Involvement of CLEC16A in Activation of Astrocytes After LPS Treated

Wu, Xinmin; Li, Jing; Chen, Chun; Yan, Yaohua; Jiang, Shengyang; Wu, Xiaohong; Shao, Bai; Xu, Jin; Kang, Lihua; Huang, Yeqing; Zhu, Lin; Ji, Yuhong; Gao, Yilu

doi:10.1007/s11064-011-0581-4

Cited by 20 publications

(13 citation statements)

References 31 publications

(23 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…CLEC16A expression was strongly induced in active astrocytes in inflamed cerebral cortex. In vitro studies indicated that the up-regulation of CLEC16A may be involved in astrocyte activation following LPS challenge [72]. …”

Section: Genetic Component In Type 1 Diabetesmentioning

confidence: 99%

Genes Involved in Type 1 Diabetes: An Update

Bakay

Pandey

Hákonarson

2013

Genes

View full text Add to dashboard Cite

Type 1 Diabetes (T1D) is a chronic multifactorial disease with a strong genetic component, which, through interactions with specific environmental factors, triggers disease onset. T1D typically manifests in early to mid childhood through the autoimmune destruction of pancreatic β cells resulting in a lack of insulin production. Historically, prior to genome-wide association studies (GWAS), six loci in the genome were fully established to be associated with T1D. With the advent of high-throughput single nucleotide polymorphism (SNP) genotyping array technologies, enabling investigators to perform high-density GWAS, many additional T1D susceptibility genes have been discovered. Indeed, recent meta-analyses of multiple datasets from independent investigators have brought the tally of well-validated T1D disease genes to almost 60. In this mini-review, we address recent advances in the genetics of T1D and provide an update on the latest susceptibility loci added to the list of genes involved in the pathogenesis of T1D.

show abstract

Section: Genetic Component In Type 1 Diabetesmentioning

confidence: 99%

Genes Involved in Type 1 Diabetes: An Update

Bakay

Pandey

Hákonarson

2013

Genes

View full text Add to dashboard Cite

show abstract

“…CLEC16A, however, could have evolved to play a much different role in humans (as seen by its preferential expression in immune cells). Another study found that CLEC16A was induced in activated rat astrocytes harvested from the inflamed cerebral cortices of rats that have been injected with lipopolysaccharide (LPS), and suggests that it may be involved in the astrocyte-mediated immune response [26]. This result merely correlates the presence of CLEC16A with astrocyte inflammation, and needs to be investigated in further detail.…”

Section: Introductionmentioning

confidence: 99%

Functional evaluation of the role of C-type lectin domain family 16A at the chromosome 16p13 locus

Zouk

d’Hennezel

et al. 2014

Clinical and Experimental Immunology

View full text Add to dashboard Cite

SummaryThe type 1 diabetes-associated 16p13 locus contains the CLEC16A gene. Its preferential immune cell expression suggests involvement in autoimmunity. Given its elevated expression in dendritic and B cells -known professional antigen-presenting cells (APCs) -we hypothesize that C-type lectin domain family 16 member A (CLEC16A) may be involved in T cell co-stimulation and consequent activation and proliferation. We also sought to identify CLEC16A's subcellular localization. The effect of the CLEC16A knock-down (KD) on B cell co-stimulation and activation of T cells was tested in human lymphoblastoid cell lines (LCLs) by co-culture with CD4 + T cells. T cell activation and proliferation were determined by flow-cytometric analysis of CD69 and CD25 expression and carboxyfluorescein succinimidyl ester (CFSE) dilution, respectively. CLEC16A subcellular localization in K562 cells was examined by immunofluorescence. We show that the CLEC16A KD did not affect the tested indices of lymphoblastoid cell line (LCL) APC capacity. Additionally, the percentage of activated T cells following LCL co-culture was not affected significantly by the CLEC16A KD. T cells co-cultured with KD or control LCLs also exhibited similar cell division profiles. CLEC16A co-localized with an endoplasmic reticulum (ER) marker, suggesting that it may be an ER protein. In conclusion, CLEC16A may not be involved in T cell co-stimulation. Additional studies on CLEC16A, accounting for its ER localization, are needed to uncover its biological role.

show abstract

“…After pulp injury regulation of innervation and inflammation is important to preserve pulpal health trough both regulation of re-innervation and intrapulpal tissue pressure. Significant markers for neural development up-regulated in pulp cells after EMD treatment were CLEC16A [33] with effect on activation and control of neuroinflammation, CNTNAP5 involved in CNS development [34] and NFASC that regulate neural development and axon innervations [35]. …”

Section: Discussionmentioning

confidence: 99%

Enamel Matrix Derivative Promote Primary Human Pulp Cell Differentiation and Mineralization

Riksen

Landin

Reppe

et al. 2014

IJMS

View full text Add to dashboard Cite

Enamel matrix derivative (EMD) has been found to induce reactive dentin formation; however the molecular mechanisms involved are unclear. The effect of EMD (5–50 μg/mL) on primary human pulp cells were compared to untreated cells and cells incubated with 10−8 M dexamethasone (DEX) for 1, 2, 3, 7, and 14 days in culture. Expression analysis using Affymetrix microchips demonstrated that 10 μg/mL EMD regulated several hundred genes and stimulated the gene expression of proteins involved in mesenchymal proliferation and differentiation. Both EMD and DEX enhanced the expression of amelogenin (amel), and the dentinogenic markers dentin sialophosphoprotein (DSSP) and dentin matrix acidic phosphoprotein 1 (DMP1), as well as the osteogenic markers osteocalcin (OC, BGLAP) and collagen type 1 (COL1A1). Whereas, only EMD had effect on alkaline phosphatase (ALP) mRNA expression, the stimulatory effect were verified by enhanced secretion of OC and COL1A from EMD treated cells, and increased ALP activity in cell culture medium after EMD treatment. Increased levels of interleukin-6 (IL-6), interleukin-8 (IL-8), and monocyte chemoattractant proteins (MCP-1) in the cell culture medium were also found. Consequently, the suggested effect of EMD is to promote differentiation of pulp cells and increases the potential for pulpal mineralization to favor reactive dentine formation.

show abstract

Involvement of CLEC16A in Activation of Astrocytes After LPS Treated

Cited by 20 publications

References 31 publications

Genes Involved in Type 1 Diabetes: An Update

Genes Involved in Type 1 Diabetes: An Update

Functional evaluation of the role of C-type lectin domain family 16A at the chromosome 16p13 locus

Enamel Matrix Derivative Promote Primary Human Pulp Cell Differentiation and Mineralization

Contact Info

Product

Resources

About