scholarly journals The association of EGF rs2237051 variant, serum EGF levels and generalized aggressive periodontitis: a preliminary study

PeerJ ◽  
2020 ◽  
Vol 8 ◽  
pp. e9212
Author(s):  
Xian’e Wang ◽  
Wenjing Li ◽  
Li Xu ◽  
Ruifang Lu ◽  
Huanxin Meng
Keyword(s):  
Inflammatory Diseases ◽  
Aggressive Periodontitis ◽  
Chinese Patients ◽  
Linear Regression Models ◽  
Flight Mass Spectrometry ◽  
Probing Depth ◽  
Proliferation And Differentiation ◽  
Epidermal Growth ◽  
Combined Genotypes ◽  
Control Study

Background Epidermal growth factor (EGF) is a pro-inflammatory small peptide that stimulates cell growth, proliferation and differentiation through binding to its receptor. EGF rs2237051 and serum EGF levels have been demonstrated to be related with a variety of diseases, including several tumors and inflammatory diseases. Therefore, this study aims to investigate the association of the EGF rs2237051 variant and serum EGF levels in Chinese patients with generalized aggressive periodontitis (GAgP). Material and Methods A case-control study was conducted among 216 patients with GAgP and 138 healthy controls. The clinical parameters of plaque index, probing depth, attachment loss and bleeding index were recorded. The EGF rs2237051 polymorphism was genotyped using time-of-flight mass spectrometry, and serum EGF levels were determined. Logistic and linear regression models were used to investigate the association between the genotypes of EGF rs2237051, serum EGF levels and GAgP risk. Results The AA genotype of EGF rs2237051 showed higher risk for GAgP than the combined genotypes GG and AG (adjusted OR = 1.65, 95% CI [1.06–2.57]). Increased serum EGF levels were associated with GAgP (adjusted OR = 1.18, 95% CI [1.14–1.22]). Moreover, the serum EGF level for the AA genotype was significantly higher than that for the AG/GG genotypes in patients with GAgP (adjusted β = 4.70, 95% CI [2.09–7.31]). Conclusion We demonstrated that EGF rs2237051 variant and the increased level of serum EGF were associated with the risk of GAgP, the serum EGF was up-regulated in patients with GAgP. It was indicated that serum EGF might be a biomarker of GAgP and EGF rs2237051 may be related to the genetic background of GAgP.

scholarly journals GC Gene Polymorphisms and Vitamin D-Binding Protein Levels Are Related to the Risk of Generalized Aggressive Periodontitis

2016 ◽  
Vol 2016 ◽  
pp. 1-8 ◽  
Author(s):  
Wenli Song ◽  
Xian’e Wang ◽  
Yu Tian ◽  
Xin Zhang ◽  
Ruifang Lu ◽  
...  
Keyword(s):  
Vitamin D ◽  
Binding Protein ◽  
Aggressive Periodontitis ◽  
Recessive Model ◽  
Strong Linkage Disequilibrium ◽  
Vitamin D Binding Protein ◽  
Protein Levels ◽  
Combined Genotypes ◽  
Gc Gene ◽  
Control Study

Objective. To explore whether GC (group-specific component) rs17467825, rs4588, and rs7041 polymorphisms are associated with generalized aggressive periodontitis.Methods. This case-control study recruited 372 patients with generalized aggressive periodontitis (group AgP) and 133 periodontal healthy subjects (group HP). GC rs17467825, rs4588, and rs7041 genotypes and plasmatic vitamin D-binding protein (DBP) were measured. Analysis of single SNP and multiple SNPs was performed and relevance between plasmatic DBP and haplotypes was analyzed.Results. GC rs17467825 GG genotype was statistically associated with lower risk for generalized aggressive periodontitis under the recessive model (OR = 0.52, 95% CI: 0.30–0.92,p=0.028). GC rs17467825 and rs4588 had strong linkage disequilibrium withr2≥0.8andD′≥0.8. Haplotype (GC rs17467825, rs4588) GC was associated with the less risk for generalized aggressive periodontitis (OR = 0.29, 95% CI: 0.09–0.96,p=0.043). In group AgP, individuals with combined genotype (GC rs17467825, rs4588) AG+CA had significantly lower plasmatic DBP level than those with the other two combined genotypes (AG+CA versus AA+CCp=0.007; AG+CA versus GG+AAp=0.026).Conclusions. GC rs17467825 genotype GG and haplotype (GC rs17467825, rs4588) GC are associated with generalized aggressive periodontitis. The association may be acquired through regulating DBP levels. The functions of GC gene and DBP in inflammatory disease need to be further studied.

Growth factor regulation of uncoupling protein-1 mRNA expression in brown adipocytes

2002 ◽  
Vol 282 (1) ◽  
pp. C105-C112 ◽  
Author(s):  
Bibian García ◽  
Maria-Jesús Obregón
Keyword(s):  
Growth Factor ◽  
Adipocyte Differentiation ◽  
Uncoupling Protein ◽  
Brown Adipocyte ◽  
Mrna Levels ◽  
Uncoupling Protein 1 ◽  
Brown Adipocytes ◽  
Proliferation And Differentiation ◽  
Epidermal Growth ◽  
Continuous Presence

To study the effect of the mitogens epidermal growth factor (EGF), acidic and basic fibroblast growth factors (aFGF and bFGF), and vasopressin on brown adipocyte differentiation, we analyzed the expression of uncoupling protein-1 (UCP-1) mRNA. Quiescent brown preadipocytes express high levels of UCP-1 mRNA in response to triiodothyronine (T3) and norepinephrine (NE). The addition of serum or the mitogenic condition aFGF + vasopressin + NE or EGF + vasopressin + NE decreases UCP-1 mRNA. A second addition of mitogens further decreases UCP-1 mRNA. Treatment with aFGF or bFGF alone increases UCP-1 mRNA, whereas the addition of EGF or vasopressin dramatically reduces UCP-1 mRNA levels. The continuous presence of T3 increases UCP-1 mRNA levels in cells treated with EGF, aFGF, or bFGF. The effect of T3 on the stimulation of DNA synthesis also was tested. T3 inhibits the mitogenic activity of aFGF and bFGF. In conclusion, mitogens like aFGF or bFGF allow brown adipocyte differentiation, whereas EGF and vasopressin inhibit the differentiation process. T3 behaves as an important hormone that regulates both brown adipocyte proliferation and differentiation.

scholarly journals Are Proteinase 3 and Cathepsin C Enzymes Related to Pathogenesis of Periodontitis?

2014 ◽  
Vol 2014 ◽  
pp. 1-7 ◽  
Author(s):  
Oya Türkoğlu ◽  
Elif Azarsız ◽  
Gülnur Emingil ◽  
Necil Kütükçüler ◽  
Gül Atilla
Keyword(s):  
Gingival Crevicular Fluid ◽  
Periodontal Diseases ◽  
Study Groups ◽  
Aggressive Periodontitis ◽  
Control Group ◽  
Proteinase 3 ◽  
Cathepsin C ◽  
Probing Depth ◽  
Inflammatory Processes ◽  
Crevicular Fluid

Aim. Cathepsin C is the activator of the polymorphonuclear leukocyte-derived proteinase 3, which contributes to inflammatory processes. The aim of the present study was to investigate gingival crevicular fluid (GCF) proteinase 3 and cathepsin C levels in periodontal diseases.Design. Eighteen patients with chronic periodontitis (CP), 20 patients with generalized aggressive periodontitis (G-AgP), 20 patients with gingivitis, and 18 healthy subjects were included in the study. Periodontal parameters including probing depth, clinical attachment level, papilla bleeding index, and plaque index were assessed in all study subjects. GCF proteinase 3 and cathepsin C levels were analyzed by ELISA.Results. GCF proteinase 3 total amount was significantly higher in diseased groups compared to control group, after adjusting ageP<0.05. No differences were found in GCF cathepsin C levels among the study groupsP>0.05. Periodontal parameters of sampling sites were positively correlated with GCF proteinase 3 total amountsP<0.01but not with cathepsin C total amountsP>0.05.Conclusions. Elevated levels of GCF proteinase 3 in CP, G-AgP, and gingivitis might suggest that proteinase 3 plays a role during inflammatory periodontal events in host response. However, cathepsin C in GCF does not seem to have an effect on the pathogenesis of periodontal diseases.

scholarly journals Gab1 and SHP-2 promote Ras/MAPK regulation of epidermal growth and differentiation

2002 ◽  
Vol 159 (1) ◽  
pp. 103-112 ◽  
Author(s):  
Ti Cai ◽  
Keigo Nishida ◽  
Toshio Hirano ◽  
Paul A. Khavari
Keyword(s):  
Epidermal Cell ◽  
Mapk Signaling ◽  
Dominant Negative ◽  
Mapk Activity ◽  
Ras Activation ◽  
Proliferation And Differentiation ◽  
Epidermal Proliferation ◽  
Epidermal Growth ◽  
Docking Protein

În epidermis, Ras can influence proliferation and differentiation; however, regulators of epidermal Ras function are not fully characterized, and Ras effects on growth and differentiation are controversial. EGF induced Ras activation in epidermal cells along with phosphorylation of the multisubstrate docking protein Gab1 and its binding to SHP-2. Expression of mutant Gab1Y627F deficient in SHP-2 binding or dominant-negative SHP-2C459S reduced basal levels of active Ras and downstream MAPK proteins and initiated differentiation. Differentiation triggered by both Gab1Y627F and SHP-2C459S could be blocked by coexpression of active Ras, consistent with Gab1 and SHP-2 action upstream of Ras in this process. To study the role of Gab1 and SHP-2 in tissue, we generated human epidermis overexpressing active Gab1 and SHP-2. Both proteins stimulated proliferation. In contrast, Gab1Y627F and SHP-2C459S inhibited epidermal proliferation and enhanced differentiation. Consistent with a role for Gab1 and SHP-2 in sustaining epidermal Ras/MAPK activity, Gab1−/− murine epidermis displayed lower levels of active Ras and MAPK with postnatal Gab1−/− epidermis, demonstrating the hypoplasia and enhanced differentiation seen previously with transgenic epidermal Ras blockade. These data provide support for a Ras role in promoting epidermal proliferation and opposing differentiation and indicate that Gab1 and SHP-2 promote the undifferentiated epidermal cell state by facilitating Ras/MAPK signaling.

scholarly journals Clinical Factors Influencing the Efficacy of Systemic Moxifloxacin in the Therapy of Patients With Generalized Aggressive Periodontitis: A Multilevel Analysis From a Clinical Trial

2015 ◽  
Vol 8 (3) ◽  
pp. 80 ◽  
Author(s):  
Carlos M. Ardila ◽  
Isabel C. Guzmán
Keyword(s):  
Clinical Trial ◽  
Multilevel Analysis ◽  
Linear Models ◽  
Clinical Results ◽  
Aggressive Periodontitis ◽  
Continuous Variables ◽  
Clinical Factors ◽  
Probing Depth ◽  
Clinical Benefits ◽  
Multilevel Linear Models

<p><strong>BACKGROUND:</strong> It has been reported that clinical results of mechanical periodontal treatment could differ between subjects and among different sites of the tooth in the patient. The objective of this multilevel analysis is to investigate clinical factors at subject and sites of the tooth that influence variations in clinical attachment (CAL) increase and probing depth (PD) diminution of adjunctive moxifloxacin (MOX) at six months post-treatment in generalized aggressive periodontitis.</p> <p><strong>METHODS:</strong> This clinical trial included 40 patients randomly distributed to two therapy protocols: scaling and root planing alone or combined with MOX. Multilevel linear models for continuous variables were formulated to evaluate the clinical impact of the hierarchical configuration of periodontal data.</p> <p><strong>RESULTS:</strong> Six months following therapy, the divergences between both protocols were statistically significant in PD diminution and CAL increase, favouring the MOX therapy (p&lt;0.001). Besides, the multilevel analysis revealed that adjunctive MOX at the subject level, non-molar and the interaction non-molar x MOX at the tooth level, interproximal sites and the interaction interproximal sites x MOX at the site level, were statistically significant factors in determining CAL increase and PD diminution.</p> <p><strong>CONCLUSIONS:</strong> The main cause of variability in CAL gain and PD reduction following adjunctive MOX was attributable to the tooth level. Adjunctive MOX and their interactions with non-molar and interproximal sites showed higher clinical benefits at the tooth and site levels which could be essential for PD reduction and CAL gain in generalized aggressive periodontitis subjects.</p>

MAPK Cascades in Cell Growth and Death

Physiology ◽  
1997 ◽  
Vol 12 (6) ◽  
pp. 286-293 ◽  
Author(s):  
JT Neary
Keyword(s):  
Gene Expression ◽  
Signal Transduction ◽  
Cellular Proliferation ◽  
Inflammatory Diseases ◽  
Growth Arrest ◽  
Therapeutic Strategies ◽  
Extracellular Signals ◽  
Mapk Cascades ◽  
Proliferation And Differentiation ◽  
Signaling Components

Distinct signal transduction cascades comprised of at least three proteinkinases mediate cellular proliferation and differentiation, growth arrest, and programmed cell death. These cytosolic enzymes relay extracellular signals from cell surface to nucleus, leading to changes in gene expression. Signaling components of these cascades offer new possibilities for therapeutic strategies in tumorigenesis, inflammatory diseases, immunopotentiation, wound healing, and regeneration.

Inappropriate expression of human transforming growth factor (TGF)-α in the uterus of transgenic mouse causes downregulation of TGF-β receptors and delays the blastocyst-attachment reaction

1997 ◽  
Vol 18 (3) ◽  
pp. 243-257 ◽  
Author(s):  
S K Das ◽  
H Lim ◽  
J Wang ◽  
B C Paria ◽  
M BazDresch ◽  
...  
Keyword(s):  
Growth Factor ◽  
Transforming Growth Factor ◽  
Receptor Subtypes ◽  
Transforming Growth Factor Α ◽  
Decidual Cells ◽  
Proliferation And Differentiation ◽  
Epidermal Growth ◽  
Β Receptor ◽  
Factor Α ◽  
Inappropriate Expression

ABSTRACT In the mouse, the initiation of the attachment reaction between the blastocyst trophectoderm and luminal epithelium of the receptive uterus occurs in the evening (2200-2300 h) of day 4 of pregnancy (day 1=vaginal plug) and is followed by proliferation and differentiation of stromal cells into decidual cells at the sites of blastocyst attachment. This investigation demonstrates that an inappropriate expression of the human transforming growth factor α (hTGF-α) transgene in the uterus under the direction of a mouse metallothionein-I promoter downregulates uterine expression of TGF-β receptor subtypes and delays the initiation of implantation (attachment reaction) resulting in delayed parturition. This delay in the attachment reaction is accompanied by deferred uterine expression of amphiregulin. The results suggest that a coordinated 'cross-talk' between the signaling pathways executed by epidermal growth factor-like growth factors and TGF-βs is important for the normal implantation process.

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