IL-1 Alpha Regulates CXCL1, CXCL10 and ICAM1 in Network Form in Oral Keratinocytes

Wu, Tong; Du, Rui; Hong, Yun; Lee, Jia; Zeng, Qi; Cheng, Bin

doi:10.7754/clin.lab.2012.121029

Cited by 15 publications

(19 citation statements)

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“…IL‐1α is reported to increase expression of CXCL10 mRNA in oral keratinocytes . These proinflammatory cytokines are known to be potent inducers for the production of chemokines including CXCL1, IL‐8, CXCL9, and CXCL10 by keratinocytes . In this study, we confirmed that IL‐1β and TNF‐α increased CXCL10 mRNA expression in HaCaT cells (Fig.…”

Section: Discussionsupporting

confidence: 81%

“…When skin is wounded, accumulated inflammatory cells produce proinflammatory cytokines including TNF-a and IL-1 [27]. Especially, TNF-a is known to be a potent inducer for the production of VEGF and several chemokines including CXCL10 in keratinocytes [28][29][30]. Consistent with these reports, we found that the CXCL10 mRNA level was increased five times by TNF-a and 1.8 times by IL-1b in HaCaT cells (Fig.…”

Section: Hgf Inhibits Cxcl10 Expression Induced By Tnf-a In Hacat Cellssupporting

confidence: 89%

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Hepatocyte growth factor reduces CXCL10 expression in keratinocytes

et al. 2016

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Keratinocytes secrete vascular endothelial growth factor (VEGF) and angioregulatory chemokines during cutaneous wound healing. Hepatocyte growth factor (HGF) promotes skin re-epithelialization by increasing VEGF expression in keratinocytes. Here, we investigated the regulatory roles of HGF in the expression of genes encoding angiogenic and angiostatic chemokines in keratinocytes and found that HGF specifically inhibits mRNA expression of the angiostatic chemokine CXCL10 in both mouse primary keratinocytes and in the human keratinocyte cell line HaCaT through the MEK/ERK cascade. Furthermore, HGF inhibited tumor necrosis factor-α-induced CXCL10 expression at both mRNA and protein levels in HaCaT cells. Thus, HGF may orchestrate angiogenesis in wounded skin by modulating both VEGF and CXCL10 expression in keratinocytes.

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Section: Discussionsupporting

confidence: 81%

Section: Hgf Inhibits Cxcl10 Expression Induced By Tnf-a In Hacat Cellssupporting

confidence: 89%

Hepatocyte growth factor reduces CXCL10 expression in keratinocytes

et al. 2016

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“…[8][9][10]20 Besides, inflammatory cytokines IL-1β, ICAM1, and CCL5 expression in OLP was reported separately. [12][13][14] However, the data of CCN1 and its related cytokines IL-1β, ICAM1, and CCL5 in OLP are not available so far in the literature. Herein, we showed that altered expression of CCN1 in OLP associated with keratinocyte activation and IL-1β, ICAM1, and CCL5 up-regulation.…”

Section: Discussionmentioning

confidence: 99%

“…10 IL-1β and related cytokines intercellular adhesion molecule (ICAM) 1 and CCL5 (also known as RANTES) are pro-inflammatory mediators that response from neonatal airway epithelial cells. 11 Although IL-1β, ICAM1, and CCL5 expression in OLP was reported separately, [12][13][14] whether aberrant expression of CCN1 and its related cytokines IL-1β, ICAM1, and CCL5 in OLP are still unknown.…”

Section: Introductionmentioning

confidence: 99%

Altered expression of CCN1 in oral lichen planus associated with keratinocyte activation and IL‐1β, ICAM1, and CCL5 up‐regulation

Wang

Shi

et al. 2020

J Oral Pathology Medicine

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Background: Emerging evidence indicates that CCN1 is a novel inflammation-regulated mediator involved in the pathogenesis of some immune-mediated inflammatory diseases. The objective of this study was to investigate the preliminary roles of CCN1 and its related cytokines IL-1β, CCL5, and ICAM1 in oral lichen planus (OLP). Methods: CCN1 expression levels in biopsies from OLP patients against normal oral mucosa (NOM) using immunohistochemistry (42 OLP vs 9 NOM) and RT-qPCR (20 OLP vs 20 NOM) were compared, respectively. The correlation of CCN1 and IL-1β, CCL5, and ICAM1 expression was examined by RT-qPCR in tissue samples and an in vitro cell culture system using keratinocyte HaCaT cells incubated with lipopolysaccharides. Results: Immunohistochemistry showed that CCN1 protein mainly expressed in the cytoplasm of epithelial keratinocytes of OLP. Consistently, RT-qPCR revealed that mRNA expression of CCN1 was increased in OLP compared with NOM (P < .05) and positively correlated with the high expression of IL-1β, ICAM1, and CCL5 (P < .001), respectively. Importantly, an in vitro study showed that keratinocyte proliferation significantly (P < .05) increased by CCN1 stimulation. Moreover, IL-1β, ICAM1, and CCL5 expression in keratinocytes stimulated by CCN1 was increased (P < .05), respectively. Conclusions: This preliminary study for the first time reported that altered expression of CCN1 was associated with high expression of IL-1β, ICAM1, and CCL5 in OLP. And we demonstrated CCN1 promoted keratinocyte activation, as well as IL-1β, ICAM1, and CCL5 production in keratinocytes. Our data indicated that the potential role of CCN1 and its related cytokines was involved in the pathogenesis of OLP.

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“…Данные работы вносят большой вклад в понимание патогенеза заболеваний и играют важную роль для выбора тактики лечения. В мире существует множество работ, посвященных идентификации генетических факторов риска развития красного плоского лишая, однако, работы, касающиеся роли цитокинов и хемокинов в развитии данного заболевания, немногочисленны [5,6,21]. Более того, мы не обнаружили ни одной российской работы, посвященной молекулярно-генетическому изучению КПЛ, и предполагаем, что подобные исследования ранее не проводились.…”

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The use of genetic markers in predicting of oral lichen planus development and recurrence

Akmalova¹,

Чуйкин²,

Chuykin

et al. 2016

Actual Problems in Dentistry

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To reveal the association of the interleukin 8 (IL-8) gene with the development and progression of oral lichen planus (OLP) we performed RT-PCR analysis of rs4073 polymorphism in the IL-8 gene in 92 oral lichen planus patients and 163 healthy individuals of Russian ethnic origin from the Volga-Ural region of Russia. The investigation showed the importance of polymorphism rs4073 of IL-8 gene for oral lichen planus development. The disease was associated with genotype rs4073*T / T which was found to be the genetic marker of high risk for oral lichen planus development, and rs4073*A / T genotype — the genetic marker of low risk for erosive-ulcerous oral lichen planus form development (p=0.016, OR=0.40) and the disease recurrence (p=0.02, OR=0.33). The results obtained in the investigation make a significant contribution to understanding the structure of hereditary predisposition to oral lichen planus development.

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IL-1 Alpha Regulates CXCL1, CXCL10 and ICAM1 in Network Form in Oral Keratinocytes

Cited by 15 publications

References 0 publications

Hepatocyte growth factor reduces CXCL10 expression in keratinocytes

Hepatocyte growth factor reduces CXCL10 expression in keratinocytes

Altered expression of CCN1 in oral lichen planus associated with keratinocyte activation and IL‐1β, ICAM1, and CCL5 up‐regulation

The use of genetic markers in predicting of oral lichen planus development and recurrence

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