Connexin37, not Cx40 and Cx43, is induced in vascular smooth muscle cells during coronary arteriogenesis.
W.-J. Cai, S. Koltai, E. Kocsis, D. Scholz, W. Schaper and J. Schaper. Connexin37, not Cx40 and Cx43, is Induced in Vascular Smooth Muscle Cells During Coronary Arteriogenesis. Journal of Molecular and Cellular Cardiology (2001) 33, 957-967. The hypothesis that an altered expression of gap junction (GJ) proteins, connexin37 (Cx37), Cx40 and Cx43 will contribute to adaptive arteriogenesis was tested in growing coronary collateral vessels (CV) of the dog heart by immunoconfocal microscopy and transmission electron microscopy (TEM). We found that: (1) in the normal coronary system Cx37 and Cx40 were only expressed in endothelial cells (EC) from artery to capillary; (2) during collateral growth Cx37 was significantly induced in smooth muscle cells (SMC) from small-large arteries to precapillary arterioles (Ø=15 microm), while Cx40 was still only present in EC; (3) both homogeneous and heterogeneous distribution of Cx37 was observed in normal vessels (NV) and growing vessels (GV); (4) in mature vessels (MV), Cx37 was downregulated, similar to NV; (5) dual immunostaining revealed an inverse correlation between expression of Cx37 and desmin in GV occurring prior to downregulation of alpha-smooth actin and calponin; (6) Cx43 was undetectable in any vascular cells, both in NV and GV; (7) GJ were not found in SMC by TEM. Our data for the first time show the profile of connexin expression in the coronary system and provide evidence for existence of GJ proteins in capillaries. It is a novel finding that an altered expression of Cx37 is characteristic of adaptive arteriogenesis in the dog heart and may be used as a marker of vascular growth. Induced Cx37 may be an early signal indicating that SMC are responding to haemodynamic changes, i.e. increased shear stress.
Cai
W J
WJ
Max Planck Institute, Dept. of Experimental Cardiology, Benekestr. 2, Bad Nauheim, 61231, Germany.
Koltai
S
S
Kocsis
E
E
Scholz
D
D
Schaper
W
W
Schaper
J
J
D000199:Actins / Q000096:biosynthesis; D000818:Animals; D002135:Calcium-Binding Proteins / Q000096:biosynthesis / Q000378:metabolism; D018031:Connexin 43 / Q000096:biosynthesis*; D017630:Connexins / Q000096:biosynthesis* / Q000378:metabolism; D003893:Desmin / Q000378:metabolism; D004285:Dogs; D015536:Down-Regulation; D004730:Endothelium, Vascular / Q000378:metabolism; D007150:Immunohistochemistry; D037102:Lectins / Q000378:metabolism; D008840:Microfilament Proteins; D018613:Microscopy, Confocal; D008854:Microscopy, Electron; D009131:Muscle, Smooth, Vascular / Q000378:metabolism*; D009206:Myocardium / Q000378:metabolism* / Q000648:ultrastructure; D018919:Neovascularization, Physiologic; D000096985:Calponins; D000097003:Gap Junction alpha-5 Protein; D000097006:Gap Junction alpha-4 Protein
D000199:Actins; D002135:Calcium-Binding Proteins; D018031:Connexin 43; D017630:Connexins; D003893:Desmin; D037102:Lectins; D008840:Microfilament Proteins; D000096985:Calponins; D000097003:Gap Junction alpha-5 Protein; D000097006:Gap Junction alpha-4 Protein