Connexin 32 fused to the green fluorescent protein retains its ability to control the proliferation of thyroid cells.
Cell Commun Adhes
; 8(4-6): 447-52, 2001.
Article
in En
| MEDLINE
| ID: mdl-12064633
ABSTRACT
Cell-to-cell exchanges of signaling molecules are thought to be involved in the control of cell proliferation. Connexins, which are encoded by a family of genes expressed in a cell type-specific manner, are considered as tumor suppressors. Thyroid epithelial cells co-express connexin 32 (Cx32) and connexin 43 (Cx43) that form distinct and delocalized gap junctions in vivo. The communication-deficient rat thyroid-derived cell lines, FRTL-5 and FRT, stably transfected with the Cx32 cDNA, have a reduced proliferation rate related to a prolonged G1 cell cycle phase. To determine whether Cx32-gap junctions exert the same regulatory role in vivo, we have undertaken a program of production of transgenic mice over-expressing Cx32 specifically in thyrocytes. To this purpose, we designed a vector in which the Cx32 cDNA was fused to the gene encoding the enhanced green fluorescent protein (EGFP) and placed under the control of a strong and thyroid-specific promoter, the thyroglobulin gene promoter (pTg). In stably transfected FRTL-5 cells, the Cx32/EGFP chimeric protein forms functional gap junction channels and induces the same proliferation slowdown as native Cx32. The pTg-Cx32/EGFP construct should thus allow us to obtain the thyroid-targeted over-expression of Cx32 in the mouse to investigate the involvement of Cx32-gap junctions in thyroid growth, functional activity and propensity to form tumors.
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Collection:
01-internacional
Database:
MEDLINE
Main subject:
Thyroid Gland
/
Cell Division
/
Connexins
Limits:
Animals
Language:
En
Journal:
Cell Commun Adhes
Year:
2001
Document type:
Article
Affiliation country:
Francia