Cutting edge: interleukin-17a prompts HIF1α for wound healing

Ahmed, Minhal; Huh, Jun R.

doi:10.1016/j.it.2022.09.013

Cited by 4 publications

(6 citation statements)

References 11 publications

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“…IL-17A is an inflammatory cytokine linked to psoriasis development and severity; using anti-IL-17 antibodies to block it is an effective existing treatment in psoriasis therapy [ 24 ]. IL-17A targets KC activation, which leads to dysfunction through the p38-MAPK and NF-κB signaling pathways [ 25 , 26 ].…”

Section: Resultsmentioning

confidence: 99%

CD147 Facilitates the Pathogenesis of Psoriasis through Glycolysis and H3K9me3 Modification in Keratinocytes

Chen,

Yi,

Liu

et al. 2023

Research

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Psoriasis is a chronic inflammatory skin disease featuring rapid proliferation of epidermal cells. Although elevated glycolysis flux has been reported in psoriasis, the molecular mechanisms underlying its pathogenesis remain unclear. We investigated the role of the integral membrane protein CD147 in psoriasis pathogenesis, observing its high expression in psoriatic skin lesions of humans and imiquimod (IMQ)-induced mouse models. In mouse models, genomic deletion of epidermal CD147 markedly attenuated IMQ-induced psoriatic inflammation. We found that CD147 interacted with glucose transporter 1 (Glut1). Depletion of CD147 in the epidermis blocked glucose uptake and glycolysis in vitro and in vivo. In CD147-knockout mice and keratinocytes, oxidative phosphorylation was increased in the epidermis, indicating CD147's pivotal role in glycolysis reprogramming during pathogenesis of psoriasis. Using non-targeted and targeted metabolic techniques, we found that epidermal deletion of CD147 significantly increased the production of carnitine and α-ketoglutaric acid (α-KG). Depletion of CD147 also increased transcriptional expression and activity of γ-butyrobetaine hydroxylase (γ-BBD/ BBOX1 ), a crucial molecule for carnitine metabolism, by inhibiting histone trimethylations of H3K9. Our findings demonstrate that CD147 is critical in metabolic reprogramming through the α-KG–H3K9me3– BBOX1 axis in the pathogenesis of psoriasis, indicating that epidermal CD147 is a promising target for psoriasis treatment.

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Section: Resultsmentioning

confidence: 99%

CD147 Facilitates the Pathogenesis of Psoriasis through Glycolysis and H3K9me3 Modification in Keratinocytes

Chen,

Yi,

Liu

et al. 2023

Research

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Section: Resultsmentioning

confidence: 99%

“…Sci. 2023, 24, 11989 3 of 26 these two viruses in the disease spectrum, the incidence of various clinical manifestations and epidemiological characteristics [35][36][37][38][39]. Most previous studies used the KOS strain of HSV-1, and significant knowledge has been accumulated regarding this strain.…”

Section: Resultsmentioning

confidence: 99%

“…Although the cellular responses induced by HSV-1 and HSV-2 are similar, they also show significant differences [35][36][37][38][39]. HSV-1 and HSV-2 have different nucleotide sequences, reactivation rates and transcriptional effects [35][36][37][38][39][40]. There is also a difference between these two viruses in the disease spectrum, the incidence of various clinical manifestations and epidemiological characteristics [35][36][37][38][39].…”

Section: Resultsmentioning

confidence: 99%

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Herpes Simplex Virus Infection Alters the Immunological Properties of Adipose-Tissue-Derived Mesenchymal-Stem Cells

Kun-Varga,

Gubán,

Miklós

et al. 2023

IJMS

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The proper functioning of mesenchymal stem cells (MSCs) is of paramount importance for the homeostasis of the body. Inflammation and infection can alter the function of MSCs, which can also affect the regenerative potential and immunological status of tissues. It is not known whether human herpes simplex viruses 1 and 2 (HSV1 and HSV2), well-known human pathogens that can cause lifelong infections, can induce changes in MSCs. In non-healing ulcers, HSV infection is known to affect deeper tissue layers. In addition, HSV infection can recur after initially successful cell therapies. Our aim was to study the response of adipose-derived MSCs (ADMSCs) to HSV infection in vitro. After confirming the phenotype and differentiation capacity of the isolated cells, we infected the cells in vitro with HSV1-KOS, HSV1-532 and HSV2 virus strains. Twenty-four hours after infection, we examined the gene expression of the cells via RNA-seq and RT-PCR; detected secreted cytokines via protein array; and determined autophagy via Western blot, transmission electron microscopy (TEM) and fluorescence microscopy. Infection with different HSV strains resulted in different gene-expression patterns. In addition to the activation of pathways characteristic of viral infections, distinct non-immunological pathways (autophagy, tissue regeneration and differentiation) were also activated according to analyses with QIAGEN Ingenuity Pathway Analysis, Kyoto Encyclopedia of Genes and Genome and Genome Ontology Enrichment. Viral infections increased autophagy, as confirmed via TEM image analysis, and also increased levels of the microtubule-associated protein light chain 3 (LC3B) II protein. We identified significantly altered accumulation for 16 cytokines involved in tissue regeneration and inflammation. Our studies demonstrated that HSV infection can alter the viability and immunological status of ADMSCs, which may have implications for ADMSC-based cell therapies. Alterations in autophagy can affect numerous processes in MSCs, including the inhibition of tissue regeneration as well as pathological differentiation.

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“…Studies conducted in recent years have demonstrated that IL-17 is responsible for driving epithelial HIF-1α [ 69 ], which in turn promotes wound repair through glycolysis [ 70 ]. IL-17 A/F, which is supplied by skin-dwelling RORγt + γδ T cells that have been expanded, is also required for optimum HIF-1α activation in wound marginal epithelial cells when hypoxia is present [ 71 ].…”

Section: Il-17 Familymentioning

confidence: 99%

IL-17 in wound repair: bridging acute and chronic responses

Mu,

Gu,

Tang

et al. 2024

Cell Commun Signal

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Chronic wounds, resulting from persistent inflammation, can trigger a cascade of detrimental effects including exacerbating inflammatory cytokines, compromised blood circulation at the wound site, elevation of white blood cell count, increased reactive oxygen species, and the potential risk of bacterial infection. The interleukin-17 (IL-17) signaling pathway, which plays a crucial role in regulating immune responses, has been identified as a promising target for treating inflammatory skin diseases. This review aims to delve deeper into the potential pathological role and molecular mechanisms of the IL-17 family and its pathways in wound repair. The intricate interactions between IL-17 and other cytokines will be discussed in detail, along with the activation of various signaling pathways, to provide a comprehensive understanding of IL-17’s involvement in chronic wound inflammation and repair.

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Cutting edge: interleukin-17a prompts HIF1α for wound healing

Cited by 4 publications

References 11 publications

CD147 Facilitates the Pathogenesis of Psoriasis through Glycolysis and H3K9me3 Modification in Keratinocytes

CD147 Facilitates the Pathogenesis of Psoriasis through Glycolysis and H3K9me3 Modification in Keratinocytes

Herpes Simplex Virus Infection Alters the Immunological Properties of Adipose-Tissue-Derived Mesenchymal-Stem Cells

IL-17 in wound repair: bridging acute and chronic responses

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