High in situ mRNA levels of IL-22, TFG-β, and ARG-1 in keloid scars

Tiveron, Luciana Rodrigues da Cunha Colombo; Silva, Isabela Rios da; Silva, Marcos; Peixoto, Alberto Borges; Rodrigues, Denise Bertulucci Rocha; Rodrigues, Virmondés

doi:10.1016/j.imbio.2018.08.010

Cited by 13 publications

(9 citation statements)

References 44 publications

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“…Similarly, Lymphoid tissue inducer (LTi) is known to be a source of IL-22 in fetal lymph nodes and spleen for its regenerative functions (143). Higher levels of IL-22 in keloid scars have also been observed, however, its exact role whether as healing or pathological factor is still needed to be explored (144).…”

Section: Wound Healing and Tissue Regenerationmentioning

confidence: 99%

A Double Edged Sword Role of Interleukin-22 in Wound Healing and Tissue Regeneration

et al. 2020

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Wound healing and tissue regeneration is an intricate biological process that involves repair of cellular damage and maintenance of tissue integrity. Cascades involved in wound healing and tissue regeneration highly overlap with cancer causing pathways. Usually, subsequent tissue damage events include release of a number of cytokines to accomplish post-trauma restoration. IL-22 is one of the cytokines that are immediately produced to initiate immune response against several tissue impairments. IL-22 is a fundamental mediator in inflammation, mucous production, protective role against pathogens, wound healing, and tissue regeneration. However, accumulating evidence suggests pivotal role of IL-22 in instigation of various cancers due to its pro-inflammatory and tissue repairing activity. In this review, we summarize how healing effects of IL-22, when executed in an uncontrollable fashion can lead to carcinogenesis.

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Section: Wound Healing and Tissue Regenerationmentioning

confidence: 99%

A Double Edged Sword Role of Interleukin-22 in Wound Healing and Tissue Regeneration

et al. 2020

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“…Thus, we confirmed that knockdown of hsa_circ_0002198 could inhibit the secretion of large amounts of ECM in keloid fibroblasts. In addition, a keloid scar is currently considered to be a chronic inflammatory process rather than a benign skin tumor, which is also defined as a highly inflamed, hyperproliferative pathological scar (Da Cunha Colombo Tiveron et al, 2018). In this study, knockdown of hsa_circ_0002198 decreased the levels of pro-inflammatory cytokines (IL-1ß and IL-33), suggesting that hsa_circ_0002198 silencing attenuates the chronic inflammatory process associated with keloid inflammatory etiopathogenesis.…”

Section: Discussionmentioning

confidence: 64%

Downregulation of hsa_circ_0002198 inhibits keloid fibroblast activities in vitro by reducing NLRP3 inflammasome activity

Fu¹,

Jingwen²,

CHEN³

et al. 2022

Biocell

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The levels of hsa circular RNA_0002198 (hsa_circ_0002198) have been found to be significantly upregulated in keloid dermal fibroblasts. However, the functional role of hsa_circ_0002198 in keloid fibroblasts and the underlying molecular mechanism for its effects have not been reported. In this study, the levels of hsa_circ_0002198 and nucleotide-binding and oligomerization domain, leucine rich repeat and pyrin domain containing 3 (NLRP3) expression in keloid scar tissues and adjacent normal skin tissues were determined by quantitative real-time PCR and western blotting, respectively. In vitro models of keloid tissue were created by culturing primary keloid fibroblasts obtained from patients. A series of functional experiments, including CCK-8 assays, Transwell assays, and ELISA assays were performed to analyze the functional role of hsa_circ_0002198/NLRP3. Our data showed that hsa_circ_0002198 and NLRP3 were upregulated in keloid scar tissues when compared with adjacent normal tissues.Knockdown of hsa_circ_0002198 expression significantly suppressed cell proliferation, migration, and invasion, and those effects could be partially reversed by forced NLRP3 overexpression in keloid fibroblasts. At the molecular level, knockdown of hsa_circ_0002198 downregulated the levels of Col I, α-SMA, and NLRP3 proteins, as well as the levels of TGF-β, IL-1ß, and IL-33, but upregulated caspase 3 expression in keloid fibroblasts. All those effects were partially reversed after NLRP3 overexpression. In conclusion, our results suggest hsa_circ_0002198 as a potential target for treating keloid lesions.

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“…In fibroblasts, IL-22 signal was activated and then guided the expression of extracellular matrix genes and differentiation of myofibroblasts. Significantly increased expression of TGF-β, IL-22 and Arg-1 in keloid was found as compared to normal scar tissue (da Cunha Colombo Tiveron et al, 2018).…”

Section: Il-22mentioning

confidence: 84%

“…Recently, researchers have also found other interleukins in scar, such as IL-22, which was activated in KFs, involved in EMC synthesis and myofibroblast transformation (da Cunha Colombo Tiveron et al, 2018). Additionally, the serum level of IL-37 was negatively correlated with the severity of keloid lesions, and IL-36, which had not been previously concerned in scars, was also mentioned (Zhao et al, 2020).…”

Section: Discussionmentioning

confidence: 99%

Therapeutic Strategies by Regulating Interleukin Family to Suppress Inflammation in Hypertrophic Scar and Keloid

Zhang

Zhao

2021

Front. Pharmacol.

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Hypertrophic scar (HS) and keloid are fibroproliferative disorders (FPDs) of the skin due to aberrant wound healing, which cause disfigured appearance, discomfort, dysfunction, psychological stress, and patient frustration. The unclear pathogenesis behind HS and keloid is partially responsible for the clinical treatment stagnancy. However, there are now increasing evidences suggesting that inflammation is the initiator of HS and keloid formation. Interleukins are known to participate in inflammatory and immune responses, and play a critical role in wound healing and scar formation. In this review, we summarize the function of related interleukins, and focus on their potentials as the therapeutic target for the treatment of HS and keloid.

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High in situ mRNA levels of IL-22, TFG-β, and ARG-1 in keloid scars

Cited by 13 publications

References 44 publications

A Double Edged Sword Role of Interleukin-22 in Wound Healing and Tissue Regeneration

A Double Edged Sword Role of Interleukin-22 in Wound Healing and Tissue Regeneration

Downregulation of hsa_circ_0002198 inhibits keloid fibroblast activities in vitro by reducing NLRP3 inflammasome activity

Therapeutic Strategies by Regulating Interleukin Family to Suppress Inflammation in Hypertrophic Scar and Keloid

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