Original Contributions |
From Humboldt University (Charité), Department of Physiology, Berlin (I.M.), and Max Delbrück Center for Molecular Medicine, Berlin-Buch (U.W., G.L., H.H., U.G., I.M.), Germany.
Correspondence to Prof Ingo Morano, Max Delbrück Center for Molecular Medicine, Robert-Rössle-Straße 10, 13122 Berlin-Buch, Germany. E-mail imorano{at}orion.rz.mdc-berlin.de
AbstractWe investigated expression
of the 5'-spliced isoform of smooth muscle myosin heavy chain
(SM-MHC-B) in smooth muscle cells of cardiac vessels of the left
ventricle of normotensive (Wistar-Kyoto) and spontaneously hypertensive
rats of the stroke-prone strain by
immunofluorescence microscopy. In parallel, liver
and bladder were studied for characterization of the nature of vessels
expressing SM-MHC-B and for semiquantitative evaluation of its
abundance. Smooth muscle cells were detected by staining with a
monoclonal antibody specific for
-smooth muscle actin. Abundance of
the SM-MHC-B isoform in these cells was evaluated by using an antibody
raised against the sevenamino acid insert at the 25K/50K junction of
the myosin head (a25K/50K) that specifically recognized SM-MHC-B. In
the ventricle, a25K/50K immunoreactivity was observed in smooth muscle
cells of precapillary arterioles but not in larger vessels or aorta.
The a25K/50K immunoresponse of those vessels with the highest
expression level of SM-MHC-B closely resembled the signal observed in
the smooth muscle layer of urinary bladder known to preferentially
express SM-MHC-B. Interestingly, in left ventricles of stroke-prone
spontaneously hypertensive rats, there was a significantly reduced
fraction of a25K/50K-positive precapillary arterioles compared with
normotensive control rats.
Key Words: smooth muscle myosin heavy chain hypertrophy hypertension cardiac vessel
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