Differential gene expression analysis identifies murine Cacnb3 as strongly upregulated in distinct dendritic cell populations upon stimulation
Author(s)
Bros, Matthias
Dexheimer, Nadine
Ross, Ralf
Trojandt, Stefanie
Hoehn, Yvette
Tampe, Jens
Sutter, Arne
Jaehrling, Frank
Grabbe, Stephan
Reske-Kunz, Angelika B
Griffith University Author(s)
Year published
2011
Metadata
Show full item recordAbstract
Langerhans cells (LCs) represent the dendritic cell (DC) population in the epidermis. Among the set of genes induced in primary mouse LCs in response to stimulation, both isoforms of the voltage-dependent Ca2+ channel (VDCC) regulatory subunit Cacnb3 as well as the DC maturation marker Fscn1 were upregulated most strongly. Comparable results were obtained for a recently described myeloid DC line (SP37A3). Other antigen presenting cell populations, namely, bone marrow-derived DCs, macrophages and primary B cells, showed no stimulation-associated upregulation of Cacnb3 expression. Pharmacological inhibition of Ca2+ channel ...
View more >Langerhans cells (LCs) represent the dendritic cell (DC) population in the epidermis. Among the set of genes induced in primary mouse LCs in response to stimulation, both isoforms of the voltage-dependent Ca2+ channel (VDCC) regulatory subunit Cacnb3 as well as the DC maturation marker Fscn1 were upregulated most strongly. Comparable results were obtained for a recently described myeloid DC line (SP37A3). Other antigen presenting cell populations, namely, bone marrow-derived DCs, macrophages and primary B cells, showed no stimulation-associated upregulation of Cacnb3 expression. Pharmacological inhibition of Ca2+ channel activity during the stimulation of SP37A3 cells enhanced their T cell stimulatory capacity, while selective inhibition of L-type VDCC had no effect. Both Cacnb3 isoforms, similar to Fscn1, required JNK and p38 kinase activity for stimulation-associated upregulation, and this process was inhibited by ERK and PI(3)K. The putative promoter region of Cacnb3 isoform 2, which we found to be less ubiquitously expressed than Cacnb3 isoform 1, exerted reporter activity in LC-like cell lines. Our findings suggest that Cacnb3 exerts its function in distinct activated DC populations. Further analysis of the regulatory region(s) facilitating stimulation-induced upregulation of Cacnb3 expression in these DC subsets will help to gain better insight into DC subset specific gene regulation.
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View more >Langerhans cells (LCs) represent the dendritic cell (DC) population in the epidermis. Among the set of genes induced in primary mouse LCs in response to stimulation, both isoforms of the voltage-dependent Ca2+ channel (VDCC) regulatory subunit Cacnb3 as well as the DC maturation marker Fscn1 were upregulated most strongly. Comparable results were obtained for a recently described myeloid DC line (SP37A3). Other antigen presenting cell populations, namely, bone marrow-derived DCs, macrophages and primary B cells, showed no stimulation-associated upregulation of Cacnb3 expression. Pharmacological inhibition of Ca2+ channel activity during the stimulation of SP37A3 cells enhanced their T cell stimulatory capacity, while selective inhibition of L-type VDCC had no effect. Both Cacnb3 isoforms, similar to Fscn1, required JNK and p38 kinase activity for stimulation-associated upregulation, and this process was inhibited by ERK and PI(3)K. The putative promoter region of Cacnb3 isoform 2, which we found to be less ubiquitously expressed than Cacnb3 isoform 1, exerted reporter activity in LC-like cell lines. Our findings suggest that Cacnb3 exerts its function in distinct activated DC populations. Further analysis of the regulatory region(s) facilitating stimulation-induced upregulation of Cacnb3 expression in these DC subsets will help to gain better insight into DC subset specific gene regulation.
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Journal Title
Gene
Volume
472
Issue
1-2
Subject
Genetics
Zoology
Allergy
Cellular immunology
Medical microbiology