Altered <scp>TGF</scp>‐β signaling in fetal fibroblasts: What is known about the underlying mechanisms?

Walraven, Maudy; Gouverneur, Mirella; Middelkoop, Esther; Beelen, R.H.J.; Ulrich, Magda M. W.

doi:10.1111/wrr.12098

Cited by 48 publications

(46 citation statements)

References 100 publications

(298 reference statements)

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“…Second, we hypothesized recently that caveolin-mediated receptor endocytosis, leading to receptor degradation, might play a role in scarless fetal wound healing [7]. Our data showed that there are significant differences in gene expression and protein levels of two markers of the receptor endocytosis pathways.…”

Section: Discussionmentioning

confidence: 78%

“…The role of TGF-β in scarless fetal healing has been a topic of investigation for decades, and it is often assumed that fetal skin has short-lived or inhibited TGF-β signaling [7]. The purpose of the present study was to evaluate the components of the canonical TGF-β pathway in healthy human fetal and adult skin.…”

Section: Discussionmentioning

confidence: 99%

“…Besides TGF-βRI and -βRII, another receptor, TGF-βRIII, is identified, but its function in wound healing and fibrosis still remains unknown. M a n u s c r i p t 4 We recently described the potential role that the different components of the TGF-β pathway might play in fetal scarless wound healing in a review article [7]. In contrast to the extensive studies on the TGF-β isoforms in the fetal skin, only little information is available about the other components of the canonical TGF-β pathway such as the TGF-βRs or the intracellular Smads.…”

Section: Introductionmentioning

confidence: 98%

See 2 more Smart Citations

Transforming growth factor-β (TGF-β) signaling in healthy human fetal skin: A descriptive study

Walraven

Beelen

Ulrich

2015

Journal of Dermatological Science

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Section: Discussionmentioning

confidence: 78%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 98%

See 1 more Smart Citation

Transforming growth factor-β (TGF-β) signaling in healthy human fetal skin: A descriptive study

Walraven

Beelen

Ulrich

2015

Journal of Dermatological Science

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“…In humans, however, scarring occurs earlier in fetal wound repair [64]. This might be due to the specific response of fetal fibroblasts to the pro-fibrotic mediator TGF-β [65]. …”

Section: Remodeling In Skin Wound Healing and Scarringmentioning

confidence: 99%

Skin Wound Healing: An Update on the Current Knowledge and Concepts

Sorg

Tilkorn²,

Hager³

et al. 2016

Eur Surg Res

829

691

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Background: The integrity of healthy skin plays a crucial role in maintaining physiological homeostasis of the human body. The skin is the largest organ system of the body. As such, it plays pivotal roles in the protection against mechanical forces and infections, fluid imbalance, and thermal dysregulation. At the same time, it allows for flexibility to enable joint function in some areas of the body and more rigid fixation to hinder shifting of the palm or foot sole. Many instances lead to inadequate wound healing which necessitates medical intervention. Chronic conditions such as diabetes mellitus or peripheral vascular disease can lead to impaired wound healing. Acute trauma such as degloving or large-scale thermal injuries are followed by a loss of skin organ function rendering the organism vulnerable to infections, thermal dysregulation, and fluid loss. Methods: For this update article, we have reviewed the actual literature on skin wound healing purposes focusing on the main phases of wound healing, i.e., inflammation, proliferation, epithelialization, angiogenesis, remodeling, and scarring. Results: The reader will get briefed on new insights and up-to-date concepts in skin wound healing. The macrophage as a key player in the inflammatory phase will be highlighted. During the epithelialization process, we will present the different concepts of how the wound will get closed, e.g., leapfrogging, lamellipodial crawling, shuffling, and the stem cell niche. The neovascularization represents an essential component in wound healing due to its fundamental impact from the very beginning after skin injury until the end of the wound remodeling. Here, the distinct pattern of the neovascularization process and the special new functions of the pericyte will be underscored. At the end, this update will present 3 topics of high interest in skin wound healing issues, dealing with scarring, tissue engineering, and plasma application. Conclusion: Although wound healing mechanisms and specific cell functions in wound repair have been delineated in part, many underlying pathophysiological processes are still unknown. The purpose of the following update on skin wound healing is to focus on the different phases and to brief the reader on the current knowledge and new insights. Skin wound healing is a complex process, which is dependent on many cell types and mediators interacting in a highly sophisticated temporal sequence. Although some interactions during the healing process are crucial, redundancy is high and other cells or mediators can adopt functions or signaling without major complications.

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“…TGF-β1 stimulates the proliferation of fibroblasts and the production of collagen, and inhibits matrix degradation, finally leading to the formation of hypertrophic scars (10). Inhibition of the TGF-β1/Smads signaling pathway was reported to suppress the formation of hypertrophic scars (11). TGF-β is a cytokine that activates the intracellular Smad signaling pathway and has a key role in promoting wound healing and tissue remodeling after repair (10).…”

Section: Introductionmentioning

confidence: 99%

Mast cell chymase promotes hypertrophic scar fibroblast proliferation and collagen synthesis by activating TGF‑β1/Smads signaling pathway

Chen

Yang

et al. 2017

Exp Ther Med

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Abstract. The present study assessed the existence of mast cell chymase in hypertrophic scars and determined whether chymase promotes fibrosis via the transforming growth factor (TGF)-β1/Smads signaling pathway. Five patients with hypertrophic scars and another five patients subjected to repair and reconstruction of other tissue defects were included in the present study. To detect the existence of mast cells and mast cell chymase in hypertrophic scars, immunohistochemistry was employed. To test the effect of chymase on TGF-β1, angiotensin, and type I and III collagen mRNA expression in isolated hypertrophic scar fibroblasts in vitro, reverse-transcription quantitative PCR was performed. To investigate how chymase affects TGF-β1, phosphorylated (P)-Smad2/3 as well as Smad4 and Smad7 protein expression, western blot analysis was used. Mast cell chymase was identified to promote the mRNA expression of TGF-β1, angiotensin, and type I and III collagen in hypertrophic scar fibroblasts in a time-and dose-dependent manner. Furthermore, treatment with 60 ng/ml mast cell chymase for 12 h led to the upregulation of TGF-β1, P-Smad2/3, Smad4 and Smad7 in hypertrophic scar fibroblasts. The present study demonstrated that mast cells and chymase are present in hypertrophic scars, and chymase promotes hypertrophic scar fibroblast proliferation and collagen synthesis by activating the TGF-β1/Smads signaling pathway.

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Altered TGF‐β signaling in fetal fibroblasts: What is known about the underlying mechanisms?

Cited by 48 publications

References 100 publications

Transforming growth factor-β (TGF-β) signaling in healthy human fetal skin: A descriptive study

Transforming growth factor-β (TGF-β) signaling in healthy human fetal skin: A descriptive study

Skin Wound Healing: An Update on the Current Knowledge and Concepts

Mast cell chymase promotes hypertrophic scar fibroblast proliferation and collagen synthesis by activating TGF‑β1/Smads signaling pathway

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