Literature DB >> 11896992

Detection of apoptosis in keloids and a comparative study on apoptosis between keloids, hypertrophic scars, normal healed flat scars, and dermatofibroma.

Y Akasaka1, K Fujita, Y Ishikawa, N Asuwa, K Inuzuka, M Ishihara, M Ito, T Masuda, Y Akishima, L Zhang, K Ito, T Ishii.   

Abstract

Recent studies have suggested that the regulation of apoptosis during wound healing is important in scar establishment and the development of pathological scarring. In this study, we demonstrate that keloid fibroblasts can be identified as apoptotic cells because of their highly condensed chromatin and discrete nuclear fragments. To further reveal the phenomenon of apoptosis, we quantified the number of terminal deoxynucleotide transferase-mediated dUTP nick-end labeling (TUNEL)-positive cells in surgically resected tissues of keloids (N = 10), hypertrophic scars (N = 10), normal healed flat scars (N = 10), and dermatofibroma (N = 10). The number of TUNEL-positive cells was relatively low, but was significantly higher for the keloid group compared with the normally healed flat scar group (p = 0.004), suggesting reduced cell survival and increased apoptotic cell death in a subpopulation of keloid fibroblasts. Furthermore, the number of TUNEL-positive cells was significantly higher for the keloid group compared with the dermatofibroma group (p = 0.044), suggesting that a subpopulation of keloid fibroblasts may suppress tumorgenicity at a greater rate than dermatofibroma by undergoing cell death. Hypertrophic scars had significantly higher levels of apoptosis than normally healed flat scars (p = 0.033). Therefore, these results suggest that selected fibroblasts in keloids and hypertrophic scars undergo apoptosis, which may play a role in the process of pathological scarring.

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Year:  2001        PMID: 11896992     DOI: 10.1046/j.1524-475x.2001.00501.x

Source DB:  PubMed          Journal:  Wound Repair Regen        ISSN: 1067-1927            Impact factor:   3.617


  14 in total

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2.  Lack of CXC chemokine receptor 3 signaling leads to hypertrophic and hypercellular scarring.

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3.  The role of the TGF-β family in wound healing, burns and scarring: a review.

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4.  Dermal fibroblast phagocytosis of apoptotic cells: A novel pathway for wound resolution.

Authors:  Bruna Romana-Souza; Lin Chen; Trevor R Leonardo; Zhenlong Chen; Luisa A DiPietro
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5.  Effects of hepatocyte growth factor on collagen synthesis and matrix metalloproteinase production in keloids.

Authors:  Won Jai Lee; Sang Eun Park; Dong Kyun Rah
Journal:  J Korean Med Sci       Date:  2011-07-27       Impact factor: 2.153

6.  BMP‑7 suppresses excessive scar formation by activating the BMP‑7/Smad1/5/8 signaling pathway.

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Review 8.  Understanding Keloid Pathobiology From a Quasi-Neoplastic Perspective: Less of a Scar and More of a Chronic Inflammatory Disease With Cancer-Like Tendencies.

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Journal:  Front Immunol       Date:  2019-08-07       Impact factor: 7.561

Review 9.  The Keloid Disorder: Heterogeneity, Histopathology, Mechanisms and Models.

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Journal:  Front Cell Dev Biol       Date:  2020-05-26

10.  RNA-seq-based analysis of the hypertrophic scarring with and without pressure therapy in a Bama minipig model.

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Journal:  Sci Rep       Date:  2018-08-07       Impact factor: 4.379

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