Effect of heat shock protein 47 on collagen accumulation in keloid fibroblast cells

Chen, JJ; Zhao, Sha; Cen, Yunyun; Xx, Liu; Yu, Rong; Dm, Wu

doi:10.1111/j.1365-2133.2007.07898.x

Cited by 37 publications

(22 citation statements)

References 24 publications

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“…The expression of HSP47 is closely correlated with that of collagen in fibrotic disorders . Some experiments, using antisense oligonucleotides against HSP47 and transfection of HSP47‐specific siRNA, revealed that the down‐regulated expression of HSP47 could suppress accumulation of collagen . We also found that HSP47 expression was markedly decreased in resveratrol‐treated keloid fibroblasts, suggesting that it might suppress collagen accumulation.…”

Section: Discussionmentioning

confidence: 98%

Resveratrol inhibits fibrogenesis and induces apoptosis in keloid fibroblasts

Ikeda

Torigoe

Matsumoto

et al. 2013

Wound Repair Regeneration

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Keloids are benign dermal fibrotic tumors arising during the wound healing process. The mechanisms of keloid formation and development still remain unknown, and no effective treatment is available. Resveratrol, a dietary compound, has anticancer properties and, from recent studies, it has been suggested that resveratrol may have an antifibrogenic effect on organs such as the liver and kidney. Based on this idea, we investigated its effect on the regulation of extracellular matrix expression, proliferation, and apoptosis of keloid fibroblasts. Type I collagen, α-smooth muscle actin, and heat shock protein 47 expression decreased in resveratrol-treated keloid fibroblasts in a dose-dependent manner. In addition, resveratrol diminished transforming growth factor-β1 production by keloid fibroblasts. We also demonstrated that it suppressed their proliferation and induced apoptosis of the fibroblasts. Conversely, resveratrol did not decrease type I collagen, α-smooth muscle actin, and heat shock protein 47 mRNA expression in normal skin fibroblasts and barely suppressed cell proliferation. Our data indicate that resveratrol may have an antifibrogenic effect on keloid fibroblasts without any adversely effects on normal skin fibroblasts, suggesting the potential application of resveratrol for the treatment of keloids.

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Section: Discussionmentioning

confidence: 98%

Resveratrol inhibits fibrogenesis and induces apoptosis in keloid fibroblasts

Ikeda

Torigoe

Matsumoto

et al. 2013

Wound Repair Regeneration

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“…Extracellular matrix (ECM) components such as collagen are also affected by heat, which can rupture the stabilizing intramolecular and molecular cross‐links of their fibers . It has been observed that under moderate heat stress most of these structures, both the junctions and the esophageal cancer component, are overexpressed by the mediation of HSP and HSF molecules . These changes take place to protect the tissues and increase tolerance to the heat.…”

Section: Heat Stressmentioning

confidence: 99%

“…45 It has been observed that under moderate heat stress most of these structures, both the junctions and the esophageal cancer component, are overexpressed by the mediation of HSP and HSF molecules. 41,46,47 These changes take place to protect the tissues and increase tolerance to the heat. However, under severe heat shock (up to 56 C) widespread cellular injury and necrotic cell death have been noted.…”

Section: Histological Modificationsmentioning

confidence: 99%

Heat‐induced inflammation and its role in esophageal cancer

Maghsudlu

Yazd

2017

J of Digest Diseases

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Esophageal cancer, the sixth most common cause of death from cancer worldwide, consists of different histological types and displays various patterns of incidence. Esophageal adenocarcinoma and esophageal squamous cell carcinoma are the most prevalent types. As epidemiological studies report that ingesting hot substances is one major risk factor for squamous cell carcinoma, evaluating the effect of this external stress on esophagus cells seems desirable. This specific kind of stress brings about cellular changes and stabilizes them by affecting different cellular features such as genetic stability, membrane integrity and the regulation of signaling pathways. It also causes tissue injury by affecting the extracellular matrix and cell viability. Thus, one of the main consequences of thermal injury is the activation of the immune system, which can result in chronic inflammation. The genetic alteration that has occurred during thermal injury and the consequent reduction in the function of repair systems is further strengthened by chronic inflammation, thereby increasing the probability that mutated cell lines may appear. The molecules that present in this circumstance, such as heat shock proteins, cytokines, chemokines and other inflammatory factors, affect intercellular signaling pathways, including nuclear factor kappa-light-chain-enhancer of activated B cells, signal transducer activator of transcription-3 and hypoxia-inducible factor 1α in supporting the survival and emergence of mutant phenotypes and the consequent malignant progression in altered cell lines. This investigation of these effective factors and their probable role in the tumorigenic path may improve current understanding.

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“…Although numerous investigations have attempted to clarify the mechanism of keloid formation, the aetiology remained unclear . It was generally thought that overexpression of transforming growth factor (TGF)‐β1, platelet‐derived growth factor (PDGF) and heat shock protein 47 (HSP47) may play the important role in keloid formation …”

Section: Introductionmentioning

confidence: 99%