ArticleCell stress & chaperones2018
Association between circulating levels of heat-shock protein 27 and aggressive periodontitis.
Article in Cell stress & chaperones, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
6 citing papers in PubMed, 7 citations in OpenAlex.
- Proteome-Wide Mendelian Randomisation Identifies Causal Links of Plasma Proteins With Periodontitis.International dental journal · 2024Article
- Mechanistic insights into heat shock protein 27, a potential therapeutic target for cardiovascular diseases.Frontiers in cardiovascular medicine · 2023Review
- Influence of Periodontal Ligament Stem Cell-Derived Conditioned Medium on Osteoblasts.Pharmaceutics · 2022Article
- Effect of nonsurgical periodontal therapy on haematological parameters in grades B and C periodontitis: an exploratory analysis.Clinical oral investigations · 2020Article
- Promising Scaffold-Free Approaches in Translational Dentistry.International journal of environmental research and public health · 2020Review
- Phosphorylated Heat Shock Protein 27 Inhibits Lipopolysaccharide-Induced Inflammation in Thp1 Cells by Promoting TLR4 Endocytosis, Ubiquitination, and Degradation.Inflammation · 2019Article
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Heat-shock protein (Hsp) 27 is a major intracellular molecular chaperone and controller of intracellular responses to inflammatory signals. In the extracellular space, recombinant Hsp27 has been described to exert anti-inflammatory activities. The aim of this study was to assess the association between circulating levels of Hsp27 and different types of periodontitis. Pro- and anti-inflammatory cytokines and the stress proteins Hsp27 and Hsp60 with proposed anti- and pro-inflammatory properties, respectively, were measured by two-site ELISA in the serum of patients with aggressive periodontitis (AgP, n = 30), chronic periodontitis (CP, n = 29) and periodontally healthy controls (H, n = 28). Furthermore, Hsp27 and Hsp60 levels were also measured longitudinally in 12 AgP patients at 6 time points up to 3 months after treatment. AgP patients had lower levels of Hsp27 compared to CP patients and healthy subjects (adjusted one-way ANOVA, p < 0.001, followed by post hoc Tukey HSD comparisons), while no differences in levels of Hsp60 or cytokines between the three groups were detected. In CP patients and H subjects, the systemic Hsp27 levels correlated with Hsp60 (r = 0.43, p < 0.001; r = 0.59, p < 0.001, respectively) and with pro-inflammatory cytokines TNF-α (r = 0.48, p < 0.001; r = 0.55, p < 0.001, respectively) and IL-6 (r = 0.44, p < 0.01). However, no such correlations were detected in AgP cases. No consistent temporal patterns of changes of Hsp27 concentration were detected across AgP patients following periodontal treatment. This study provides the first evidence that Hsp27 may be differentially expressed and regulated in AgP patients as compared with CP patients and healthy individuals.
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