Human gingiva transcriptome during wound healing

Wang, Yun; Tatakis, Dimitris N.

doi:10.1111/jcpe.12669

Cited by 40 publications

(46 citation statements)

References 41 publications

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“…However, collective evidence from this study and that of Lundmark et al () supports the absence of MUC4 in healthy keratinized oral epithelia. We further confirm and extend reports of transcripts for MUC16 in buccal epithelium (Hori et al, ) and MUC21 in gingival tissue (Wang & Tatakis, ). MUCs 15, 16, 20, and 21 are localized to all cell layers above basal cells, in both buccal and palatal epithelia, suggesting they are functionally important as cells differentiate during transition to the uppermost layer.…”

Section: Discussionsupporting

confidence: 91%

Oral epithelial membrane‐associated mucins and transcriptional changes with Sjögren's syndrome

2019

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Objectives To determine expression and localization of membrane‐associated mucins within human keratinized and non‐keratinized oral epithelia, and to explore transcriptional changes associated with primary Sjögren's syndrome. Subjects and Methods Mucin transcripts and glycoproteins were determined by RT‐PCR and immunohistochemistry, respectively, in oral keratinized (hard palate) and non‐keratinized (buccal) epithelia obtained from three cadavers. Mucin transcripts assessed by quantitative PCR were compared between cells harvested by brushing buccal and palatal epithelia of 25 female primary Sjögren's syndrome patients vs 25 healthy age‐matched female control subjects. Results In hard palate, MUC4 is absent and MUC1 localized to deeper cell layers. Both mucins are within the apical layers of buccal epithelium. MUC15 is localized throughout all palatal cell layers and in all but the basal layer of buccal epithelia. MUC16, MUC20, and MUC21 glycoproteins are localized within all but the basal cell layer of both tissue types. In buccal cells of primary Sjögren's patients, MUC21 transcripts are down‐regulated 3.4‐fold and MUC20 2.6‐fold. Dysregulation of select epithelial mucins may therefore contribute to xerostomia. Conclusions Differential expression of multiple mucins and down‐regulation in Sjögren's syndrome support further study of oral epithelial mucin physiology and pathophysiology, including their functions in hydration and lubrication of the oral mucosal pellicle.

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Section: Discussionsupporting

confidence: 91%

Oral epithelial membrane‐associated mucins and transcriptional changes with Sjögren's syndrome

2019

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“…Nearly all other oral mucosal wounds heal faster than skin wounds, with minimal scar formation (Glim, Niessen, Everts, Van Egmond, & Beelen, 2013;Szpaderska et al, 2005). Periodontists experienced that gingival wounds, in particular, heal without scars (Larjava et al, 2011;Wang & Tatakis, 2017;Wong et al, 2009). However, in the scientific landscape on this topic, a direct comparison between oral mucosa and gingiva in the early phases of wound healing is missing.…”

Section: Discussionmentioning

confidence: 99%

Autophagy activation is required for myofibroblast differentiation during healing of oral mucosa

Vescarelli

Pilloni

Dominici

et al. 2017

J Clinic Periodontology

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“…8 SPOCD1 was initially found to interact with testis protein phosphatase 1 which is a major eukaryotic serine/threonine-specific phosphatase regulating cellular signaling. 9 However, the exact role of SPOCD1 in biological processes remains unknown. Recent studies have shown that SPOCD1 can predict progression and prognosis in T1G3 bladder cancer.…”

Section: Introductionmentioning

confidence: 99%

<p>SPOCD1 accelerates ovarian cancer progression and inhibits cell apoptosis via the PI3K/AKT pathway</p>

Liu

Yang

Yan

et al. 2020

OTT

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Background: Ovarian cancer (OC) is the most common type of gynecological malignant tumors with poor prognosis. The spen paralogue and orthologue C-terminal domain containing 1 (SPOCD1) is a newly identified molecule that has been indicated to discriminate progressive in human solid tumors. However, the role of SPOCD1 in OC remains unknown. Methods: The expression of SPOCD1 in OC and non-cancerous tissue was detected by Realtime polymerase chain reaction and immunohistochemical staining. The expression of SPOCD1 in OC cells (SKOV3 and CAOV3) was also detected by immunohistochemical staining. The effect of SPOCD1 on cell proliferation was analyzed by Cell Counting Kit 8 and colony formation assay, and cell migration was analyzed by transwell assay. Apoptosis was analyzed by flow cytometry. The protein expression of SPOCD1, PTEN, PI3K, p-AKT, and mTOR in OC cells was measured by Western blot. Results: SPOCD1 expression was significantly upregulated in OC tissues compared with non-cancerous tissues (P<0.01), and was positively correlated to FIGO stage and tumor grade of OC. Also, SPOCD1 was significantly expressed in nucleus and cytoplasm of SKOV3 and CAOV3 cells. Kaplan-Meier analysis indicated that patients with high SPOCD1 expression had shorter overall survival (HR =1.512, 95%CI: 1.321-2.793, P=0.031) and progression-free survival (HR =1.875, 95%CI: 1.435-3.157, P=0.028). SPOCD1 was upregulated in OC SKOV3 and CAOV3 cells. Further investigation revealed that downregulation of SPOCD1 inhibited the SKOV3 and CAOV3 cells proliferation and migration. In addition, the deficit of SPOCD1 increased the apoptosis in SKOV3 and CAOV3 cells. PI3K/AKT pathway was inhibited by knockdown of SPOCD1 in SKOV3 and CAOV3 cells. Conclusions: Our data suggest that SPOCD1 may act as a carcinogenesis factor by activating the PI3K/AKT pathway to restrained cell apoptosis in OC.

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Human gingiva transcriptome during wound healing

Cited by 40 publications

References 41 publications

Oral epithelial membrane‐associated mucins and transcriptional changes with Sjögren's syndrome

Oral epithelial membrane‐associated mucins and transcriptional changes with Sjögren's syndrome

Autophagy activation is required for myofibroblast differentiation during healing of oral mucosa

<p>SPOCD1 accelerates ovarian cancer progression and inhibits cell apoptosis via the PI3K/AKT pathway</p>

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