CHRFAM7A reduces monocyte/macrophage migration and colony formation in vitro.
Animals
Cell Adhesion
/ physiology
Cell Movement
/ genetics
Cell Proliferation
/ physiology
Gene Expression
Gene Expression Regulation
HEK293 Cells
Humans
Leukocytes
Macrophages
/ physiology
Mice
Monocytes
/ physiology
RAW 264.7 Cells
Stem Cells
/ physiology
THP-1 Cells
Transduction, Genetic
alpha7 Nicotinic Acetylcholine Receptor
/ antagonists & inhibitors
Dup α7-nicotinic acetylcholine receptor
Human-specific genes
Monocyte migration
Myeloid cell self-renewal
α7-nicotinic acetylcholine receptor
Journal
Inflammation research : official journal of the European Histamine Research Society ... [et al.]
ISSN: 1420-908X
Titre abrégé: Inflamm Res
Pays: Switzerland
ID NLM: 9508160
Informations de publication
Date de publication:
Jul 2020
Jul 2020
Historique:
received:
02
04
2020
accepted:
10
04
2020
revised:
08
04
2020
pubmed:
19
4
2020
medline:
7
10
2020
entrez:
19
4
2020
Statut:
ppublish
Résumé
CHRFAM7A is a unique human gene that encodes a dominant negative inhibitor of the α7 nicotinic acetylcholine receptor. We have recently shown that CHRFAM7A is expressed in human leukocytes, increases cel-cell adhesion, and regulates the expression of genes associated with leukocyte migration. Human THP-1, RAW264.7 and HEK293 cells. Cell migration, cell proliferation and colony formation in soft agar to compare the biological activity of vector vs. CHRFAM7A-transduced cells. We show that gene delivery of CHRFAM7A into the THP-1 human monocytic cell line reduces cell migration, reduces chemotaxis to monocyte chemoattractant protein, and reduces colony formation in soft agar. Taken together, the findings demonstrate that CHRFAM7A regulates the biological activity of monocytes/macrophages to migrate and undergo anchorage-independent growth in vitro.
Identifiants
pubmed: 32303780
doi: 10.1007/s00011-020-01349-7
pii: 10.1007/s00011-020-01349-7
pmc: PMC7263946
mid: NIHMS1585796
doi:
Substances chimiques
Chrna7 protein, human
0
alpha7 Nicotinic Acetylcholine Receptor
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
631-633Subventions
Organisme : NIGMS NIH HHS
ID : R01 GM121530
Pays : United States
Organisme : NIDCD NIH HHS
ID : 5T32DC000028-27
Pays : United States
Organisme : NIGMS NIH HHS
ID : 5R01GM121530-03
Pays : United States
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