Immunohistochemical analyses of survivin and heat shock protein 90 expression in patients with oral lichen planus

Chaiyarit, Ponlatham; Jintakanon, Darunee; Klanrit, Poramate; Siritapetawee, Mookhda; Thongprasom, Kobkan

doi:10.1111/j.1600-0714.2008.00713.x

Cited by 18 publications

(22 citation statements)

References 59 publications

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“…Considering these observations, an increased expression of NLRP3 inflammasome in oral epithelial cells and infiltrated immune cells at the sites of OLP lesional mucosae possibly reflects cellular responses to pathological stimuli. Previous studies have demonstrated aberrant expression of HSP60 and HSP90 in OLP lesions [44,45]. Previous studies have demonstrated aberrant expression of HSP60 and HSP90 in OLP lesions [44,45].…”

Section: Discussionmentioning

confidence: 98%

New evidence of connections between increased O-GlcNAcylation and inflammasome in the oral mucosa of patients with oral lichen planus

Thi

Phoomak

Champattanachai

et al. 2018

Clinical and Experimental Immunology

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Oral lichen planus (OLP) is considered a chronic inflammatory immune-mediated disease of the oral mucosa. Immunopathogenesis of OLP is thought to be associated with cell-mediated immune dysregulation. O-GlcNAcylation is a form of reversible glycosylation. It has been demonstrated that O-GlcNAcylation promoted nuclear factor kappa B (NF-κB) signalling. Activation of NF-кB can induce expression of nucleotide-binding domain-like receptor family pyrin domain containing 3 (NLRP3) inflammasome, which is a large intracellular multi-protein complex involving an immune response. Dysregulated expression of the NLRP3 inflammasome was reported to be associated with autoinflammatory diseases. No integrative studies between O-GlcNAcylation and NLRP3 inflammasome in OLP patients have been reported. The present study aimed to determine the immunohistochemical expression of O-GlcNAcylation, NF-κB signalling molecules and NLRP3 inflammasome in oral mucosae of OLP patients. Oral tissue samples were collected from 30 OLP patients and 30 healthy individuals. Immunohistochemical staining and analyses of immunostaining scores were performed to evaluate expression of O-GlcNAcylation, NF-κB signalling molecules and NLRP3 inflammasome. According to observations in this study, significantly higher levels of O-GlcNAcylation, NF-κB signalling molecules and NLRP3 inflammasome were demonstrated in OLP patients compared with control subjects (P < 0·001). Positive correlations among O-GlcNAcylation, NF-κB signalling molecules and NLRP3 inflammasome were also observed in OLP samples (P < 0·01). In conclusion, the present study provides supportive evidence that increased O-GlcNAcylation is associated with increased expression of NLRP3 inflammasome via the NF-κB signalling pathway. These findings provide a new perspective on immunopathogenesis of OLP in relation to autoinflammation.

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Section: Discussionmentioning

confidence: 98%

New evidence of connections between increased O-GlcNAcylation and inflammasome in the oral mucosa of patients with oral lichen planus

Thi

Phoomak

Champattanachai

et al. 2018

Clinical and Experimental Immunology

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“…In addition, HSPs can be released extracellularly in response to a number of stressful conditions, but this mechanism, independent of necrotic cell death, is not clear (Tsan and Gao, 2004). Both Sugerman et al (1995) and Chaiyarit et al (2009) detected the expression of hsp70 and hsp90 , respectively in some lymphocytes at the connective tissue in OLP lesions. We should also consider the fact that not all the HSPs, or at least hsp27 , might interact directly with lymphocytes considering the possibility for intermediary molecules carrying out that role.…”

Section: Discussionmentioning

confidence: 94%

Analysis of the expression of heat‐shock protein 27 in patients with oral lichen planus

et al. 2012

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“…16,17 The alterations present in the mucosa of OLP patients may involve the homeostatic activities of oral epithelial cells, possibly resulting in an imbalance between cell proliferation and apoptosis. 31 Survivin, a member of IAP family protein, plays a pivotal role in cell survival with a double function: controlling cell division and interacting with several caspases to inhibit apoptosis. 24,25 It is reasonable to think that Survivin is involved in OLP, although studies conducted to date were focused on oral squamous cell carcinoma, [28][29][30] while only one study investigated the expression of Survivin in OLP.…”

Section: Discussionmentioning

confidence: 99%

“…[24][25][26][27] There are many studies focused on the relationship between oral squamous cell carcinoma and Survivin, [28][29][30] while the expression of this protein in the context of its relationship to chronic inflammatory diseases were limited, with only one study regarding the expression of survivin in OLP. 31 The aim of this study is to evaluate the expression of OPN, CD44, and Survivin in a group of patients affected by OLP, and assess if there are any differences in the expression levels of these proteins between erosive and reticular form of OLP.…”

Section: Introductionmentioning

confidence: 99%

Active inflammatory biomarkers in oral lichen planus

Santarelli

Mascitti

Rubini

et al. 2015

Int J Immunopathol Pharmacol

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Oral lichen planus (OLP) is a chronic disease, with a central role to cell-mediated autoimmunity. Osteopontin promotes migration and recruitment of immune cells, CD44 is its receptor, and Survivin seems to be important in skin/mucosa homeostasis. The aim of this study was to investigate their expression in biopsy specimens of patients with different OLP clinical types and healthy controls.Biopsy specimens from 30 patients with OLP (15 atrophic and 15 hyperplastic) and 15 healthy controls were subjected to immune-histochemical analysis, to detect the expression of osteopontin, CD44, and Survivin in oral epithelia. The distributions of positively stained cells were evaluated with a quantitative method, while the inflammation degree was evaluated with a semi-quantitative one.Expression of osteopontin and CD44 was higher in OLP than controls, while Survivin expression was lower in OLP patients. There was a greater reduction of Survivin expression in atrophic OLP than hyperplastic OLP. A correlation between osteopontin expression and a high degree of inflammation was found. Furthermore, Survivin expression was higher in cases with low intensity of inflammation.Osteopontin, CD44, and Survivin seem to be involved in OLP pathogenesis, and further investigations are needed for clarifying their role in this oral disease.

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Immunohistochemical analyses of survivin and heat shock protein 90 expression in patients with oral lichen planus

Abstract: Our results provided additional evidence that alterations in the expression of survivin and Hsp90 in oral epithelia might be associated with pathological stress, such as chronic inflammation, in patients with OLP.

Cited by 18 publications

References 59 publications

New evidence of connections between increased O-GlcNAcylation and inflammasome in the oral mucosa of patients with oral lichen planus

New evidence of connections between increased O-GlcNAcylation and inflammasome in the oral mucosa of patients with oral lichen planus

Analysis of the expression of heat‐shock protein 27 in patients with oral lichen planus

Active inflammatory biomarkers in oral lichen planus

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