PMID- 15063830
OWN - NLM
STAT- MEDLINE
DCOM- 20040809
LR  - 20131121
IS  - 1537-1891 (Print)
IS  - 1537-1891 (Linking)
VI  - 40
IP  - 6
DP  - 2004 Jan
TI  - Aldosterone signaling modifies capillary formation by human bone marrow 
      endothelial cells.
PG  - 269-77
AB  - We investigated the regulation of the epithelial sodium channel (ENaC) in human 
      bone marrow endothelial cells (HBMEC) responding to mineralocorticoid hormones 
      and other accessory effectors. The message for both the mineralocorticoid 
      receptor (MCR) and the alpha subunit of ENaC was expressed in HBMEC as predicted 
      bands of 838 and 521 bp, respectively. In Western blots, the MCR of about 107 kDa 
      was localized primarily in the cytoplasmic compartment but migrated to the 
      nucleus when cell cultures were exposed to exogenous aldosterone. On the other 
      hand, the alphaENaC was revealed as a membrane-bound protein of approximately 82 
      kDa, whose abundance increased after aldosterone treatment. Confocal microscopy 
      confirmed the presence of both the MCR and ENaC as nucleocytoplasmic and 
      membrane-bound proteins, respectively, and both colocalized with tubulin in situ. 
      On Matrigel, the mineralocorticoid aldosterone, by itself, did not influence 
      capillary formation by HBMEC, but the diuretic amiloride reduced the organization 
      of HBMEC into capillary-like networks; curiously, aldosterone further exacerbated 
      this inhibitory effect of amiloride. On the fibrin matrix, aldosterone had no 
      influence at all on the length of the newly formed capillaries, but the capillary 
      diameter was highly increased over the control. Aldosterone-mediated capillary 
      swelling was totally reversed by amiloride, which, by itself, also inhibited 
      capillary elongation by HBMEC. Thus, cell signaling by mineralocorticoid hormones 
      in HBMEC appears to proceed in a manner very similar to that in the epithelial 
      cell, thereby leading to an increase in the endothelial cell volume, which may 
      underline the hypertensive state and which may also modify angiogenesis.
FAU - Chen, W
AU  - Chen W
AD  - Inserm and Cnrs, Paris, France.
FAU - Valamanesh, F
AU  - Valamanesh F
FAU - Mirshahi, T
AU  - Mirshahi T
FAU - Soria, J
AU  - Soria J
FAU - Tang, R
AU  - Tang R
FAU - Agarwal, M K
AU  - Agarwal MK
FAU - Mirshahi, M
AU  - Mirshahi M
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PL  - United States
TA  - Vascul Pharmacol
JT  - Vascular pharmacology
JID - 101130615
RN  - 0 (Diuretics)
RN  - 0 (Protein Subunits)
RN  - 0 (Receptors, Mineralocorticoid)
RN  - 0 (Sodium Channels)
RN  - 0 (Tubulin)
RN  - 4964P6T9RB (Aldosterone)
RN  - 7DZO8EB0Z3 (Amiloride)
SB  - IM
MH  - Aldosterone/*pharmacology/physiology
MH  - Amiloride/pharmacology
MH  - Blotting, Western
MH  - Bone Marrow Cells/cytology/*drug effects/metabolism
MH  - Capillaries/*drug effects/physiology
MH  - Cell Line
MH  - Diuretics/pharmacology
MH  - Endothelium, Vascular/cytology/*drug effects/metabolism
MH  - Humans
MH  - Immunohistochemistry
MH  - Microscopy, Confocal
MH  - Neovascularization, Physiologic/*drug effects
MH  - Polymerase Chain Reaction
MH  - Protein Subunits/biosynthesis/drug effects/genetics
MH  - Receptors, Mineralocorticoid/biosynthesis/drug effects/genetics
MH  - Signal Transduction/*drug effects
MH  - Sodium Channels/biosynthesis/drug effects/genetics
MH  - Tubulin/metabolism
EDAT- 2004/04/06 05:00
MHDA- 2004/08/10 05:00
CRDT- 2004/04/06 05:00
PHST- 2003/06/30 00:00 [received]
PHST- 2003/08/25 00:00 [accepted]
PHST- 2004/04/06 05:00 [pubmed]
PHST- 2004/08/10 05:00 [medline]
PHST- 2004/04/06 05:00 [entrez]
AID - S1537189104000199 [pii]
AID - 10.1016/j.vph.2003.08.003 [doi]
PST - ppublish
SO  - Vascul Pharmacol. 2004 Jan;40(6):269-77. doi: 10.1016/j.vph.2003.08.003.