Erratum to: High-Glucose Environment Inhibits p38MAPK Signaling and Reduces Human β-Defensin-3 Expression in Keratinocytes

Lan, Cheng‐Che E.; Wu, Ching‐Shuang; Huang, Shu‐Mei; Kuo, H.-Y.; Wu, I-Hui; Wen, Chien-Hui; Chai, Chee-Yin; Fang, Ai-Hui; Chen, Gwo‐Shing

doi:10.2119/molmed.2011.00002.erratum

Cited by 10 publications

(20 citation statements)

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“…The question about the biological link between type 2 DM and periodontal diseases has been the focus of several studies. Type 2 diabetes has been associated with a reduction in tissue AMP production in some studies, while Brauner et al . found no difference in serum levels of AMP in such subjects.…”

Section: Resultsmentioning

confidence: 93%

“…Together, these results could be suggestive of common genetic susceptibility features underlying suboptimal AMP regulation and function in both DM and periodontal disease. Besides possible genetic predisposition, high levels of hyperglycemia and periodontal infection can both independently affect AMP expression and function in epithelial cells . The compounds, dicarbonyls methylgloxal and glyoxal are produced in response to hypergylcemia, and it shows that they can damage HBD‐2; the mechanism of immunosuppression underlies the increased susceptibility to intracellular invasion by gram‐negative pathogens, which is noted in DM …”

Section: Resultsmentioning

confidence: 99%

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Antimicrobial peptides as a possible interlink between periodontal diseases and its risk factors: A systematic review

Schmalz

Schmidt

et al. 2017

J of Periodontal Research

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Antimicrobial peptides (AMPs) play a critical role in controlling innate and acquired immune responses. Local dysregulation of AMP is implicated in the pathogenesis of periodontal diseases as a response to periodontal pathogen challenge. Changes in AMP expression also characterize tobacco smoking, diabetes mellitus, obesity and rheumatoid arthritis, which are established risk factors of periodontal diseases, suggesting AMP may act as putative mechanistic links between these. The aim was to evaluate and summarize critically the current evidence pertaining to interrelationships between AMPs, periodontal diseases and selected periodontal disease risk factors. General and theme specific keywords were used to search the PUBMED database for studies relevant to AMP, periodontal diseases, smoking, diabetes mellitus, obesity and rheumatoid arthritis and critically reviewed. A total of 131 abstracts and 119 full text articles were screened for relevance; 13 studies were selected for inclusion after critical review. Local AMP dysregulation characteristic to periodontal diseases appears to occur within a broader landscape of complex systemic immune perturbations independently induced by smoking, metabolic and rheumatoid disease. The nature of these interactions and mechanistic pathways involved are inadequately understood. AMPs could be possible mechanistic interlinks between periodontal diseases and its risk factors. However, such evidence is very limited and more in vivo and in vitro studies are necessary to clarify the nature of such relationships. A greater understanding of AMPs as shared mediators is essential for unraveling their value as therapeutic or biomarker candidates.

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Section: Resultsmentioning

confidence: 93%

Section: Resultsmentioning

confidence: 99%

Antimicrobial peptides as a possible interlink between periodontal diseases and its risk factors: A systematic review

Schmalz

Schmidt

et al. 2017

J of Periodontal Research

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“…Lan et al . determined the molecular effects of a high‐glucose environment on hBD‐3 expression in their skin‐lesion models; in their results, they found that treating keratinocytes with glycation end‐products significantly decreased the levels of hBD3 produced, although hyperglycemic conditions inhibited constitutive expression of hBD‐3 on keratinocytes and resulted in inadequate up‐regulation of hBD‐3 upon stimulation. Hiratsuka et al .…”

Section: Discussionmentioning

confidence: 99%

Gingival crevicular fluid levels of human beta‐defensins 1 and 3 in subjects with periodontitis and/or type 2 diabetes mellitus: a cross‐sectional study

Ertuğrul

Dikilitaş

Sahin

et al. 2012

J of Periodontal Research

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As a result of the observed vascular and cell activity changes that occur within patients diagnosed with DM, periodontal diseases become more severe. These changes hinder the migration and the ability of chemotactic factors and leukocytes to protect periodontal tissues from the effects of microorganisms. In order to eliminate microorganisms, the epithelial cells in patients with DM may release more hBD-1 and hBD-3 into the gingival crevicular fluid. Determining the amount of hBD-1 and hBD-3 in the gingival crevicular fluid of patients with and without DM will help to elucidate the relationship among hBD-1, hBD-3, DM and periodontal disease.

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“…Intriguingly, it was shown that skin wounding induced cutaneous hBD2 expression; 17,18 however, for diabetic wounds, inadequate upregulation of hBD2 has been suggested to play a pathogenic role 19 . Recently, we demonstrated that diabetic rat skin showed inadequate β‐defensin expression after wounding compared with control 20 . Therefore, the current study was launched to evaluate the impact of a high‐glucose environment on cultured keratinocytes in terms of hBD2 expression.…”

mentioning

confidence: 99%

High-glucose environment reduces human β-defensin-2 expression in human keratinocytes: implications for poor diabetic wound healing

Lan

Huang

et al. 2012

British Journal of Dermatology

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Erratum to: High-Glucose Environment Inhibits p38MAPK Signaling and Reduces Human β-Defensin-3 Expression in Keratinocytes

Cited by 10 publications

References 0 publications

Antimicrobial peptides as a possible interlink between periodontal diseases and its risk factors: A systematic review

Antimicrobial peptides as a possible interlink between periodontal diseases and its risk factors: A systematic review

Gingival crevicular fluid levels of human beta‐defensins 1 and 3 in subjects with periodontitis and/or type 2 diabetes mellitus: a cross‐sectional study

High-glucose environment reduces human β-defensin-2 expression in human keratinocytes: implications for poor diabetic wound healing

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