Ask about this productRelated genes to: Sdc3 Blocking Peptide
- Gene:
- SDC3 NIH gene
- Name:
- syndecan 3
- Previous symbol:
- -
- Synonyms:
- N-syndecan, SYND3
- Chromosome:
- 1p35.2
- Locus Type:
- gene with protein product
- Date approved:
- 1994-05-16
- Date modifiied:
- 2014-11-19
Related products to: Sdc3 Blocking Peptide
Related articles to: Sdc3 Blocking Peptide
- Low back pain is a leading cause of disability worldwide, and lumbar intervertebral disc degeneration (IVDD) is strongly associated with its development. Recent studies have shown that the gut microbiota (GM) and its metabolites may be involved in the occurrence and development of IVDD through the gut-disc axis. However, the key microbes mediating this process and their specific molecular mechanisms remain unclear. - Source: PubMed
Publication date: 2026/04/24
Liu HaoXie BinZhuo HangHe BowenDai JiahuiZhou ZelinShen GengyangChen BinweiTang JingjingRen HuiJiang Xiaobing - Reliable and disease-specific blood biomarkers are critically needed for Alzheimer's disease (AD), particularly in early stages when interventions are most effective. Although phosphorylated tau and neurofilament light chain (NfL) are widely used, their diagnostic specificity has been reported to decrease in elderly populations with multimorbidities. Syndecan-3 (SDC3), a heparan sulfate proteoglycan implicated in amyloid and tau aggregation, has recently emerged as a mechanistically relevant biomarker candidate. In this clinically realistic cohort study, we examined 46 participants, including 23 clinically diagnosed AD patients and 23 age-matched non-AD individuals with psychiatric and/or metabolic comorbidities. SDC3 expression was quantified in peripheral blood mononuclear cells (PBMCs), while soluble SDC3 and NfL were measured in plasma. Both PBMC-expressed and plasma SDC3 levels were elevated in AD compared with non-AD participants and showed a strong intercorrelation, whereas plasma NfL was likewise increased in AD. Individually, PBMC-SDC3, plasma SDC3, and NfL demonstrated moderate discriminatory performance. However, multivariable models integrating SDC3 (PBMC or plasma), NfL, and age achieved substantially improved discrimination (AUC > 0.8). SDC3 did not correlate with NfL, consistent with a biological signal distinct from neuroaxonal injury and reflective of peripheral immune-metabolic remodeling. Together, these findings identify SDC3 as a blood-based biomarker associated with systemic immune remodeling that complements established neuronal markers in a clinically realistic AD versus non-AD comparison. While exploratory, this study supports further investigation of SDC3 within integrated, multi-domain biomarker strategies in larger and independent cohorts. - Source: PubMed
Publication date: 2026/02/06
Hudák AnettLetoha AnnamáriaLetoha Tamás - Our earlier study demonstrated that metabolic disorders increase the expression of Syndecan-3 (Sdc-3), a heparan sulfate proteoglycan (HSPG) in erythrocytes, contributing to adhesion through the glycosaminoglycan chain. Reactive oxygen species (ROS) could be one of the factors for increased expression. This study aimed to determine whether quercetin, a bioactive antioxidant commonly found in food, could modulate Sdc-3 expression. Male Wistar rats were made dyslipidemic and diabetic, after which they were treated with quercetin at doses of 50 and 100 mg/kg body weight for a duration of 2 months. Sdc-3 expression in erythrocytes was assessed by Western blot, and erythrocyte adhesion to fibronectin was evaluated in-vitro. The quercetin-supplemented diet reduced circulating lipids, blood glucose, and MDA levels, mitigated changes in Sdc-3 expression, and decreased erythrocyte adhesion to fibronectin. These effects may be attributed to quercetin's antioxidant properties, as was seen by the positive correlation between MDA levels and Sdc-3 expression. Sdc-3 levels in erythrocytes could serve as a prognostic marker for assessing the impact of dietary compounds on complications linked to metabolic disorders. - Source: PubMed
Mallanna Smitha HonnalagereChilkunda Nandini D - Oral leukoplakia and proliferative verrucous leukoplakia represent oral potentially malignant disorders. Oral leukoplakia typically presents as solitary lesions, while proliferative verrucous leukoplakia manifests as multifocal lesions with higher malignant potential. This study aimed to investigate the genetic heterogeneity between these disorders through differential gene expression, genetic variants, and microRNA profiling to identify potential biomarkers for diagnosis and prognosis. - Source: PubMed
Publication date: 2026/03/01
Pérez-Sayáns MVieira-E-Silva F-FFernández-Rozadilla CCarracedo ÁCarlés-González SLorenzo-Pouso A-IPérez-Jardón AGándara-Vila PGarcía-García ASuárez-Peñaranda J-MBlanco-Carrión AChamorro-Petronacci C-M - Amyotrophic lateral sclerosis (ALS) is a multisystem progressive neurodegenerative disease. A recent theory of ALS onsetting pathogenesis proposed that the initiating primary damage is an acquired irreversible intrafusal proprioceptive terminal PIEZO2 channelopathy with underlying genetic and environmental risk factors. This Piezo2 channelopathy may also disrupt the ultrafast proton-based oscillatory signaling to motor neurons through vesicular transporter 1 (VGLUT1) and to the hippocampus through VGLUT2. As a result, it may gradually degenerate motor neurons in which process K1.2 ion channels are gradually depleted. It also gradually depletes heat shock transcription factor-1 (HSF-1) in the hippocampus, hence negatively affecting adult hippocampal neurogenesis. Syndecans, especially syndecan-3 (SDC3) in the nervous system, may act as critical players in the maintenance of the crosstalk between Piezo ion channels. Hence, our goal was to reanalyze the potential pathogenic gene variants from the cohort of our previous ALS study with a special focus on the aforementioned genes. Reanalysis of data formerly acquired by whole-exome sequencing of 21 non-related adult ALS patients was carried out with a focus on 28 genes. Accordingly, we identified charge-altering variants of SDC3 in 13 patients out of 21 that may contribute to the impairment of the Piezo crosstalk, and the progressive loss of the proposed proton-based signaling to motor neurons and to the hippocampus. A variant of uncertain significance was identified in the gene that may facilitate the faster loss of K1.2 ion function on motor neurons when Piezo2 channelopathy prevails. Not to mention that one variant was identified in the potassium current rectifying ion channels encoding and genes that may also propel the ALS disease process and provide the autoimmune-like pathogenic background. Moreover, Piezo2 channelopathy likely promotes diminishing HSF1 function in the hippocampus in the presence of the identified variant. The current findings may support the ALS onsetting acquired irreversible Piezo2 channelopathy-induced pathogenesis. However, the preliminary nature of these findings needs validation and further functional studies on cohorts with a larger sample size in the future. - Source: PubMed
Publication date: 2025/10/21
Sonkodi BalázsNagy Zsófia FlóraKeller-Pintér AnikóKlivényi PéterMolnár Mária JuditSzéll Márta