Keloid scars are abnormal benign fibroproliferative tumors with high recurrence rates and no current efficacious treatment. Accumulating evidence suggests that human umbilical cord Wharton's jelly-derived mesenchymal stem cells (WJ-MSCs) have antifibrotic properties. Paracrine signaling is considered one of the main underlying mechanisms behind the therapeutic effects of mesenchymal stem cells. However, the paracrine signaling effects of WJ-MSCs on keloids have not yet been reported. The aim of this study is to investigate paracrine signaling effects of human WJ-MSCs on keloid fibroblasts in vitro. Human umbilical cords and keloid skin samples were obtained, and WJ-MSCs and keloid fibroblasts were isolated and cultured. One-way and two-way paracrine culture systems between both cell types were investigated. Plasminogen activator inhibitor-I and transforming growth factor-β2 (TGF-β2) transcripts were upregulated in keloid fibroblasts cultured with WJ-MSC-conditioned medium (WJ-MSC-CM) and cocultured with inserts, while showing lower TGF-β3 gene expression. Interleukin (IL)-6, IL-8, TGF-β1, and TGF-β2 protein expression was also enhanced. The WJ-MSC-CM-treated keloid fibroblasts showed higher proliferation rates than their control keloid fibroblasts with no significant change in apoptosis rate or migration ability. In our culture conditions, the indirect application of WJ-MSCs on keloid fibroblasts may enhance their profibrotic phenotype.
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http://dx.doi.org/10.5966/sctm.2013-0120 | DOI Listing |
J Control Release
January 2025
Department of Plastic and Cosmetic Surgery, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430074, China. Electronic address:
Keloids are pathological scars characterized by excessive fibroblast proliferation, abnormal collagen deposition, and chronic inflammation, which often result in high recurrence rates and limited treatment success. Targeting BACH1 with gene therapy has shown promise in regulating fibroblast activity and reducing inflammation. However, effective delivery systems for targeted gene therapy in keloids remain a major challenge.
View Article and Find Full Text PDFClin Cosmet Investig Dermatol
December 2024
Plastic Surgery Department, The Second Affiliated Hospital of Harbin Medical University, Harbin, Peoples Republic of China'.
Background: Recent evidence suggests a crucial biological role for Circular RNAs (circRNAs) in keloid diseases, yet the underlying mechanisms remain unclear. This study explored the biological effects and molecular mechanisms of hsa_circ_0002198 in keloid formation.
Methods: Real-time quantitative PCR (qRT-PCR) was employed to assess the expression of circ_0002198 in keloid tissues, normal skin tissues, keloid fibroblasts (KFs), and normal skin fibroblasts (NFs) from nine patients.
Exp Cell Res
January 2025
Department of Plastic Surgery, The First Affiliated Hospital of Anhui Medical University, Anhui, 230032, China. Electronic address:
Keloids are disfiguring proliferative scars, and their pathological mechanisms are still unclear. We have previously established that FoxC1 plays a significant role in rheumatoid arthritis and osteoarthritis, but its molecular mechanisms in pathological scar formation remain elusive. In this study, we analyzed keloid tissue characteristics using HE staining and immunohistochemistry, revealing abnormal expression of FoxC1 and Notch3 in keloids.
View Article and Find Full Text PDFCommun Biol
December 2024
Department of Plastic and Reconstructive Surgery, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Keloid is a dermatofibrotic disease known for its aggressive nature and characterized by pathological scarring, which often leads to disfigurement and frequent recurrences. Effective therapies for keloids are still limited, presumably due to the inadequate comprehension of their aggressive mechanisms. In our study, we examined the unique scenario where both keloid and non-aggressive pathological scar originate from the same patient, providing a rare opportunity to explore the aggressive mechanisms of keloids through single-cell RNA sequencing.
View Article and Find Full Text PDFInt J Mol Sci
December 2024
Department for Orthopedics and Trauma Surgery, Medical Faculty and University Hospital Düsseldorf, Heinrich Heine University Düsseldorf, 40225 Dusseldorf, Germany.
Wound healing as a result of a skin injury involves a series of dynamic physiological processes, leading to wound closure, re-epithelialization, and the remodeling of the extracellular matrix (ECM). The primary scar formed by the new ECM never fully regains the original tissue's strength or flexibility. Moreover, in some cases, due to dysregulated fibroblast activity, proliferation, and differentiation, the normal scarring can be replaced by pathological fibrotic tissue, leading to hypertrophic scars or keloids.
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