Related Experiment Video
Updated: Dec 23, 2025
05:37
Experimental Model of Ligature-Induced Peri-Implantitis in Mice
Published on: May 17, 2024
3.1K
Sdccag3 Promotes Implant Osseointegration during Experimental Hyperlipidemia
1Department of Prosthodontics, School and Hospital of Stomatology, Shandong University & Shandong Provincial Key Laboratory of Oral Tissue Regeneration & Shandong Engineering Laboratory for Dental Materials and Oral Tissue Regeneration, Jinan, Shandong, China.
Journal of Dental Research
|April 28, 2020
Summary
This study reveals that Serologically defined colon cancer antigen 3 (Sdccag3) protein enhances implant osseointegration in hyperlipidemic rats by interacting with lncRNA-MSTRG.97162.4. Modulating this network may improve dental implant success rates.
Area of Science:
- Biomedical Engineering
- Molecular Biology
- Regenerative Medicine
Background:
- Hyperlipidemia negatively impacts bone metabolism and osseointegration, leading to implant failure.
- Understanding genetic networks is crucial for improving osseointegration, especially in metabolic disorders.
- The role of Serologically defined colon cancer antigen 3 (Sdccag3) in osteogenesis and osseointegration under hyperlipidemia remains unexplored.
Purpose of the Study:
- To investigate the role of Sdccag3 and its associated noncoding RNAs (ncRNAs) in implant osseointegration in a hyperlipidemic rat model.
- To elucidate the molecular mechanisms underlying Sdccag3-mediated effects on bone-implant integration.
- To identify potential therapeutic targets for enhancing osseointegration in hyperlipidemic conditions.
Main Methods:
- Microarray and RNA sequencing were employed to analyze gene and ncRNA expression in bone tissues around implants in hyperlipidemic rats.
- Overexpression and downregulation experiments were conducted for Sdccag3, lncRNA-MSTRG.97162.4, and miR-193a-3p.
- RNA pulldown assays were used to confirm direct interactions between Sdccag3 protein and lncRNA-MSTRG.97162.4.
Main Results:
- Sdccag3 and lncRNA-MSTRG.97162.4 were downregulated, while miR-193a-3p was upregulated in hyperlipidemic rats.
- Overexpression of Sdccag3 significantly improved new bone formation, bone volume/total volume (BV/TV), and bone-implant contact ratio (BIC%).
- Sdccag3 directly targets lncRNA-MSTRG.97162.4, and their co-regulation significantly enhances osseointegration, whereas miR-193a-3p negatively impacts this process.
Conclusions:
- Sdccag3 overexpression promotes implant osseointegration in hyperlipidemia by interacting with lncRNA-MSTRG.97162.4.
- The lncRNA-MSTRG.97162.4/miR-193a-3p/Sdccag3 axis plays a critical role in regulating osseointegration under hyperlipidemic conditions.
- Targeting this network presents a promising therapeutic strategy for improving dental implantation success rates.
Related Concept Videos
01:06Lipid Digestion
98.2K
Lipids are large molecules that are generally not water-soluble. Since most of the digestive enzymes in the human body are water-based, there are specific steps the body must take to break down lipids and make them available for use.
98.2K
01:24Lipid Absorption
2.3K
Dietary triglycerides from chyme in the duodenum are mixed with bile salts produced by the liver to emulsify fats. As a result, large droplets are broken down into smaller ones, increasing the surface area for enzymatic action. Once emulsified, pancreatic lipases hydrolyze the triglycerides into free fatty acids and monoglycerides.
These breakdown products bind with bile salts and lecithin to form micelles, which quickly pass between microvilli to come in close contact with the apical...
These breakdown products bind with bile salts and lecithin to form micelles, which quickly pass between microvilli to come in close contact with the apical...
2.3K