Modulatory Effect of Glycated Collagen on Oral Streptococcal Nanoadhesion

2020 ◽  
Vol 100 (1) ◽  
pp. 82-89
Author(s):  
C.M.A.P. Schuh ◽  
B. Benso ◽  
P.A. Naulin ◽  
N.P. Barrera ◽  
L. Bozec ◽  
...  
Keyword(s):  
Dental Caries ◽  
Biofilm Formation ◽  
Type I Collagen ◽  
Type I ◽  
Oral Streptococci ◽  
Oral Diseases ◽  
Collagen Crosslinking ◽  
Initial Adhesion ◽  
Collagen Glycation ◽  
The Impact

Biofilm-mediated oral diseases such as dental caries and periodontal disease remain highly prevalent in populations worldwide. Biofilm formation initiates with the attachment of primary colonizers onto surfaces, and in the context of caries, the adhesion of oral streptococci to dentinal collagen is crucial for biofilm progression. It is known that dentinal collagen suffers from glucose-associated crosslinking as a function of aging or disease; however, the effect of collagen crosslinking on the early adhesion and subsequent biofilm formation of relevant oral streptococci remains unknown. Therefore, the aim of this work was to determine the impact of collagen glycation on the initial adhesion of primary colonizers such as Streptococcus mutans UA159 and Streptococcus sanguinis SK 36, as well as its effect on the early stages of streptococcal biofilm formation in vitro. Type I collagen matrices were crosslinked with either glucose or methylglyoxal. Atomic force microscopy nanocharacterization revealed morphologic and mechanical changes within the collagen matrix as a function of crosslinking, such as a significantly increased elastic modulus in crosslinked fibrils. Increased nanoadhesion forces were observed for S. mutans on crosslinked collagen surfaces as compared with the control, and retraction curves obtained for both streptococcal strains demonstrated nanoscale unbinding behavior consistent with bacterial adhesin-substrate coupling. Overall, glucose-crosslinked substrates specifically promoted the initial adhesion, biofilm formation, and insoluble extracellular polysaccharide production of S. mutans, while methylglyoxal treatment reduced biofilm formation for both strains. Changes in the adhesion behavior and biofilm formation of oral streptococci as a function of collagen glycation could help explain the biofilm dysbiosis seen in older people and patients with diabetes. Further studies are necessary to determine the influence of collagen crosslinking on the balance between acidogenic and nonacidogenic streptococci to aid in the development of novel preventive and therapeutic treatment against dental caries in these patients.

scholarly journals Virtual Screening and Biological Evaluation of Anti-Biofilm Agents Targeting LuxS in the Quorum Sensing System

2021 ◽  
Vol 16 (6) ◽  
pp. 1934578X2110196
Author(s):  
Zheng Liu ◽  
Lihua Zhang ◽  
Jincai Wang ◽  
Yanping Li ◽  
Yiqun Chang ◽  
...  
Keyword(s):  
Dental Caries ◽  
Quorum Sensing ◽  
Biofilm Formation ◽  
Binding Mode ◽  
Biological Evaluation ◽  
Oral Diseases ◽  
Traditional Use ◽  
New Approach ◽  
Sensing System ◽  
Plaque Biofilm

Biofilm formation is considered as a crucial factor in various oral diseases, such as dental caries. The quorum sensing (QS) signaling system was proved to have a crucial role in the microbial dental plaque biofilm formation of Streptococcus mutans ( S. mutans). LuxS was critical to regulating the QS system and survival of the bacterium, and, therefore, compounds which target LuxS may be a potential therapy for dental caries. The binding activities of 37,170 natural compounds to LuxS were virtually screened in this study. Baicalein and paeonol were chosen for further research of the binding mode and ΔG values with LuxS. Both baicalein and paeonol inhibited the biofilm formation without influence on the growth of S. mutans. Baicalein also distinctly reduced the production of both rhamnolipids and acids. The results provide us with a new approach to combat dental caries instead of the traditional use of antibacterial chemicals.

scholarly journals The Dynamic Interaction between Extracellular Matrix Remodeling and Breast Tumor Progression

Cells ◽  
2021 ◽  
Vol 10 (5) ◽  
pp. 1046
Author(s):  
Jorge Martinez ◽  
Patricio C. Smith
Keyword(s):  
Extracellular Matrix ◽  
Type I Collagen ◽  
Cell Metabolism ◽  
Breast Tumors ◽  
Extracellular Matrix Remodeling ◽  
Type I ◽  
Matrix Remodeling ◽  
Desmoplastic Reaction ◽  
The Impact

Desmoplastic tumors correspond to a unique tissue structure characterized by the abnormal deposition of extracellular matrix. Breast tumors are a typical example of this type of lesion, a property that allows its palpation and early detection. Fibrillar type I collagen is a major component of tumor desmoplasia and its accumulation is causally linked to tumor cell survival and metastasis. For many years, the desmoplastic phenomenon was considered to be a reaction and response of the host tissue against tumor cells and, accordingly, designated as “desmoplastic reaction”. This notion has been challenged in the last decades when desmoplastic tissue was detected in breast tissue in the absence of tumor. This finding suggests that desmoplasia is a preexisting condition that stimulates the development of a malignant phenotype. With this perspective, in the present review, we analyze the role of extracellular matrix remodeling in the development of the desmoplastic response. Importantly, during the discussion, we also analyze the impact of obesity and cell metabolism as critical drivers of tissue remodeling during the development of desmoplasia. New knowledge derived from the dynamic remodeling of the extracellular matrix may lead to novel targets of interest for early diagnosis or therapy in the context of breast tumors.

Trabecular Bone is Increased in a Rat Model of Polycystic Ovary Syndrome

2020 ◽  
Author(s):  
Lady Katerine Serrano Mujica ◽  
Werner Giehl Glanzner ◽  
Amanda Luiza Prante ◽  
Vitor Braga Rissi ◽  
Gabrielle Rebeca Everling Correa ◽  
...  
Keyword(s):  
Polycystic Ovary Syndrome ◽  
Bone Formation ◽  
Type I Collagen ◽  
Polycystic Ovary ◽  
Osteoclast Differentiation ◽  
Bone Volume ◽  
Negative Regulator ◽  
Type I ◽  
Ovary Syndrome ◽  
The Impact

AbstractPolycystic ovary syndrome (PCOS) in an intricate disorder characterized by reproductive and metabolic abnormalities that may affect bone quality and strength along with the lifespan. The present study analysed the impact of postnatal androgenization (of a single dose of testosterone propionate 1.25 mg subcutaneously at day 5 of life) on bone development and markers of bone metabolism in adult female Wistar rats. Compared with healthy controls, the results of measurements of micro-computed tomography (microCT) of the distal femur of androgenized rats indicated an increased cortical bone volume voxel bone volume to total volume (VOX BV/TV) and higher trabecular number (Tb.n) with reduced trabecular separation (Tb.sp). A large magnitude effect size was observed in the levels of circulating bone formation Procollagen I N-terminal propeptide (P1NP) at day 60 of life; reabsorption cross-linked C-telopeptide of type I collagen (CTX) markers were similar between the androgenized and control rats at days 60 and 110 of life. The analysis of gene expression in bone indicated elements for an increased bone mass such as the reduction of the Dickkopf-1 factor (Dkk1) a negative regulator of osteoblast differentiation (bone formation) and the reduction of Interleukin 1-b (Il1b), an activator of osteoclast differentiation (bone reabsorption). Results from this study highlight the possible role of the developmental programming on bone microarchitecture with reference to young women with PCOS.

Osteogenesis Imperfecta: The Impact of Genotype and Clinical Phenotype on Adiposity and Resting Energy Expenditure

2021 ◽  
Author(s):  
Kaitlin L Ballenger ◽  
Nicol Tugarinov ◽  
Sara K Talvacchio ◽  
Marianne M Knue ◽  
An N Dang Do ◽  
...  
Keyword(s):  
Energy Expenditure ◽  
Osteogenesis Imperfecta ◽  
Type I Collagen ◽  
Resting Energy Expenditure ◽  
Type I ◽  
Healthy Controls ◽  
Type Iv ◽  
Reduced Mobility ◽  
The Impact ◽  
Resting Energy

Abstract Context Mutations in type I collagen or collagen-related proteins cause Osteogenesis Imperfecta (OI). Energy expenditure and body composition in OI could reflect reduced mobility, or intrinsic defects in osteoblast differentiation increasing adipocyte development. Objective Compare adiposity and resting energy expenditure (REE) in OI and healthy controls (HC), for OI genotype- and Type-associated differences. Design/Setting/Participants We studied 90 participants, 30 with OI (13 COL1A1 Gly, 6 COL1A2 Gly, 3 COL1A1 non-Gly, 2 COL1A2 non-Gly, 6 non-COL; 8 Type III, 16 Type IV, 4 Type VI, 1 Type VII, 1 Type XIV) and 60 HC with sociodemographic characteristics/BMI/BMIz similar to the OI group. Participants underwent dual-energy X-ray absorptiometry to determine lean mass and fat mass percentage (FM%) and REE. FM% and REE were compared, adjusting for covariates to examine the relationship of OI genotypes and phenotypic Types. Results FM% did not differ significantly in all patients with OI versus HC (OI: 36.6±1.9%, HC: 32.7±1.2%, p =0.088). FM% was, however, greater than HC for those with non-COL variants (p=0.018). FM% did not differ from HC among OI Types (p’s>0.05). Overall, covariate-adjusted REE did not differ significantly between OI and HC (OI: 1376.5±44.7 kcal/d, healthy controls: 1377.0±96 kcal/d p=0.345). However, those with non-COL variants (p=0.034) and Type VI OI (p=0.04) had significantly lower REE than HC. Conclusions Overall, patients with OI did not significantly differ in either extra-marrow adiposity or REE from BMI-similar HC. However, reduced REE among those with non-COL variants may contribute to greater adiposity.

scholarly journals ΕGFR/ERβ-Mediated Cell Morphology and Invasion Capacity Are Associated with Matrix Culture Substrates in Breast Cancer

Cells ◽  
2020 ◽  
Vol 9 (10) ◽  
pp. 2256
Author(s):  
Konstantina Kyriakopoulou ◽  
Eirini Riti ◽  
Zoi Piperigkou ◽  
Konstantina Koutroumanou Sarri ◽  
Heba Bassiony ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Cell Morphology ◽  
Breast Cancer Cells ◽  
Type I Collagen ◽  
Morphological Characteristics ◽  
Migration And Invasion ◽  
Type I ◽  
Egfr Inhibition ◽  
The Impact

Breast cancer accounts for almost one in four cancer diagnoses in women. Studies in breast cancer patients have identified several molecular markers, indicators of aggressiveness, which help toward more individual therapeutic approaches. In triple-negative breast cancer (TNBC), epidermal growth factor receptor (EGFR) overexpression is associated with increased metastatic potential and worst survival rates. Specifically, abnormal EGFR activation leads to altered matrix metalloproteinases’ (MMPs) expression and, hence, extracellular matrix (ECM) degradation, resulting in induced migration and invasion. The use of matrix substrates for cell culture gives the opportunity to mimic the natural growth conditions of the cells and their microenvironment, as well as cell–cell and cell–matrix interactions. The aim of this study was to evaluate the impact of EGFR inhibition, estrogen receptor beta (ERβ) and different matrix substrates [type I collagen and fibronectin (FN)] on the functional properties, expression of MMPs and cell morphology of ERβ-positive TNBC cells and shERβ ones. Our results highlight EGFR as a crucial regulator of the expression and activity levels of MMPs, while ERβ emerges as a mediator of MMP7 and MT1-MMP expression. In addition, the EGFR/ERβ axis impacts the adhesion and invasion potential of breast cancer cells on collagen type I. Images obtained by scanning electron microscope (SEM) from cultures on the different matrix substrates revealed novel observations regarding various structures of breast cancer cells (filopodia, extravesicles, tunneling nanotubes, etc.). Moreover, the significant contribution of EGFR and ERβ in the morphological characteristics of these cells is also demonstrated, hence highlighting the possibility of dual pharmacological targeting.

scholarly journals Suppressive Effects of Octyl Gallate on Streptococcus mutans Biofilm Formation, Acidogenicity, and Gene Expression

Molecules ◽  
2019 ◽  
Vol 24 (17) ◽  
pp. 3170 ◽  
Author(s):  
Vika Gabe ◽  
Tomas Kacergius ◽  
Saleh Abu-Lafi ◽  
Mouhammad Zeidan ◽  
Basheer Abu-Farich ◽  
...  
Keyword(s):  
Gene Expression ◽  
Dental Caries ◽  
Streptococcus Mutans ◽  
Biofilm Formation ◽  
Colorimetric Method ◽  
Solid Surfaces ◽  
Dependent Manner ◽  
Oral Diseases ◽  
Expression Change ◽  
Biofilm Development

The accumulation of biofilm by Streptococcus mutans bacteria on hard tooth tissues leads to dental caries, which remains one of the most prevalent oral diseases. Hence, the development of new antibiofilm agents is of critical importance. The current study reports the results from testing the effectiveness of octyl gallate (C8-OG) against: (1) S. mutans biofilm formation on solid surfaces (polystyrene, glass), (2) acidogenicity, (3) and the expression of biofilm-related genes. The amount of biofilm formed by S. mutans bacteria was evaluated using the colorimetric method and optical profilometry. The pH of the biofilm growth medium was measured with microelectrode. A quantitative reverse transcription-polymerase chain reaction (RT-qPCR) was used to assess the expression of genes encoding glucan binding protein B (gbpB), glucosyltransferases B, -C, -D (gtfB, -C, -D), and the F-ATPase β subunit of the F1 protein (atpD). The results show that C8-OG significantly diminished biofilm formation by exposed S. mutans on solid surfaces and suppressed acidogenicity in a dose-dependent manner, compared to unexposed bacteria (p < 0.05). The C8-OG concentration of 100.24 µM inhibited S. mutans biofilm development on solid surfaces by 100% and prevented a decrease in pH levels by 99%. In addition, the RT-qPCR data demonstrate that the biofilm-producing bacteria treated with C8-OG underwent a significant reduction in gene expression in the case of the four genes under study (gbpB, gtfC, gtfD, and atpD), and there was a slight decrease in expression of the gtfB gene. However, C8-OG treatments did not produce significant expression change compared to the control for the planktonic cells, although there was a significant increase for the atpD gene. Therefore, C8-OG might be a potent antibiofilm and/or anticaries agent for oral formulations that aim to reduce the prevalence of dental caries.

scholarly journals Contractile properties of EDL and soleus muscles of myostatin-deficient mice

2006 ◽  
Vol 101 (3) ◽  
pp. 898-905 ◽  
Author(s):  
Christopher L. Mendias ◽  
James E. Marcin ◽  
Daniel R. Calerdon ◽  
John A. Faulkner
Keyword(s):  
Type I Collagen ◽  
Contractile Properties ◽  
Negative Regulator ◽  
Type I ◽  
Lengthening Contractions ◽  
Tetanic Force ◽  
The Difference ◽  
The Impact ◽  
Deficient Mice

Myostatin is a negative regulator of muscle mass. The impact of myostatin deficiency on the contractile properties of healthy muscles has not been determined. We hypothesized that myostatin deficiency would increase the maximum tetanic force (Po), but decrease the specific Po(sPo) of muscles and increase the susceptibility to contraction-induced injury. The in vitro contractile properties of extensor digitorum longus (EDL) and soleus muscles from wild-type ( MSTN+/+), heterozygous-null ( MSTN+/−), and homozygous-null ( MSTN−/−) adult male mice were determined. For EDL muscles, the Poof both MSTN+/−and MSTN−/−mice were greater than the Poof MSTN+/+mice. For soleus muscles, the Poof MSTN−/−mice was greater than that of MSTN+/+mice. The sPoof EDL muscles of MSTN−/−mice was less than that of MSTN+/+mice. For soleus muscles, however, no difference in sPowas observed. Following two lengthening contractions, EDL muscles from MSTN−/−mice had a greater force deficit than that of MSTN+/+or MSTN+/−mice, whereas no differences were observed for the force deficits of soleus muscles. Myostatin-deficient EDL muscles had less hydroxyproline, and myostatin directly increased type I collagen mRNA expression and protein content. The difference in the response of EDL and soleus muscles to myostatin may arise from differences in the levels of a myostatin receptor, activin type IIB. Compared with the soleus, the amount of activin type IIB receptor was approximately twofold greater in EDL muscles. The results support a significant role for myostatin not only in the mass of muscles but also in the contractility and the composition of the extracellular matrix of muscles.

Anti-Biofilm Formation of Streptococcus mutans by Jasmine Mouthwash

2018 ◽  
Vol 773 ◽  
pp. 323-327
Author(s):  
Sroisiri Thaweboon ◽  
Boonyanit Thaweboon
Keyword(s):  
Dental Caries ◽  
Streptococcus Mutans ◽  
Biofilm Formation ◽  
Antimicrobial Activities ◽  
Inhibitory Effect ◽  
Negative Control ◽  
Oral Streptococci ◽  
Drug Of Choice ◽  
Causative Microorganism ◽  
Warm Temperate

Streptococcus mutans has been reported to be a major causative microorganism for oral biofilm associated with dental caries. Jasmine sambac or Arabian jasmine is a species of jasmine native to tropical and warm temperate regions particularly West and Southeast Asia. The antimicrobial activities of essential oil extracted from the flowers of J. sambac have been shown to attract researchers. Objective: To determine the anti-biofilm formation of S. mutans by mouthwash containing jasmine oil. Materials and Methods: S. mutans KPSK2, the cariogenic strain of oral streptococci was used in the study. The 24-h biofilms of S. mutans were formed on polystyrene plates treated with jasmine mouthwash. The 0.2% chlorhexidine gluconate and phosphate buffer saline mouthwash were used as a positive and negative control respectively. The amount of biofilm was quantified by crystal violet staining and spectrophotometry at an optical density of 595 nm. Results: Jasmine mouthwash showed a significant inhibitory effect on S. mutans biofilm formation by decreasing 43% of biofilm whereas that of chlorhexidine showed 71% reduction. Conclusion: The anti-biofilm formation property of jasmine mouthwash was elucidated; therefore it might be another drug of choice that can be used as an adjunct to control the oral health in the prevention of dental caries.

scholarly journals Impact of acetaminophen consumption and resistance exercise on extracellular matrix gene expression in human skeletal muscle

2017 ◽  
Vol 313 (1) ◽  
pp. R44-R50 ◽  
Author(s):  
Shivam H. Patel ◽  
Andrew C. D’Lugos ◽  
Erica R. Eldon ◽  
Donald Curtis ◽  
Jared M. Dickinson ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Extracellular Matrix ◽  
Resistance Exercise ◽  
Mrna Expression ◽  
Human Skeletal Muscle ◽  
Type I Collagen ◽  
Type Iii Collagen ◽  
Type I ◽  
Matrix Gene ◽  
The Impact

Acetaminophen (APAP) given during chronic exercise reduces skeletal muscle collagen and cross-linking in rats. We propose that the effect of APAP on muscle extracellular matrix (ECM) may, in part, be mediated by dysregulation of the balance between matrix metalloproteinases (MMPs) and tissue inhibitors of MMPs (TIMPs). The purpose of this study was to evaluate the impact of APAP consumption during acute resistance exercise (RE) on several regulators of the ECM in human skeletal muscle. In a double-blinded, placebo-controlled, randomized crossover design, recreationally active men ( n = 8, 25 ± 2 yr) performed two trials of knee extension. Placebo (PLA) or APAP (1,000 mg/6 h) was given for 24 h before and immediately following RE. Vastus lateralis biopsies were taken at baseline and 1 and 3 h post-RE. Quantitative RT-PCR was used to determine differences in mRNA expression. MMP-2, type I collagen, and type III collagen mRNA expression was not altered by exercise or APAP ( P > 0.05). When compared with PLA, TIMP-1 expression was lower at 1 h post-RE during APAP conditions but greater than PLA at 3 h post-RE ( P < 0.05). MMP-9 expression and protein levels were elevated at 3 h post-RE independent of treatment ( P < 0.05). Lysyl oxidase expression was greater at 3 h post-RE during APAP consumption ( P < 0.05) compared with PLA. MMP-2 and TIMP-1 protein was not altered by RE or APAP ( P > 0.05). Phosphorylation of ERK1/2 and p38-MAPK increased ( P < 0.05) with RE but was not influenced by APAP. Our findings do not support our hypothesis and suggest that short-term APAP consumption before RE has a small impact on the measured ECM molecules in human skeletal muscle following acute RE.

NP603, a novel and potent inhibitor of FGFR1 tyrosine kinase, inhibits hepatic stellate cell proliferation and ameliorates hepatic fibrosis in rats

2011 ◽  
Vol 301 (2) ◽  
pp. C469-C477 ◽  
Author(s):  
Nan Lin ◽  
Si Chen ◽  
Weidong Pan ◽  
Linan Xu ◽  
Kunpeng Hu ◽  
...  
Keyword(s):  
Tyrosine Kinase ◽  
Hepatic Fibrosis ◽  
Hepatic Stellate Cell ◽  
Type I Collagen ◽  
Kinase Inhibitor ◽  
Stellate Cell ◽  
Smooth Muscle Actin ◽  
Type I ◽  
Promising Therapeutic Approach ◽  
The Impact

Fibroblast growth factor 2 (FGF-2) and its main receptor FGFR1 have been shown to promote hepatic stellate cell (HSC) activation and proliferation. However, scant information is available on the anti-fibrogenic activity of FGFR1 inhibitors. The aim of this study was to assess the impact of a selective FGFR1 tyrosine kinase inhibitor NP603 on HSC proliferation and hepatic fibrosis. We demonstrated that rat primary HSCs secreted significant amounts of FGF-2, and its tyrosine phosphorylation of FGFR1 was attenuated by NP603. NP603 inhibited HSC activaton by measuring the expression of α-smooth muscle actin (α-SMA) and the production of type I collagen using ELISA. Furthermore, NP603 (25 μM) in vitro strongly suppressed HSC growth induced by FGF-2 (10 ng/ml) and FCS. This effect correlated with the suppression of extracellular-regulated kinase (ERK) activity and its downstream targets cyclin D1 and p21. In addition, PO NP603 (20 mg·kg−1·day−1) administration significantly decreased hepatic collagen deposition and α-SMA expression in CCl4-treated rats. Collectively, these studies suggest that selective blocking of the FGFR1-mediated pathway could be a promising therapeutic approach for the treatment of hepatic fibrosis.

Sign in / Sign up

Export Citation Format

Share Document