Phosphorylation of α-CateninS641 Suppresses the NF-κB Pathway in Fibroblasts to Activate Skin Wound Repair

Shen, Yingjie; Zhu, Zhongxin; Cong, Weitao; Jiang, Mengying; Wang, Jianan; Chen, Xixi; Wang, Nan; Yu, Ying; Dong, Yetong; Liu, Zhili; Sun, Jia; Gong, Wenjie; Zhang, Siyi; Kim, Kwonseop; Jin, Litai

doi:10.1016/j.jid.2021.09.037

Cited by 3 publications

(3 citation statements)

References 16 publications

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“…It was reported that the NF-κB/IκB signaling pathway played an important role in wound healing [ 43 ]. Suppression of the NF-κB/p65 pathway in fibroblasts promoted skin wound repair [ 44 ]. Hence, blockade of SENP3 repressed inflammation via the Smad6/IκB/p65 pathway, further implicating SENP3 as a promising therapeutic strategy in wound healing.…”

Section: Discussionmentioning

confidence: 99%

SENP3 deletion promotes M2 macrophage polarization and accelerates wound healing through smad6/IκB/p65 signaling pathway

Ma¹,

Hu²,

Xue³

et al. 2023

Heliyon

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Section: Discussionmentioning

confidence: 99%

SENP3 deletion promotes M2 macrophage polarization and accelerates wound healing through smad6/IκB/p65 signaling pathway

Ma¹,

Hu²,

Xue³

et al. 2023

Heliyon

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“…These findings showed that IL‐1β inhibited IGF‐1 synthesis in DETCs. NF‐κB proteins are one of the key transcription factors in the inflammatory response 13,14 . Our group showed that IL‐1β promoted the intracellular phosphorylation of NF‐κB p65 as well as the translocation of NF‐κB p65 from the cytoplasm to the nucleus 3 .…”

Section: Introductionmentioning

confidence: 93%

“…NF-κB proteins are one of the key transcription factors in the inflammatory response. 13,14 Our group showed that IL-1β promoted the intracellular phosphorylation of NF-κB p65 as well as the translocation of NF-κB p65 from the cytoplasm to the nucleus. 3 The expression of IGF-1 in DETCs was dramatically enhanced when NF-κb signaling was blocked.…”

Section: Introductionmentioning

confidence: 99%

IL-1β/NF-κB signaling inhibits IGF-1 production via let-7f-5p in dendritic epidermal T cells

Wang

et al. 2022

Journal of Leukocyte Biology

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Dendritic epidermal T cells (DETCs) are the main source of insulin‐like growth factor‐1 (IGF‐1) in epidermal tissue, which promote re‐epithelialization and wound healing. In refractory wounds, IL‐1β has been shown to activate NF‐κB and suppress IGF‐1 expression in DETCs. Nevertheless, the underlying mechanisms remain unclear. In this study, chromatin immunoprecipitation analysis revealed that IL‐1β did not inhibit NF‐κB binding to IGF‐1 promoter, indicating that IL‐1β/NF‐κB may suppress IGF‐1 expression by alternative mechanisms. MiRNAs negatively regulate gene expression predominantly by base pairing to the 3′ untranslation region (UTR) of target mRNAs. Let‐7f‐5p, miR‐1a‐3p, and miR‐98‐5p have been identified as IGF‐1‐specific miRNAs that can bind directly to the 3′UTR of IGF‐1 mRNA and dysregulate IGF‐1 mRNA and protein levels. In IL‐1β‐treated epidermis around wounds or DETCs in vitro, NF‐κB promoted the expression of let‐7f‐5p, and IGF‐1 expression was impeded via NF‐κB/let‐7f‐5p pathway. As pre‐let‐7f‐5p, let‐7f‐1 is located in the 3′UTR of LOC118568094, and let‐7f‐2 is located in the intron of HUWE1. We discovered that NF‐κB p65 bound to the promoters of LOC118568094 and HUWE1 to accelerate let‐7f‐5p expression, but NF‐κB p65 did not affect the methylation levels of LOC118568094 and HUWE1 CpG islands. Injections of Let‐7f‐5p antagomir into IL‐1β‐treated and ischemic wound margins restored IGF‐1 secretion in DETCs and promoted wound healing. In conclusion, we demonstrated that NF‐κB signaling pathway activated by IL‐1β could increase let‐7f‐5p expression to inhibit IGF‐1 production in DETCs and delay wound healing. And let‐7f‐5p antagomir utilized in wound margin could effectively promote refractory wound healing.

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IKZF3 modulates cerebral ischemia/reperfusion injury by inhibiting neuroinflammation

Meng

Chen

et al. 2023

International Immunopharmacology

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Phosphorylation of α-CateninS641 Suppresses the NF-κB Pathway in Fibroblasts to Activate Skin Wound Repair

Cited by 3 publications

References 16 publications

SENP3 deletion promotes M2 macrophage polarization and accelerates wound healing through smad6/IκB/p65 signaling pathway

SENP3 deletion promotes M2 macrophage polarization and accelerates wound healing through smad6/IκB/p65 signaling pathway

IL-1β/NF-κB signaling inhibits IGF-1 production via let-7f-5p in dendritic epidermal T cells

IKZF3 modulates cerebral ischemia/reperfusion injury by inhibiting neuroinflammation

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