Proteomic Profiling and Differential Messenger RNA Expression Correlate HSP27 and Serpin Family B Member 1 to Apical Periodontitis Outcomes

Cavalla, Franco; Biguetti, Cláudia Cristina; Jain, Sameer; Johnson, Cleverick D; Letra, Ariadne; Garlet, Gustavo; Silva, Renato

doi:10.1016/j.joen.2017.03.014

Cited by 11 publications

(10 citation statements)

References 34 publications

(34 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…TIMP1 is a matrix metalloproteinase inhibitor with a critical role in bone remodeling and homeostasis; imbalances in TIMP gene expression may be related to increased or decreased bone resorption 33 . Interestingly, previous studies showed that SERPINB1, TIMP1 and COL1A1 were upregulated in AP lesions 30,34 . The expression of TIMP1 and COL1A1 was significantly higher in inactive AP lesions when compared to active lesions 30 .…”

Section: Discussionmentioning

confidence: 95%

WNT gene polymorphisms and predisposition to apical periodontitis

Souza

Cavalla

Maili

et al. 2019

Sci Rep

Self Cite

View full text Add to dashboard Cite

Single nucleotide polymorphisms (SNPs) in WNT genes may impact gene/protein function and contribute to individual predisposition to apical periodontitis (AP). Here, we investigated the association of SNPs in/nearby WNT3, WNT3A, WNT5A, WNT8A, WNT9B and WNT11 genes with AP using a case-control dataset. Cases were defined as individuals with deep caries and AP (n = 188); controls had deep caries and no AP (n = 230). Genotyping was performed using Taqman chemistry in real time PCR. Data analyses was performed using Fisher Exact tests assuming a Bonferroni correction threshold value of 0.005. Single-SNP association analysis revealed a trend for association with WNT3 rs9890413 genotypes (P = 0.009) under a dominant model and allelic association for WNT3A rs1745420 (P = 0.009). Haplotypes involving WNT3-WNT9B-WNT3A alleles were also significantly associated with AP (P ≤ 0.003). Luciferase reporter assays showed higher transcriptional activity (1.4-fold) with the alternate G allele in rs1745420. Expression of WNT3, WNT3A and WNT5A in AP tissues was significantly higher than in control tissues, and inversely correlated with the expression of SERPINB1, COL1A1 and TIMP1 (P < 0.05). Our results suggest that WNT genes have a role in modulating AP and polymorphisms in these genes may increase susceptibility to AP.

show abstract

Section: Discussionmentioning

confidence: 95%

WNT gene polymorphisms and predisposition to apical periodontitis

Souza

Cavalla

Maili

et al. 2019

Sci Rep

Self Cite

View full text Add to dashboard Cite

show abstract

“…Despite being mainly associated with the direct killing of bacteria and tissue necrosis, neutrophils are also capable of releasing molecular mediators into the extracellular compartment and influencing the later stages of the response (117, 118). Accordingly, a significant increase in heat shock protein 27 (HSP27) and Serpin Family B member 1 (SERPINB1) protein levels were identified in apical periodontitis compared to healthy tissues (119). HSP27 belongs to the heat shock protein gene family and has an essential role in the inhibition of apoptosis in thermal and chemical stress, protecting the cells from injury in hostile environments (120).…”

Section: Apical Periodontitismentioning

confidence: 99%

“…The role of another Serpin family member (SERPINE1) has been demonstrated in the stabilization of apical lesions (122), thus pointing to a molecular pathway of Serpin family proteins regulating PMN functions and periodontal destruction in apical periodontitis. Importantly, this increased expression of HSP27 and SERPINB1 was compartmentalized to epithelial cells and infiltrating neutrophils in the inflammatory front (119). The expression of HSP27 and SERPINB1 was inversely correlated with markers of acute inflammation and markedly increased in apical lesion characterized as “stable/inactive.” This evidence suggests that HSP27 and SERPINB1 could be putative markers of lesion regression and useful to follow the outcome of endodontic treatment…”

Section: Apical Periodontitismentioning

confidence: 99%

Osteoimmunology of Oral and Maxillofacial Diseases: Translational Applications Based on Biological Mechanisms

et al. 2019

Self Cite

View full text Add to dashboard Cite

The maxillofacial skeleton is highly dynamic and requires a constant equilibrium between the bone resorption and bone formation. The field of osteoimmunology explores the interactions between bone metabolism and the immune response, providing a context to study the complex cellular and molecular networks involved in oro-maxillofacial osteolytic diseases. In this review, we present a framework for understanding the potential mechanisms underlying the immuno-pathobiology in etiologically-diverse diseases that affect the oral and maxillofacial region and share bone destruction as their common clinical outcome. These otherwise different pathologies share similar inflammatory pathways mediated by central cellular players, such as macrophages, T and B cells, that promote the differentiation and activation of osteoclasts, ineffective or insufficient bone apposition by osteoblasts, and the continuous production of osteoclastogenic signals by immune and local stromal cells. We also present the potential translational applications of this knowledge based on the biological mechanisms involved in the inflammation-induced bone destruction. Such applications can be the development of immune-based therapies that promote bone healing/regeneration, the identification of host-derived inflammatory/collagenolytic biomarkers as diagnostics tools, the assessment of links between oral and systemic diseases; and the characterization of genetic polymorphisms in immune or bone-related genes that will help diagnosis of susceptible individuals.

show abstract

“…MMPs are synthesized and secreted as inactive precursors and their activation is a cascade process. Besides their natural substrates in the extracellular matrix, they are also able to degrade and modulate the biological activity of other molecules such as cytokines, growth factors and chemokines involved in periodontal diseases [17]. In oral diseases, a significant up-regulation of saliva levels of MMPs indicates that most extracellular matrix components undergo digestion to lower molecular weight forms [18].…”

Section: Introductionmentioning

confidence: 99%

Gelatinolytic activity in gingival crevicular fluid and saliva of growing patients with Marfan syndrome: a case-control study

Laganà¹,

Fasciglione²,

Biondi³

et al. 2019

BMC Oral Health

View full text Add to dashboard Cite

Background Aim of the study was to evaluate the gelatinolytic activity in the saliva and gingival crevicular fluid from a sample group of subjects with Marfan syndrome. Methods Two groups were analyzed in this case-control study. A group of 28 subjects with Marfan syndrome (MG) was recruited from the Centre for Rare Disease, Marfan Clinic of Tor Vergata University Hospital. The second sample, 23 subjects, with the same characteristics and without any syndrome, was the control group (CG). Saliva and gingival crevicular fluid were collected and transferred to a sterile test tube and stored frozen at − 20 °C until analysis at the Medical Chemistry Laboratory. Gelatin substrate zymography was used for the evaluation and characterization of saliva and crevicular fluid proteinases. Correlation test and Student’s t-test have been used to analyze data. Results In all samples different gelatin-degrading activities were observed. Two bands, which are related to the molecular weights of pro-MMP-9 and active MMP-9, respectively, were detectable in 100% of Marfan and control samples. MMP-2 activity was higher in Marfan group. Additional bands (55/48 kDa), corresponding to the activated forms of collagenase (MMP-13), were observed in saliva samples of both groups. Conclusions The association of an enhanced activity by MMP-13 with an increased amount of active MMP-9 might be an important biomarker for the diagnosis of Marfan syndrome.

show abstract

Proteomic Profiling and Differential Messenger RNA Expression Correlate HSP27 and Serpin Family B Member 1 to Apical Periodontitis Outcomes

Cited by 11 publications

References 34 publications

WNT gene polymorphisms and predisposition to apical periodontitis

WNT gene polymorphisms and predisposition to apical periodontitis

Osteoimmunology of Oral and Maxillofacial Diseases: Translational Applications Based on Biological Mechanisms

Gelatinolytic activity in gingival crevicular fluid and saliva of growing patients with Marfan syndrome: a case-control study

Contact Info

Product

Resources

About