scholarly journals Calsequestrin is a component of smooth muscles: the skeletal- and cardiac-muscle isoforms are both present, although in highly variable amounts and ratios

1994 ◽  
Vol 301 (2) ◽  
pp. 465-469 ◽  
Author(s):  
P Volpe ◽  
A Martini ◽  
S Furlan ◽  
J Meldolesi

Expression by smooth-muscle cells of calsequestrin (CS), the low-affinity/high-capacity Ca(2+)-binding protein of striated-muscle sarcoplasmic reticulum (SR), has been investigated in recent years with conflicting results. Here we report the purification and characterization from rat vas deferens of two CS isoforms, the first deemed skeletal muscle, the second cardiac type, on account of their N-terminal amino acids and other relevant biochemical and molecular properties. Compared with vas deferens, the smooth muscles from aorta and stomach, in that order, were found to express lower amounts of CS, whereas in the uterus and bladder the protein was not detectable. The ratio between the two CS isoforms was also variable, with the stomach and aorta predominantly expressing the skeletal-muscle type and the vas deferens expressing the two CSs in roughly similar amount. Because of the property of CSs to localize within the skeletal-muscle SR lumen not uniformly, but according to the distribution of their anchorage membrane proteins, the expression of the protein suggests the existence in smooth-muscle cells of discrete endoplasmic-reticulum areas specialized in the rapidly exchanging Ca2+ storage and release, and thus in the control of a variety of functions, including smooth-muscle contraction.

2001 ◽  
Vol 94 (4) ◽  
pp. 683-693 ◽  
Author(s):  
Michiaki Yamakage ◽  
Xiangdong Chen ◽  
Naoki Tsujiguchi ◽  
Yasuhiro Kamada ◽  
Akiyoshi Namiki

Background The distal airway is more important in the regulation of airflow resistance than is the proximal airway, and volatile anesthetics have a greater inhibitory effect on distal airway muscle tone. The authors investigated the different reactivities of airway smooth muscles to volatile anesthetics by measuring porcine tracheal or bronchial (third to fifth generation) smooth muscle tension and intracellular concentration of free Ca2+ ([Ca2+]i) and by measuring inward Ca2+ currents (ICa) through voltage-dependent Ca2+ channels (VDCs). Methods Intracellular concentration of free Ca2+ was monitored by the 500-nm light emission ratio of Ca2+ indicator fura-2. Isometric tension was measured simultaneously. Whole-cell patch clamp recording techniques were used to investigate the effects of volatile anesthetics on ICa in dispersed smooth muscle cells. Isoflurane (0-1.5 minimum alveolar concentration) or sevoflurane (0-1.5 minimum alveolar concentration) was introduced into a bath solution. Results The volatile anesthetics tested had greater inhibitory effects on carbachol-induced bronchial smooth muscle contraction than on tracheal smooth muscle contraction. These inhibitory effects by the anesthetics on muscle tension were parallel to the inhibitory effects on [Ca2+]i. Although tracheal smooth muscle cells had only L-type VDCs, some bronchial smooth muscle cells (approximately 30%) included T-type VDC. Each of the two anesthetics significantly inhibited the activities of both types of VDCs in a dose-dependent manner; however, the anesthetics had greater inhibitory effects on T-type VDC activity in bronchial smooth muscle. Conclusions The existence of the T-type VDC in bronchial smooth muscle and the high sensitivity of this channel to volatile anesthetics seem to be, at least in part, responsible for the different reactivities to the anesthetics in tracheal and bronchial smooth muscles.


1998 ◽  
Vol 76 (7-8) ◽  
pp. 802-806 ◽  
Author(s):  
J Noireaud ◽  
O Souilem ◽  
S Baudet ◽  
J -C Bidon ◽  
M Gogny ◽  
...  

Smooth muscles hyperresponsiveness is a common feature in anaphylaxis and allergic diseases. The aim of the present work was to investigate whether the enhanced reactivity of sensitized guinea-pig vas deferens was associated with changes in the resting membrane potential (Er) of the smooth muscle cells. Active sensitization was performed by subcutaneous injection of egg albumen. Er was measured in vitro in isolated vas deferens with conventional KCl-filled microelectrodes. Quantification of [3H]ouabain binding sites, measurements of 86Rb efflux, and measurements of Na and K contents were also performed. In normal physiological solution, at 35°C, Er was a mean of -54.1 ± 0.3 mV (mean ± SEM) in control vas deferens. Sensitization resulted in depolarizing Er by about 7 mV. In control and sensitized preparations, the 3H-ouabain binding site concentration, the efflux of 86Rb, and the K content were similar. In guinea-pig vas deferens, active sensitization induced a partial depolarization of the resting membrane potential of the smooth muscle cells, which did not result from a downregulation of Na+-K+ pump sites.Key words: hyperreactivity, sensitization, Na+-K+ ATPase, guinea-pig, vas deferens, smooth muscle.


1987 ◽  
Vol 88 (1) ◽  
pp. 25-34
Author(s):  
P.J. Kronebusch ◽  
S.J. Singer

In most animal cells, the microtubule-organizing centre (MTOC) and the Golgi apparatus (GA) are co-localized on one side of the nucleus, an arrangement that allows these cells to acquire a functional polarity. An exception has been reported in the skeletal muscle myotube, where the MTOC and GA exhibit a circumnuclear distribution. We wished to determine if this unusual distribution of the MTOC and GA was peculiar to syncytial myotubes or reflected a pattern found in muscle cells generally. Immunofluorescence microscopic studies of cultured chicken skeletal muscle, cardiac muscle and gizzard smooth muscle cells were carried out using preimmune sera that recognized the pericentriolar material, anti-tubulin antibodies to label the MTOC, and fluorescent wheat-germ agglutinin to label the GA. These studies have shown that cardiac myocytes possess a circumnuclear distribution of their MTOC and GA as do skeletal myotubes, but smooth muscle cells exhibit the centrosomal MTOC and GA distribution found in most other cells. The circumnuclear MTOC/GA distribution therefore is associated with striated muscle cells. We also found that as embryonic cardiac myocytes pass through the cell cycle the microtubule-organizing activity in these cells switches from a circumnuclear distribution in interphase to the conventional centrosomal location during mitosis. Thus, cardiac myocytes provide a rare example of mononucleated animal cells that do not display a centrosomal MTOC or a polarized GA, and also reveal a system in which the MTOC structure can be reversibly altered in a cell cycle-dependent manner.


1968 ◽  
Vol 37 (3) ◽  
pp. 794-817 ◽  
Author(s):  
Neil C. R. Merrillees

Smooth muscle cells of the external longitudinal coat of the guinea pig vas deferens were followed for 480 µ at 4.5-µ intervals. Muscle bundles and fibers interwove, facilitating intermuscular and neuromuscular contacts. The ribbon- or rodlike muscle cells were about 450 µ long, 3,000 µ3 in volume, and 4,500 µ2 in area. The thickened nuclear zone lay anywhere along the middle one-third of the cell. Intercellular distances were 500–800 A. Intrusions were rare, and tight-junctions absent. At any level in a field of 80 muscle fibers there were 10–15 nerve bundles, each containing several varicose axons. Bundles and axons divided. Axons, en passage, were frequently within 500–1,000 A of a muscle fiber. En passage close contacts were rate. Axon terminations were bare, and bare axons invariably terminated. Bare terminations had scattered vesicle-laden varicosities and were from 10µ-60 µ in length, and all ended within 500 A of muscle fibers. Some made close contact with muscle fibers. Less than half of the muscle cells received this close contact, but some cells were approached by more than one termination. Most terminations involved more than one cell. Some cells had little or no innervation. Some groups of cells had a rich innervation. There was very little evidence of sensory innervation. These conclusions are not valid for other smooth muscles.


2001 ◽  
Vol 534 (2) ◽  
pp. 313-326 ◽  
Author(s):  
Yoshiaki Ohi ◽  
Hisao Yamamura ◽  
Norihiro Nagano ◽  
Susumu Ohya ◽  
Katsuhiko Muraki ◽  
...  

Author(s):  
T.C. Steven Keller ◽  
Christophe Lechauve ◽  
Alexander S Keller ◽  
Steven Brooks ◽  
Mitchell J Weiss ◽  
...  

Globin proteins exist in every cell type of the vasculature, from erythrocytes to endothelial cells, vascular smooth muscle cells, and peripheral nerve cells. Many globin subtypes are also expressed in muscle tissues (including cardiac and skeletal muscle), in other organ-specific cell types, and in cells of the central nervous system. The ability of each of these globins to interact with molecular oxygen (O2) and nitric oxide (NO) is preserved across these contexts. Endothelial α-globin is an example of extra-erythrocytic globin expression. Other globins, including myoglobin, cytoglobin, and neuroglobin are observed in other vascular tissues. Myoglobin is observed primarily in skeletal muscle and smooth muscle cells surrounding the aorta or other large arteries. Cytoglobin is found in vascular smooth muscle but can also be expressed in non-vascular cell types, especially in oxidative stress conditions after ischemic insult. Neuroglobin was first observed in neuronal cells, and its expression appears to be restricted mainly to the central and peripheral nervous systems. Brain and central nervous system neurons expressing neuroglobin are positioned close to many arteries within the brain parenchyma and can control smooth muscle contraction and, thus, tissue perfusion and vascular reactivity. Overall, reactions between NO and globin heme-iron contribute to vascular homeostasis by regulating vasodilatory NO signals and scaveging reactive species in cells of the mammalian vascular system. Here, we discuss how globin proteins affect vascular physiology with a focus on NO biology, and offer perspectives for future study of these functions.


1995 ◽  
Vol 269 (3) ◽  
pp. G370-G377 ◽  
Author(s):  
K. N. Bitar ◽  
H. Yamada

We have investigated the effect of sphingosylphosphorylcholine (SPC), a synthetic product that was implicated in the sphingomyelin cycle, and have assessed its role in intracellular signaling. SPC induced a dose-dependent contractile effect of smooth muscle cells isolated from the rectosigmoid of the rabbit. Maximal contraction occurred at 10(-6) M. The response started early, 25.4 +/- 6% shortening at 15 s, peaked at 30 s (32.5 +/- 2%), and remained sustained at 8 min (30.0 +/- 3.5%). Preincubation of the cells with thapsigargin had no effect on contraction induced by SPC. The response to a combination of threshold concentrations of inositol 1,4,5-trisphosphate (IP3) and SPC was additive and was significantly different from the maximal response elicited by each agent alone. SPC also induced activation of mitogen-activated protein kinase (MAP kinase). This study demonstrates that SPC is important in cellular signaling of gastrointestinal smooth muscle cells through a mechanism that is independent of IP3-sensitive calcium release and probably through activation of a protein kinase C-mediated activation of MAP kinase.


1990 ◽  
Vol 259 (4) ◽  
pp. C675-C686 ◽  
Author(s):  
C. B. Neylon ◽  
J. Hoyland ◽  
W. T. Mason ◽  
R. F. Irvine

Vasoconstrictor agonists stimulate smooth muscle contraction by inducing a rise in intracellular free Ca2+. Digital-imaging microscopy of fura-2 fluorescence from single vascular smooth muscle cells cultured from the human internal mammary artery has allowed us to record the subcellular alterations in Ca2+ that occur immediately after stimulation by receptor agonists. The thrombin-induced rise in cytoplasmic free Ca2+ begins in a discrete region typically located close to the end of the cell. Subsequently, this region of elevated Ca2+ expands until Ca2+ is elevated throughout the cell cytoplasm. The rate of spreading in the region of elevated Ca2+ in a linear direction averaged 10.1 microns/s, enabling it to traverse the length of most cells within approximately 5 s, and involved rises in Ca2+ of between 200 and 500 nM. In some cells, the Ca2+ rise began at both ends and collided midway. Similar dynamic changes in the spatial distribution of Ca2+ were recorded in cells stimulated by acetylcholine. The novel observation that vasoconstrictor agonists induce an elevation of Ca2+ in a localized region which subsequently expands throughout the cytoplasm of single smooth muscle cells may provide new insight into the nature of Ca2+ signaling in vascular tissue.


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