Buccal Mucosal Epithelial Cells Downregulate CTGF Expression in Buccal Submucosal Fibrosis Fibroblasts

Gottipamula, Sanjay; Sundarrajan, Sudarson; Moorthy, Aditya; Padmanabhan, Sriram; Sridhar, Koteshwar N.

doi:10.1007/s12663-017-1056-1

Cited by 14 publications

(12 citation statements)

References 25 publications

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“…The prevalence is reported to be 0.9–4.7% in China [ 9 ], 0.62–6.42% in India, 0.15–14.6% in Vietnam [ 10 ], and 0.086–17.6% in Taiwan [ 11 ]. Based on the World Health Organization statistics, there are more than 5 million OSF patients globally [ 12 , 13 ]. The ages of OSF patients range from 8 to 80 years [ 14 ], with varying mean age across different studies.…”

Section: Epidemiology Of Osfmentioning

confidence: 99%

Oral Submucous Fibrosis: A Review on Biomarkers, Pathogenic Mechanisms, and Treatments

Shen

Shih

Fuh

et al. 2020

IJMS

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Oral submucous fibrosis (OSF) is a collagen deposition disorder that affects a patient’s oral function and quality of life. It may also potentially transform into malignancy. This review summarizes the risk factors, pathogenic mechanisms, and treatments of OSF based on clinical and bio-molecular evidence. Betel nut chewing is a major risk factor that causes OSF in Asia. However, no direct evidence of arecoline-induced carcinogenesis has been found in animal models. Despite identification of numerous biomarkers of OSF lesions and conducting trials with different drug combinations, clinicians still adopt conservative treatments that primarily focus on relieving the symptoms of OSF. Treatments focus on reducing inflammation and improving mouth opening to improve a patient’s quality of life. In conclusion, high-quality clinical studies are needed to aid clinicians in developing and applying molecular biomarkers as well as standard treatment guidelines.

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Section: Epidemiology Of Osfmentioning

confidence: 99%

Oral Submucous Fibrosis: A Review on Biomarkers, Pathogenic Mechanisms, and Treatments

Shen

Shih

Fuh

et al. 2020

IJMS

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“…Reinstating the renewal ability of the basal layer of oral mucosa should reverse fibrosis and prevent malignancy. 2 , 8 , 126 – 129 Indeed, the coculture of normal buccal mucosal epithelial cell fibrotic fibroblasts causes the downregulation of connective tissue growth factor (CTGF), 128 a profibrotic mediator in OSF. 2 The undifferentiated keratinocytes reinstate the normal healing patterns in fibrosis through the downregulation of TGF-β and the stabilization of desmosomal assembly.…”

Section: Future Perspectivesmentioning

confidence: 99%

Loss of oral mucosal stem cell markers in oral submucous fibrosis and their reactivation in malignant transformation

Sharma¹,

Fonseca

Hunter

et al. 2020

Int J Oral Sci

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The integrity of the basal stem cell layer is critical for epithelial homoeostasis. In this paper, we review the expression of oral mucosal stem cell markers (OM-SCMs) in oral submucous fibrosis (OSF), oral potentially malignant disorders (OPMDs) and oral squamous cell carcinoma (OSCC) to understand the role of basal cells in potentiating cancer stem cell behaviour in OSF. While the loss of basal cell clonogenicity triggers epithelial atrophy in OSF, the transition of the epithelium from atrophic to hyperplastic and eventually neoplastic involves the reactivation of basal stemness. The vacillating expression patterns of OM-SCMs confirm the role of keratins 5, 14, 19, CD44, β1-integrin, p63, sex-determining region Y box (SOX2), octamer-binding transcription factor 4 (Oct-4), c-MYC, B-cell-specific Moloney murine leukaemia virus integration site 1 (Bmi-1) and aldehyde dehydrogenase 1 (ALDH1) in OSF, OPMDs and OSCC. The downregulation of OM-SCMs in the atrophic epithelium of OSF and their upregulation during malignant transformation are illustrated with relevant literature in this review.

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“…Biopsies of urethral scar tissues from male USD patients undergoing urethroplasty (n=6, 42-72 years) were transported to the cell isolation facility in a cold medium containing Hank's Balanced Salt Solution (Gibco, USA) and 1% antibioticantimycotic (Gibco, USA). The USF cells were isolated and expanded as per our previously published protocol [24]. The USF cells isolated by digesting stricture tissues in Collagenase Type IV (Life Technologies, USA) were cultured in Dulbecco's Modified Eagle Medium (DMEM) (Life Technologies, USA) supplemented with 10% fetal bovine serum (FBS) (Hyclone, USA) in standard conditions till passage 2 (P2).…”

Section: Isolation and Cell Culturementioning

confidence: 99%

“…The RNA concentration was measured using NanoDrop (Thermo Scientific, USA). Total RNA was equalized in all samples and subjected to HL-ds DNase (ArcticZymes, Norway) treatment to remove genomic DNAs and then transcribed to cDNA using SuperScript III Platinum one-step quantitative reverse transcription-polymerase chain reaction (PCR) kit (Invitrogen, USA) as previously described [24]. About 2 µl of the prepared cDNA was subjected to quantitative PCR (qPCR) using Maxima SYBR Green qPCR master mix to determine the expression of α-SMA, TIMP-1, and glyceraldehyde-3-phosphate dehydrogenase (GAPDH).…”

Section: Gene Expression Studiesmentioning

confidence: 99%

The effect of human amniotic epithelial cells on urethral stricture fibroblasts

2019

J Clin Transl Res

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Background: Urethral stricture disease (USD) is effectively managed by buccal mucosa (BM) urethroplasty. Lack of adequate healthy BM has led to the use of autologous tissue-engineered BM grafts. Such grafts are costly, not easily scalable and recurrence of the stricture is still a problem. Hence, there is a requirement for cost-effective, scalable cells with innate antifibrotic properties which seem to be fulfilled by human amniotic epithelial cells (HAMECs). The effect of HAMECs on USD is unknown. Aim: To study the effect of HAMECs-CM on human urethral stricture fibroblast (USF) cells by using in-vitro migration assay and molecular techniques. Materials and Methods: USF cells were derived from six patients undergoing urethroplasty. HAMECs were derived from one placenta after delivery. The effect of HAMECs-CM on USF cell migration was observed using a standard in vitro scratch assay over a period of 3 days. The effect of HAMECs-CM on the expression levels of markers alpha-smooth muscle actin (α-SMA) and tissue inhibitor of metalloproteinases (TIMP-1) in USF cells was also examined. Results: The HAMECs-CM suppressed the migration of USF cells in in vitro scratch assay. The HAMECs-CM consistently downregulated α-SMA, but not TIMP-1. Conclusions: HAMECs have shown antifibrotic activity on USF cells in this in vitro study. Relevance for Patients: HAMECs could serve as an alternative cell source for tissue-engineered urethroplasty.

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Buccal Mucosal Epithelial Cells Downregulate CTGF Expression in Buccal Submucosal Fibrosis Fibroblasts

Cited by 14 publications

References 25 publications

Oral Submucous Fibrosis: A Review on Biomarkers, Pathogenic Mechanisms, and Treatments

Oral Submucous Fibrosis: A Review on Biomarkers, Pathogenic Mechanisms, and Treatments

Loss of oral mucosal stem cell markers in oral submucous fibrosis and their reactivation in malignant transformation

The effect of human amniotic epithelial cells on urethral stricture fibroblasts

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