Bone marrow derived mesenchymal stem cells inhibit the proliferative and profibrotic phenotype of hypertrophic scar fibroblasts and keloid fibroblasts through paracrine signaling

Fang, Fengjun; Huang, Ru‐Lin; Zheng, Yongchao; Liu, Ming; Huo, Ran

doi:10.1016/j.jdermsci.2016.03.003

Cited by 68 publications

(56 citation statements)

References 35 publications

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“…One previous study reported that the expression of type I and III collagen was found to be significantly higher in HS tissues and HSFs than in NS tissues and NSFs [22]. In humans, imbalanced cell proliferation of HSFs would cause hypertrophic scar formation [21]. Our study found for the first time that the long non-coding RNA lncRNA8975-1 inhibited cell proliferation as well as collagen and α-SMA expression in hypertrophic scar fibroblasts.…”

Section: Discussionsupporting

confidence: 49%

“…Therefore, even lncRNA8975-1 inhibits α-SMA or collagen expression, other fibrotic factors such as connective tissue growth factors, Th2 cytokines and insulin-like growth factor-1 (IGF-1) could increase collagen synthesis and α-SMA expression [1] bypass the role of lncRNA8975-1. Excess deposition of extracellular matrix proteins particularly type I collagen (which consists of a1 (I) and a2 (I) collagen) and type III collagen by fibroblasts is responsible for hypertrophic scar formation [21]. One previous study reported that the expression of type I and III collagen was found to be significantly higher in HS tissues and HSFs than in NS tissues and NSFs [22].…”

Section: Discussionmentioning

confidence: 99%

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The Long Non-Coding RNA LncRNA8975-1 is Upregulated in Hypertrophic Scar Fibroblasts and Controls Collagen Expression

Chen

Cao

et al. 2016

Cell Physiol Biochem

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Background/Aims: Long non-coding RNAs (lncRNAs) are thought to play crucial roles in human diseases. However, the function of lncRNAs in hypertrophic scar formation remains poorly understood. Methods: In this study, we investigated the expression of lncRNA8975-1 in hypertrophic scar tissues and fibroblasts by quantitative reverse transcription PCR (qRT-PCR). To investigate its function, overexpression and knockdown of lncRNA8975-1 were performed using lentivirus infection and Stealth RNAi transfection, respectively. Cell proliferation was detected by CCK-8 assay. The protein levels of collagens and alpha-smooth muscle actin (α-SMA) were analysed by western blot. Results: We found that lncRNA8975-1 was overexpressed in hypertrophic scar tissues and dermal fibroblasts. Overexpression of lncRNA8975-1 inhibited cell proliferation and reduced the protein expression levels of COL1A2, COL1A1, COL3A1 and α-SMA in hypertrophic scar fibroblasts, whereas knockdown of lncRNA8975-1 had the opposite effect. Conclusion: Our results show that the long non-coding RNA lncRNA8975-1 is upregulated in hypertrophic scar fibroblasts; furthermore, it inhibits fibroblast proliferation and reduces collagen and α-SMA expression. Further studies on the mechanisms regulated by lncRNA8975-1 would lead to a better understanding of the pathogenesis of hypertrophic scar formation.

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Section: Discussionsupporting

confidence: 49%

Section: Discussionmentioning

confidence: 99%

The Long Non-Coding RNA LncRNA8975-1 is Upregulated in Hypertrophic Scar Fibroblasts and Controls Collagen Expression

Chen

Cao

et al. 2016

Cell Physiol Biochem

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“…Second, MSC can act on myofibroblasts, the main effector cells in HS formation. It was proved that bone marrow‐derived MSCs inhibit myofibroblasts proliferation, migration, ECM synthesis, and scar formation through paracrine signalling . Moreover, not only stem cells themselves, the conditioned medium of MSCs and exosomes can be used as the treatment of anti‐scarring.…”

Section: Conclusion and Prospectmentioning

confidence: 99%

“…It was proved that bone marrow-derived MSCs inhibit myofibroblasts proliferation, migration, ECM synthesis, and scar formation through paracrine signalling. 199 Moreover, not only stem cells themselves, the conditioned medium of MSCs and exosomes can be used as the treatment of anti-scarring. The exosomes secreted by human adipose mesenchymal stem cells could benefit wound healing and promote scarless cutaneous repair by regulating ECM remodelling.…”

Section: Conclusion and Prospectmentioning

confidence: 99%

Biological approaches for hypertrophic scars

Zhong

2019

International Wound Journal

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Scar formation is usually the pathological consequence of skin trauma. And hypertrophic scars (HSs) frequently occur in people after being injured deeply. HSs are unusually considered as the result of tissue contraction and excessive extracellular matrix component deposition. Myofibroblasts, as the effector cells, mainly differentiated from fibroblasts, play the crucial role in the pathophysiology of HSs. A number of growth factors, inflammatory cytokines involved in the process of HS occurrence. Currently, with in‐depth exploration and clinical research of HSs, various creative and effective treatments budded. In here, we summarize the progress in the molecular mechanism of HSs, and review the available biotherapeutic methods for their pathophysiological characteristics. Additionally, we further prospected that the comprehensive therapy may be more suitable for HS treatment.

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“…The second co‐culture model would be the culturing of both effector cells and cells of interest in a plate with inserts. Both methods have been utilized in further understanding keloid pathobiology …”

Section: Two‐dimensional Modelsmentioning

confidence: 99%

Multi‐dimensional models for functional testing of keloid scars: In silico, in vitro, organoid, organotypic, ex vivo organ culture, and in vivo models

Lebeko

Khumalo

2019

Wound Repair Regeneration

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Keloid scars are described as benign fibro‐proliferative dermal outgrowths that commonly occur in pigmented skin post cutaneous injury, and continue to grow beyond the boundary of the original wound margin. There is a lack of thorough understanding of keloid pathogenesis and thus keloid therapeutic options remain ill‐defined. In view of the poor response to current therapy and high recurrence rates, there is an unmet need in improving our knowledge and therefore in identifying targeted and effective treatment strategies in management of keloids. Keloid research however, is hampered by a lack of relevant animal models as keloids do not spontaneously occur in animals and are unique to human skin. Therefore, developing novel animal models and nonanimal models for functional evaluation of keloid cells and tissue for better understanding their pathobiology and response to putative candidate therapies are essential. Here, we present the key concepts and relevant emerging research on two‐dimensional and three‐dimensional cell and tissue models for functional testing of keloid scars. We will describe in detail current models including in vitro mono‐ and co‐cultures, multi‐cellular spheroids (organoids) and organotyopic cultures, ex vivo whole skin keloid tissue organ culture models as well as in vivo human patient models. Finally, we discuss the role played by time as the fourth dimension in a novel model that involves sequential temporal biopsies of human patients with keloids (a so called 4D in vivo human model). The use of these unique models will no doubt prove pivotal in identification of new drug targets as well as biomarkers, in functional testing of emerging novel therapeutics, and in enhancing our understanding of keloid disease biology.

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Bone marrow derived mesenchymal stem cells inhibit the proliferative and profibrotic phenotype of hypertrophic scar fibroblasts and keloid fibroblasts through paracrine signaling

Cited by 68 publications

References 35 publications

The Long Non-Coding RNA LncRNA8975-1 is Upregulated in Hypertrophic Scar Fibroblasts and Controls Collagen Expression

The Long Non-Coding RNA LncRNA8975-1 is Upregulated in Hypertrophic Scar Fibroblasts and Controls Collagen Expression

Biological approaches for hypertrophic scars

Multi‐dimensional models for functional testing of keloid scars: In silico, in vitro, organoid, organotypic, ex vivo organ culture, and in vivo models

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