High glucose induces inflammatory cytokine through protein kinase C-induced toll-like receptor 2 pathway in gingival fibroblasts
| Autor: | Jia-Yin Deng, Ting-Ting Shang, Shao-Yun Jiang, Qi Lian, Chen-Xuan Wu, Cong-Cong Wei |
|---|---|
| Rok vydání: | 2012 |
| Předmět: |
medicine.medical_specialty
Protein Kinase C-alpha medicine.medical_treatment Interleukin-1beta Biophysics Gingiva Alpha (ethology) Inflammation Biology Biochemistry Internal medicine Protein Kinase C beta medicine Humans RNA Messenger Receptor Molecular Biology Protein kinase C Cells Cultured Protein Kinase C Cell Nucleus Tumor Necrosis Factor-alpha Transcription Factor RelA Cell Biology Fibroblasts Toll-Like Receptor 2 TLR2 Cytokine Endocrinology Glucose Gene Knockdown Techniques Hyperglycemia Tumor necrosis factor alpha Cytokine secretion medicine.symptom |
| Zdroj: | Biochemical and biophysical research communications. 427(3) |
| ISSN: | 1090-2104 |
| Popis: | Highlights: Black-Right-Pointing-Pointer High glucose significantly induced TLR2 expression in gingival fibroblasts. Black-Right-Pointing-Pointer High glucose increased NF-{kappa}B p65 nuclear activity, IL-1{beta} and TNF-{alpha} levels. Black-Right-Pointing-Pointer PKC-{alpha}/{delta}-TLR2 pathway is involved in periodontal inflammation under high glucose. -- Abstract: Toll-like receptors (TLRs) play a key role in innate immune response and inflammation, especially in periodontitis. Meanwhile, hyperglycemia can induce inflammation in diabetes complications. However, the activity of TLRs in periodontitis complicated with hyperglycemia is still unclear. In the present study, high glucose (25 mmol/l) significantly induced TLR2 expression in gingival fibroblasts (p < 0.05). Also, high glucose increased nuclear factor kappa B (NF-{kappa}B) p65 nuclear activity, tumor necrosis factor-{alpha} (TNF-{alpha}) and interleukin-l{beta} (IL-1{beta}) levels. Protein kinase C (PKC)-{alpha} and {delta} knockdown with siRNA significantly decreased TLR2 and NF-{kappa}B p65 expression (p < 0.05), whereas inhibition of PKC-{beta} had no effect on TLR2 and NF-{kappa}B p65 under high glucose (p < 0.05). Additional studies revealed that TLR2 knockdown significantly abrogated high-glucose-induced NF-{kappa}B expression and inflammatory cytokine secretion. Collectively, these data suggest that high glucose stimulates TNF-{alpha} and IL-1{beta} secretion via inducing TLR2 through PKC-{alpha} and PKC-{delta} in human gingival fibroblasts. |
| Databáze: | OpenAIRE |
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