Here, we explored the role of S. mutans’s whole cell and discrete fractions in the degradation of type I collagen and dentinal collagen. Type I collagen gels and human demineralized dentin slabs (DS) were incubated in media alone or with one of the following: overnight (O/N) or newly inoculated (NEW) cultures of S. mutans UA159; intracellular proteins, supernatant or bacterial membranes of O/N cultures. Media from all groups were analyzed for protease-mediated release of the collagen-specific imino acid hydroxyproline. Images of type I collagen and DS were analyzed, respectively. Type I collagen degradation was highest for the supernatant (p < 0.05) fractions, followed by intracellular components and O/N cultures. Collagen degradation for DS samples was highest for O/N samples, followed by supernatant, and intracellular components (p < 0.05). There was lower detectable degradation for both type I collagen and DS from NEW culture samples (p < 0.05), and there was no type I collagen or DS degradation detected for bacterial membrane samples. Structural changes to type I collagen gel and dentinal collagen were observed, respectively, following incubation with S. mutans cultures (O/N and NEW), intracellular components, and supernatant. This study demonstrates that intracellular and extracellular proteolytic activities from S. mutans enable this cariogenic bacterium to degrade type I and dentinal collagen in a growth-phase dependent manner, potentially contributing to the progression of dental caries.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9776523 | PMC |
| http://dx.doi.org/10.3390/dj10120223 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Multifunctional DNA-Collagen Biomaterials: Developmental Advances and Biomedical Applications.
ACS Biomater Sci Eng
January 2025
J. Crayton Pruitt Family Department of Biomedical Engineering, University of Florida, Gainesville, Florida 32611, United States.
The complexation of nucleic acids and collagen forms a platform biomaterial greater than the sum of its parts. This union of biomacromolecules merges the extracellular matrix functionality of collagen with the designable bioactivity of nucleic acids, enabling advances in regenerative medicine, tissue engineering, gene delivery, and targeted therapy. This review traces the historical foundations and critical applications of DNA-collagen complexes and highlights their capabilities, demonstrating them as biocompatible, bioactive, and tunable platform materials.
View Article and Find Full Text PDFThe underlying mechanisms of the association of bone health with depression - an experimental study.
Mol Biol Rep
January 2025
Medical Sociology and Psychobiology, Department of Health and Physical Activity, University of Potsdam, 14469, Potsdam, Germany.
Background: Depression constitutes a risk factor for osteoporosis, but underlying molecular and cellular mechanisms are not fully understood. MiRNAs influence gene expression and are carried by extracellular vesicles (EV), affecting cell-cell communication.
Aims: (1) Identify the difference in miRNA expression between depressed patients and healthy controls; (2) Analyze associations of these miRNAs with bone turnover markers; (3) Analyze target genes of differentially regulated miRNAs and predict associated pathways regarding depression and bone metabolism.
A facile combined therapy of chemotherapeutic agent and microRNA for hepatocellular carcinoma using non-cationic nanogel.
J Mater Chem B
January 2025
Department of Radiology, The Third Affiliated Hospital, Sun Yat-Sen University, Guangzhou 510630, P. R. China.
High drug resistance remains a challenge for chemotherapy against hepatocellular carcinoma (HCC). Combining chemotherapeutic agents with microRNA (miRNA), which simultaneously regulates multiple pathways, offers a promising approach to improve therapeutic efficacy against HCC. Although cationic amphiphilic copolymers have been used to co-deliver these agents, their effectiveness is often limited by low co-encapsulation efficiency and inherent cationic toxicity.
View Article and Find Full Text PDFA Novel COL7A1 Mutation in a Patient With Dystrophic Epidermolysis Bullosa. Successful Treatment With Upadacitinib.
Clin Cosmet Investig Dermatol
January 2025
Department of Dermatology, Candidate Branch of National Clinical Research Centre for Skin and Immune Diseases, First Affiliated Hospital of Gannan Medical University, Ganzhou, 341000, People's Republic of China.
Dystrophic epidermolysis bullosa (DEB) is a heterogeneous and rare genetic skin disease caused by mutations in the gene, which encodes Type VII collagen. The absence or dysfunction of Type VII collagen can cause the dense lower layer of the basal membrane zone of the skin to separate from the dermis, leading to blister formation and various complications. In different DEB subtypes, the severity of the phenotype is associated, to some extent, with the outcome of Type VII collagen caused by mutations in the gene, which may be reduced in expression, remarkably reduced, or completely absent.
View Article and Find Full Text PDFType IV collagen derived non-collagenous domain α6 (IV) NC1 and its derivative fragments inhibit endothelial cell proliferation and attenuates chorioallantoic membrane angiogenesis.
Cytotechnology
April 2025
Department of Genetics, Osmania University, Hyderabad, Telangana State India.
Targeting tumor angiogenesis with safe endogenous protein inhibitors is a promising therapeutic approach despite the plethora of the first line of emerging chemotherapeutic drugs. The extracellular matrix network in the blood vessel basement membrane and growth factors released from endothelial and tumor cells promote the neovascularization which supports the tumor growth. Contrastingly, small cleaved cryptic fragments of the C-terminal non collagenous domains of the same basement membrane display antiangiogenic effect.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!