PMID- 29636699
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20200929
IS  - 1664-042X (Print)
IS  - 1664-042X (Electronic)
IS  - 1664-042X (Linking)
VI  - 9
DP  - 2018
TI  - Dendritic Cell Migration Toward CCL21 Gradient Requires Functional Cx43.
PG  - 288
LID - 10.3389/fphys.2018.00288 [doi]
LID - 288
AB  - Dendritic cells (DCs) travel through lymphatic vessels to transport antigens and 
      present them to T cells in lymph nodes. DCs move directionally toward lymphatics 
      by virtue of their CCR7 and a CCL21 chemotactic gradient. We evaluated in vivo 
      and in bone marrow-derived dendritic cells (BMDCs) whether the gap junction 
      protein Cx43 contributes to CCL21/CCR7-dependent DC migration in wild-type (WT) 
      mice, heterozygous (Cx43(+/-)) mice and mice expressing a truncated form of Cx43 
      lacking its regulatory C-terminus (Cx43(K258/-)). In a model of flank skin 
      inflammation, we found that the recruitment of myeloid DCs (mDCs) to skin 
      draining lymph nodes was reduced in Cx43(K258/-) mice as compared to WT and 
      Cx43(+/-) mice. In addition, the migration of Cx43(K258/-) BMDCs toward CCL21 was 
      abolished in an in vitro chemotactic assay while it was only reduced in Cx43(+/-) 
      cells. Both mutant genotypes showed defects in the directionality of BMDC 
      migration as compared to WT BMDCs. No difference was found between the three 
      populations of BMDCs in terms of expression of surface markers (CD11c, CD86, 
      CD80, CD40, MHC-II, and CCR7) after differentiation and TLR activation. Finally, 
      examination of the CCR7-induced signaling pathways in BMDCs revealed normal 
      receptor-induced mobilization of intracellular Ca(2+). These results demonstrate 
      that full expression of an intact Cx43 is critical to the directionality and rate 
      of DC migration, which may be amenable to regulation of the immune response.
FAU - Ruez, Richard
AU  - Ruez R
AD  - Department of Pediatrics, Cell Physiology, and Metabolism, Geneva University 
      Hospitals, University of Geneva, Geneva, Switzerland.
FAU - Dubrot, Juan
AU  - Dubrot J
AD  - Department of Pathology and Immunology, University of Geneva, Geneva, 
      Switzerland.
FAU - Zoso, Alice
AU  - Zoso A
AD  - Department of Pediatrics, Cell Physiology, and Metabolism, Geneva University 
      Hospitals, University of Geneva, Geneva, Switzerland.
FAU - Bacchetta, Marc
AU  - Bacchetta M
AD  - Department of Pediatrics, Cell Physiology, and Metabolism, Geneva University 
      Hospitals, University of Geneva, Geneva, Switzerland.
FAU - Molica, Filippo
AU  - Molica F
AD  - Department of Pathology and Immunology, University of Geneva, Geneva, 
      Switzerland.
FAU - Hugues, Stephanie
AU  - Hugues S
AD  - Department of Pathology and Immunology, University of Geneva, Geneva, 
      Switzerland.
FAU - Kwak, Brenda R
AU  - Kwak BR
AD  - Department of Pathology and Immunology, University of Geneva, Geneva, 
      Switzerland.
FAU - Chanson, Marc
AU  - Chanson M
AD  - Department of Pediatrics, Cell Physiology, and Metabolism, Geneva University 
      Hospitals, University of Geneva, Geneva, Switzerland.
LA  - eng
PT  - Journal Article
DEP - 20180327
PL  - Switzerland
TA  - Front Physiol
JT  - Frontiers in physiology
JID - 101549006
PMC - PMC5880903
OTO - NOTNLM
OT  - chemotaxis
OT  - connexins
OT  - dendritic cells
OT  - mice
OT  - migration
EDAT- 2018/04/11 06:00
MHDA- 2018/04/11 06:01
PMCR- 2018/03/27
CRDT- 2018/04/12 06:00
PHST- 2018/01/12 00:00 [received]
PHST- 2018/03/12 00:00 [accepted]
PHST- 2018/04/12 06:00 [entrez]
PHST- 2018/04/11 06:00 [pubmed]
PHST- 2018/04/11 06:01 [medline]
PHST- 2018/03/27 00:00 [pmc-release]
AID - 10.3389/fphys.2018.00288 [doi]
PST - epublish
SO  - Front Physiol. 2018 Mar 27;9:288. doi: 10.3389/fphys.2018.00288. eCollection 
      2018.