lncRNA DNM1P35 is elevated in ovarian tumors compared to normal tissues, and demonstrated that lncRNA DNM1P35 promoted cancer cell proliferation, migration and invasion in SK-OV-3 and OVCAR-3 cell lines. Furthermore, lncRNA DNM1P35 also facilitated the epithelial-mesenchymal transition (EMT) of ovarian cancer cells.
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December 2024
Department of Dermatology, Hebei Medical University Third Hospital, 139 Ziqiang Road, Shijiazhuang, 050000, Hebei, China.
To investigate CHD1L's impacts and molecular processes in hypoxic cutaneous squamous cell carcinoma. Monoclonal proliferation assays and CCK-8 were used to detect the proliferation capacity of A431 cells and Colon16 cells; wound healing experiments and Transwell assays were used to examine the migration and invasion capacity of A431 cells and Colon16 cells; angiogenesis experiments were conducted to assess the influence of A431 cells on angiogenesis; a nude mouse tumor xenograft experiment and HE staining were utilized to evaluate the impact of CHD1L on the progression of cutaneous squamous cell carcinoma; western blot analysis was performed to detect the expression of p-PI3K, p-AKT, and PD-L1 in A431 cells, as well as CD9, TSG101, PD-L1 in exosomes, and CD206, Arginase-1, iNOS, IL-1β, p-AKT, p-mTOR, VEGF, COX-2, MMP2, MMP9, p-ERK1/2 in tumor-associated macrophages. Under hypoxic conditions, CHD1L promoted the proliferation, migration, invasion, and angiogenesis of cutaneous squamous cell carcinoma.
View Article and Find Full Text PDFCancer Cell Int
December 2024
Department of Plastic and Aesthetic Surgery, the Second Affiliated Hospital of Harbin Medical University, Harbin, 150086, China.
Background: Cutaneous melanoma is one of the most invasive and lethal skin malignant tumors. Compared to primary melanoma, metastatic melanoma (MM) presents poorer treatment outcomes and a higher mortality rate. The tumor microenvironment (TME) plays a critical role in MM progression and immunotherapy resistance.
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