ANGPTL1

Last update 08 May 2025

Basic Info

Synonyms

ANG-3, ANG3, angiopoietin like 1

+ [7]

Introduction-

100 Clinical Results associated with ANGPTL1

100 Translational Medicine associated with ANGPTL1

0 Patents (Medical) associated with ANGPTL1

114

Literatures (Medical) associated with ANGPTL1

01 May 2025·International Endodontic Journal

FoxO1 mediates odontoblast differentiation of hDPSCs via B cell‐derived ANGPTL1 in dental caries: A laboratory investigation

Article

Author: Zhan, Peimeng ; Lin, Zhengmei ; Shen, Zongshan ; Wang, Runfu ; Xie, Zhuo ; Huang, Qiting ; Zhang, Xinfang ; Chen, Lingling ; Huang, Zhu ; Huang, Shuheng

AbstractAimClinical and in vitro evidence indicates that chronic inflammatory responses initiated by dental caries can persist in the dental pulp even after treatment, necessitating the formation of reparative dentin to restore tissue homeostasis and health. Human dental pulp stem cells (hDPSCs) serve as crucial precursors in this reparative process. This study explores the role of B cells and their secreted factor, Angiopoietin Like 1 (ANGPTL1), in promoting hDPSCs differentiation into odontoblasts under carious conditions, with a particular focus on the activation of Forkhead box O1 (FoxO1).MethodologySingle‐cell RNA sequencing (scRNA‐Seq) data from the GEO database were analysed to explore cellular interactions and molecular mechanisms in dental pulp. Immunofluorescence staining was used to investigate the expression patterns of B cells or hDPSCs in dental pulp and hydroxyapatite/tricalcium phosphate (HA/TCP) scaffolds. The expression levels of ANGPTL1 were quantified using enzyme‐linked immunosorbent assay (ELISA). Odontoblast differentiation capacity was assessed by alkaline phosphatase activity, alizarin red S staining, and western blotting analysis. hDPSCs were overexpressed or knocked down FoxO1 with lentiviruses. The regulatory interaction between FoxO1 and the DSPP promoter was evaluated through dual‐luciferase reporter assay and chromatin immunoprecipitation assay. Statistical analyses were conducted using Student's t‐test or one‐way analysis of variance (anova) with a p‐value of <.05 considered statistically significant.ResultsscRNA‐Seq data indicated a significant increase in B cells and ANGPTL1 expression in carious dental pulp. Functional analyses confirmed that ANGPTL1 secreted by B cells activated FoxO1 expression in hDPSCs, enhancing their differentiation into odontoblast‐like cells. Blocking ANGPTL1 signalling with a specific antibody reduced FoxO1 expression, indicating a regulatory link between ANGPTL1 and FoxO1. Overexpression of FoxO1 in hDPSCs promoted their differentiation into odontoblasts and facilitated mineralized matrix formation. Mechanistic studies revealed that FoxO1 directly binds to the DSPP promoter, thereby inducing its expression.ConclusionsOur study reveals a novel mechanism in which ANGPTL1 secreted by B cells in a carious environment promotes the odontoblast differentiation of hDPSCs by upregulating FoxO1. This finding highlights a potential therapeutic target for enhancing dental pulp repair and regeneration.

01 Apr 2025·Journal of Cellular and Molecular Medicine

Associations Between APOC3 and ANGPTL8 Gene Polymorphisms With MASLD Risk and the Mediation Effect of Triglyceride on MASLD in the Chinese Population

Article

Author: Wang, Xue ; Song, Yongyan ; Zhang, Xiaoli ; Wang, Ting ; Zhang, Youjin ; Zhou, Yuanyuan ; Pan, Jia ; Lv, Saiqun ; Peng, Tao

ABSTRACTApolipoprotein C3 (APOC3) and angiopoietin‐like protein 8 (ANGPTL8) genes are related to lipid metabolism. The relationships between single nucleotide polymorphisms (SNPs) in the APOC3 and ANGPTL8 genes with metabolic dysfunction‐associated steatotic liver disease (MASLD) remain controversial. This study aimed to investigate the associations between specific SNPs in the APOC3 and ANGPTL8 genes and MASLD risk, with a particular focus on the mediating role of triglycerides (TG). A total of 440 participants were enrolled and categorised into MASLD and control groups. Genotyping of APOC3 SNPs (rs5128, rs2854116 and rs2854117) and ANGPTL8 SNP (rs2278426) was conducted using polymerase chain reaction–restriction fragment length polymorphism or Sanger sequencing methods. Multivariate logistic regression was employed to estimate the associations between these SNPs and MASLD risk, and mediation analysis was performed to assess the potential mediating effect of TG. We found that APOC3 SNPs were associated with MASLD risk, with increased odds ratios (ORs) indicating a higher risk of MASLD: rs5128 CG + GG genotype (OR = 1.8, 95% CI = 1.1–2.8), rs2854116 TC + CC genotype (OR = 1.9, 95% CI = 1.1–3.1) and rs2854117 CT + TT genotype (OR = 1.9, 95% CI = 1.2–3.2). No association was found between ANGPTL8 rs2278426 and MASLD (p > 0.05). Mediation analysis revealed that TG significantly mediated these relationships, accounting for 80.25% of the effect for rs5128, 64.61% for rs2854116 and 62.59% for rs2854117. In summary, polymorphisms in APOC3 (rs5128, rs2854116 and rs2854117) were associated with MASLD risk, with TG serving as a potential mediating factor. In contrast, ANGPTL8 rs2278426 polymorphism did not show any association with MASLD.

01 Oct 2024·Computational Biology and Chemistry

Single-cell transcriptome sequencing revealed the metabolic changes and microenvironment changes of cardiomyocytes induced by diabetes

Article

Author: Yu, Haiqiao ; Yan, Shuang ; Zhou, Weiyu

PURPOSEDiabetes is a chronic metabolic disorder characterized by elevated blood glucose levels. This study aimed to analyze the changes underlying heterogeneities and communication properties of CMs in diabetes mellitus (DM).METHODSGSE213337 dataset was retrieved from NCBI Gene Expression Omnibus, containing the single-cell RNA sequencing data of hearts from the control and streptozotocin-induced diabetic mice. GSEA and GSVA were used to explore the function enrichment of DEGs in CM. Cell communication analysis was carried out to study the altered signals and significant ligand-receptor interactions.RESULTSSeventeen cell types were identified between DM and the controls. The increasing ratio of CM suggested the occurrence of diabetes induces potential pathological changes of CM proliferation. A total of 1144 DEGs were identified in CM. GSEA and GSVA analysis indicated the enhancing lipid metabolism involving in DM. The results of cell communication analysis suggested that high glucose activated the ability of CM receiving fibroblast and LEC, while inhibited the capacity of receiving ECC and pericyte. Furthermore, GAS and ANGPTL were significantly decreased under DM, which was consistent with the results of GSEA and GSVA. Finally, the ligand-receptor interactions such as vegfc-vegfr2, angptl1 were changes in CM.CONCLUSIONSThe CM showed the significant heterogeneities in DM, which played an important role in myocardial fibrosis induce by hyperglycemia.

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ANGPTL1

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