Presence of smooth-muscle cells in the subdural neomembrane

1981 ◽  
Vol 54 (5) ◽  
pp. 646-651 ◽  
Author(s):  
Nobuyuki Kawano ◽  
Kinuko Suzuki
Keyword(s):  
Electron Microscopy ◽  
Smooth Muscle ◽  
Light Microscopy ◽  
Smooth Muscle Cells ◽  
Subdural Hematoma ◽  
Light And Electron Microscopy ◽  
Chronic Subdural Hematoma ◽  
Muscle Cells ◽  
Content Type ◽  
Fine Print

✓ The authors encountered a case of chronic subdural hematoma of which the subdural neomembrane (SN) showed numerous spindle-shaped cells identified as smooth-muscle cells (SMC's) by electron microscopy. On reexamination of 214 cases from the files, SMC's were found with light microscopy in seven cases. In these cases, the SN was well organized (collagenized). In three additional cases examined with both light and electron microscopy, SMC's were not apparent with light microscopy. However, in all cases, cells with ultrastructural features of both fibroblasts and SMC's were observed. Well formed SMC's were found in two additional cases of well organized membrane. Based on these observations, it is concluded that the presence of SMC's in the SN is not a rare phenomenon. The possible origin of SMC's in the SN and their pathological significance to the organizing process of chronic subdural hematoma are discussed.

Immediate early gene expression in vascular smooth-muscle cells synergistically induced by hemolysate components

1999 ◽  
Vol 90 (6) ◽  
pp. 1083-1090 ◽  
Author(s):  
Xiaoyu Wang ◽  
Linda S. Marton ◽  
Bryce K. A. Weir ◽  
R. Loch Macdonald
Keyword(s):  
Gene Expression ◽  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Synergistic Effects ◽  
Muscle Cells ◽  
Immediate Early Gene ◽  
Early Gene ◽  
Immediate Early ◽  
Content Type ◽  
Fine Print

Object. Vasospasm after subarachnoid hemorrhage is associated with changes in modulators of vascular tone in the arterial wall and is related to the presence of erythrocyte hemolysate in the subarachnoid space. The purpose of this study was to determine the compounds in erythrocyte hemolysate that are responsible for changing smooth-muscle cell gene expression.Methods. Rat aorta smooth-muscle cells were exposed to erythrocyte hemolysate in vitro and the effects on immediate early gene messenger (m)RNA levels were determined by competitive reverse transcriptase—polymerase chain reaction.Message levels for c-fos, jun B, and c-jun were increased in the presence of hemolysate, reaching maximum expression between 30 and 60 minutes, whereas the level of jun D mRNA was unaffected. Increasing doses of hemolysate caused greater expression of c-fos and jun B, but not c-jun. Adenosine triphosphate and hemoglobin, possible spasmogens present in hemolysate, caused much smaller and more rapid increases in c-fos expression than whole hemolysate. Size fractionation showed that all of the c-fos mRNA—inducing activity of hemolysate was recovered with molecules greater than 6 kD. Following separation of hemolysate proteins by hydrophobic interaction chromatography, only one of the three fractions had partial activity. Recombining the three fractions, however, yielded greater c-fos activation than any combination of two.Conclusions. Multiple high-molecular-weight components present in erythrocytes have synergistic effects on gene expression in smooth-muscle cells. The differences in patterns of gene induction suggest that multiple signaling pathways are activated.

Role of protein tyrosine phosphorylation in erythrocyte lysate—induced intracellular free calcium concentration elevation in cerebral smooth-muscle cells

1999 ◽  
Vol 90 (4) ◽  
pp. 743-751 ◽  
Author(s):  
Satoshi Iwabuchi ◽  
Linda S. Marton ◽  
John H. Zhang
Keyword(s):  
Molecular Weight ◽  
Smooth Muscle ◽  
Tyrosine Kinase ◽  
Smooth Muscle Cells ◽  
Tyrosine Phosphorylation ◽  
Kinase Inhibitors ◽  
Weight Fraction ◽  
Muscle Cells ◽  
Content Type ◽  
Fine Print

Object. Tyrosine kinases play an important role in the regulation of systemic vascular smooth-muscle tone. The authors studied the involvement of protein tyrosine kinase activity in erythrocyte lysate—mediated signal transduction in cerebral smooth-muscle cells.Methods. Tyrosine kinase phosphorylation and intracellular free Ca++ ([Ca++]i) were measured in rat aortic and basilar artery smooth-muscle cells by using Western blot and fura 2-acetoxymethyl ester microfluorimetry. Erythrocyte lysate enhanced tyrosine phosphorylation in cultured rat aortic and basilar smooth-muscle cells and induced a rapid transient and a prolonged plateau phase of [Ca++]i response in rat basilar smooth-muscle cells. The tyrosine kinase inhibitors genistein and tyrphostin A51 (administered at concentrations of 30 or 100 µM) attenuated both phases of erythrocyte lysate—induced [Ca++]i elevation. Erythrocyte lysate was separated into low- (< 10 kD, which contains adenine nucleotides) and high- (> 10 kD, which contains hemoglobin) molecular-weight fractions; these fractions were tested separately in these cells. The low-molecular-weight fraction produced a similar [Ca++]i response to that of erythrocyte lysate and the high-molecular-weight fraction produced a small response. The [Ca++]i responses from both fractions were inhibited by tyrosine kinase inhibitors.Conclusions. To the authors' knowledge, this is the first report to show that tyrosine phosphorylation may be involved in erythrocyte lysate—induced signal transduction and [Ca++]i responses in cerebral smooth-muscle cells.

The effect of hemoglobin and its metabolites on energy metabolism in cultured cerebrovascular smooth-muscle cells

1995 ◽  
Vol 82 (2) ◽  
pp. 244-249 ◽  
Author(s):  
Kazuhiko Nagatani ◽  
Jeffery E. Masciopinto ◽  
Peter B. Letarte ◽  
Robert A. Haworth ◽  
Thomas A. Duff
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Energy Levels ◽  
Cerebral Arteries ◽  
Muscle Cells ◽  
Inhibitory Effect ◽  
Intact Cells ◽  
Content Type ◽  
Cerebrovascular Smooth Muscle Cells ◽  
Fine Print

✓ Cerebral arteries in spasm have been found to contain low levels of adenosine triphosphate (ATP), and it has been postulated that this change in levels results from hypoxia produced by arterial encasement in clotted material. This study was undertaken to determine whether any of four blood-derived agents, ferrous hemoglobin, methemoglobin, hemin, or bilirubin, is capable of reducing energy levels in cerebral artery smooth-muscle cells. Twenty-four-hour exposure of cultured canine basilar artery cells to ferrous hemoglobin and bilirubin led to a significant decline in ATP levels (to 8.9 nmol/mg protein and 2.8 nmol/mg protein, respectively) versus control (16.6 nmol/mg protein); methemoglobin and hemin showed no effect. Bilirubin but not hemoglobin was found to interfere with electron transport and with creatine phosphokinase activity in intact cells; however, bilirubin showed no inhibitory effect on this enzyme in cell-free conditions. The findings indicate that hemoglobin and bilirubin may be responsible for diminished energy levels in cerebral arteries. These observations also suggest that bilirubin may exert its effect on ATP by impairing mitochondrial function.

Cerebral arterial pathology in experimental subarachnoid hemorrhage

1983 ◽  
Vol 58 (6) ◽  
pp. 843-850 ◽  
Author(s):  
Tetsumori Yamashima ◽  
Shinjiro Yamamoto
Keyword(s):  
Smooth Muscle ◽  
Subarachnoid Hemorrhage ◽  
Smooth Muscle Cells ◽  
Morphological Changes ◽  
Autologous Blood ◽  
Cerebral Arteries ◽  
Muscle Cells ◽  
Internal Elastic Lamina ◽  
Content Type ◽  
Fine Print

✓ Pathological changes of the cerebral arteries were studied in 30 dogs after subarachnoid injections of saline, fresh autologous blood, epinephrine, blood plus epinephrine, norepinephrine, or blood plus norepinephrine. Macroscopically, the circle of Willis was maximally dilated after the injection of epinephrine and was constricted following administration of blood plus epinephrine. Microscopically, neither saline nor blood produced abnormalities, except for minor changes of the adventitia in the latter. Epinephrine produced frank necrosis of smooth-muscle cells, which was subsequently replaced by fibrosis in the media of larger subarachnoid arteries, and the leakage of necrotic material from the infarcted hypothalamus contributed to these lesions. Blood plus epinephrine produced marked changes in the internal elastic lamina and tortuosities of the nuclei of smooth-muscle cells, while norepinephrine and blood plus norepinephrine produced only minor changes. Previously reported findings of morphological changes due to vasospasm after subarachnoid hemorrhage were confirmed experimentally, but such changes were found only after application of epinephrine. It is suggested that epinephrine produced the most severe vasospasm among the five substances tested.

Glutathione monoethyl ester and inhibition of the oxyhemoglobin-induced increase in cytosolic calcium in cultured smooth-muscle cells

1999 ◽  
Vol 90 (3) ◽  
pp. 527-532 ◽  
Author(s):  
Takashi Arai ◽  
Naoshi Takeyama ◽  
Takaya Tanaka
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Smooth Muscle Cell ◽  
Muscle Cell ◽  
Muscle Cells ◽  
Cytosolic Calcium ◽  
Acetoxymethyl Ester ◽  
Content Type ◽  
Transient Elevation ◽  
Fine Print

Object. The mechanism of arterial vasoconstriction caused by oxyhemoglobin production after subarachnoid hemorrhage was investigated.Methods. Using a fluorescent Ca++ indicator (fura-2 acetoxymethyl ester), the change in the cytosolic intracellular Ca++ concentration, [Ca++]i, was measured in cultured rat vascular smooth-muscle cells exposed to oxyhemoglobin and other substances. Oxyhemoglobin induced transient elevation of smooth-muscle cell [Ca++]i in either the presence or absence of ethyleneglycol-bis (β-aminoethylether)-N,N′-tetraacetic acid, indicating that Ca++ released by oxyhemoglobin was derived from [Ca++]i stores. In contrast, methemoglobin had no effect on the smooth-muscle cells. Exposure of the cells to reactive oxygen species generated by xanthine plus xanthine oxidase yielded the same results as with oxyhemoglobin, that is, transient elevation of smooth-muscle cell [Ca++]i. Procaine (a Ca++ channel blocker) failed to inhibit the oxyhemoglobin-induced elevation of [Ca++]i. Ryanodine (a Ca++ channel opener) plus oxyhemoglobin caused markedly greater elevation of [Ca++]i than ryanodine alone, whereas thapsigargin (an adenosine triphosphate [ATP]-dependent Ca++ pump inhibitor) plus oxyhemoglobin had no additional effect when compared with thapsigargin alone. The oxyhemoglobin-induced elevation of [Ca++]i could be blocked by an Fe++ chelator (ferene), but not by an Fe+++ chelator (deferoxamine mesylate). Treatment with either dithiothreitol or glutathione monoethyl ester markedly inhibited the oxyhemoglobin-induced elevation of [Ca++]i.Conclusions. These results indicate that Fe++-catalyzed hydroxyl radicals generated from oxyhemoglobin-derived free radicals induce the elevation of [Ca++]i by inhibiting the ATP-dependent Ca++ pump rather than the Ca++ channels in the sarcoplasmic reticulum and that thiols may prevent Ca++ pump inactivation by inhibiting the oxidation of membrane sulfhydryl groups.

Experimental vasospasm in cultured arterial smooth-muscle cells

1988 ◽  
Vol 69 (1) ◽  
pp. 92-97 ◽  
Author(s):  
Satoshi Fujii ◽  
Kazuhiko Fujitsu
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Muscle Cells ◽  
Ultrastructural Changes ◽  
Vasoactive Agents ◽  
Arterial Smooth Muscle ◽  
Content Type ◽  
Aortic Media ◽  
Arterial Smooth Muscle Cells ◽  
Fine Print

✓ Smooth-muscle cells were cultured from rat aortic media, then oxyhemoglobin and other agents including serotonin, norepinephrine, and angiotensin II were added separately to the medium. Contractile and ultrastructural changes of the cells were examined with electron microscopy during the first 2 weeks of incubation. Oxyhemoglobin not only produced progressive contraction of the arterial smooth-muscle cells, but it also caused ultrastructural changes that resembled myonecrosis. In contrast, there was no evidence of progressive contraction or ultrastructural changes either in control cultures or in cultures with the other vasoactive agents. Although washout of oxyhemoglobin 3 hours after administration prevented continued contraction of the cells, washout 24 hours or longer after administration had no preventive effect. Judging from these results and from the fact that the culture medium was changed every 2 days, it is unlikely that accumulation of exogenous vasoactive agents caused these changes. The contraction and suggestive myonecrosis of the arterial smooth-muscle cells are probably caused by some intrinsic process initiated by oxyhemoglobin. The culture of cerebral arterial smooth-muscle cells requires further technical improvement; nevertheless, these results obtained with the smooth-muscle cells of rat aortic media indicate that arterial smooth-muscle cells in culture provide a promising new experimental model for chronic in vitro study of cerebral arterial spasm. It is suggested from these results that cerebral arteries are particularly prone to vasospasm because of structural differences as compared to noncerebral arteries.

Effects of erythrocyte lysate of different incubation times on intracellular free calcium in rat basilar artery smooth-muscle cells

1998 ◽  
Vol 89 (6) ◽  
pp. 1007-1014 ◽  
Author(s):  
Yong-Yuan Guan ◽  
Bryce K. A. Weir ◽  
Linda S. Marton ◽  
R. Loch Macdonald ◽  
He Zhang
Keyword(s):  
Molecular Weight ◽  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Transient Response ◽  
Basilar Artery ◽  
Incubation Time ◽  
Muscle Cells ◽  
Free Calcium ◽  
Content Type ◽  
Fine Print

Object. The purpose of this study was to characterize substance(s) in the erythrocytes that increase intracellular free Ca++ concentration ([Ca++]i) in smooth-muscle cells and that therefore may be involved in the pathogenesis of vasospasm. Methods. Because vasospasm occurs days after subarachnoid hemorrhage (SAH), the authors studied the effects of aged human erythrocyte hemolysate and its low-molecular-weight (LMW) and high-molecular-weight (HMW) fractions on [Ca++]i in freshly isolated rat basilar artery smooth-muscle cells. Fresh hemolysate (Day 0) produced a biphasic response consisting of a transient peak and a sustained plateau increase in [Ca++]i, whereas hemolysate prepared from cells incubated for 3, 7, or 14 days induced only a transient response without a sustained phase. The effect of hemolysate declined with increasing incubation time. The HMW fraction and purified human oxyhemoglobin (OxyHb) did not evoke a response. The LMW fraction from Days 3, 7, or 14 produced no response at low concentrations (<10%) and a transient response at high concentrations (> 20%), and the effect diminished with increasing incubation time. Unfractionated hemolysate or the LMW fraction of hemolysate incubated for 21 days produced no response. The combination of the 10% LMW fraction from Day 3 plus the 10% HMW fraction (Days 3, 7, 14, or 21) transiently increased [Ca++]i. However, [Ca++]i was not changed by the 10% LMW fraction from Day 14 plus the 10% HMW fraction from Day 3 or 14. In the presence of OxyHb, [Ca++]i was increased by the 10% LMW fraction on Days 3 and 7, but not by the LMW fraction from Days 14 or 21. Conclusions. The decline over time in the effect of hemolysate on [Ca++]i indicates either that the time that substances are released from erythrocytes is important in the generation of vasospasm or that this experimental system as used is not representative of conditions present after SAH. The data indicate that the ability to elevate [Ca++]i in smooth-muscle cells with hemolysate is provided by multiple substances, including OxyHb. These substances may interact during specific times after incubation of erythrocytes in vitro.

Intercellular granules and vesicles in prolonged cerebral vasospasm

1978 ◽  
Vol 48 (2) ◽  
pp. 179-189 ◽  
Author(s):  
Eiichi Tani ◽  
Shogo Yamagata ◽  
Yuko Ito
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Extracellular Space ◽  
Muscle Cells ◽  
Characteristic Change ◽  
Content Type ◽  
Arterial Blood ◽  
Basilar Arteries ◽  
Elastic Lamina ◽  
Fine Print

✓ Prolonged vasospasm was produced in the dog basilar arteries by introduction of fresh arterial blood or norepinephrine into the chiasmatic cistern. Myonecrosis was limited to a small number of smooth-muscle cells, and a large number of muscle cells appeared intact. The most characteristic change was the appearance of aggregated granules and vesicles in the widened extracellular space between smooth-muscle cells, particularly near the adventitia and the elastic lamina. The granules were spherical, 50 to 100 nm in diameter, often surrounded by a single membrane, and contained a dense osmiophilic core, about 40 to 90 nm in diameter. In addition, the elastic lamina often became loose and corrugated or broken.

Role of transforming growth factor—β1 in the pathogenesis of moyamoya disease

1998 ◽  
Vol 89 (4) ◽  
pp. 623-629 ◽  
Author(s):  
Masato Hojo ◽  
Minoru Hoshimaru ◽  
Susumu Miyamoto ◽  
Waro Taki ◽  
Izumi Nagata ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Growth Factor ◽  
Serum Level ◽  
Smooth Muscle Cells ◽  
Cerebrovascular Disease ◽  
Moyamoya Disease ◽  
Transforming Growth Factor ◽  
Muscle Cells ◽  
Content Type ◽  
Fine Print

Object. Prominent features of moyamoya disease are intimal thickening of the cerebral arterial trunks and abundant angiogenesis for collateral blood supplies, but its pathogenesis is still unknown. The aim of this study was to test the possibility that transforming growth factor—β1 (TGFβ1) may play a role in the pathogenesis of moyamoya disease. Methods. The authors used reverse transcription—polymerase chain reaction to analyze the expression level of TGFβ1 in smooth-muscle cells cultured from the superficial temporal arteries (STAs) and measured the serum level of TGFβ1 by using enzyme-linked immunosorbent assay. Although the STA is not predominantly involved with moyamoya disease, it has been used in studies of the pathogenesis of this disease. In this report, the STAs from six patients with moyamoya disease and four with arteriosclerotic cerebrovascular disease, along with sera from 14 patients with moyamoya disease and 10 normal healthy volunteers, were studied. The expression of TGFβ1 was significantly higher in cultured smooth-muscle cells derived from the STAs of patients with moyamoya disease than in those derived from the STAs of patients with arteriosclerotic cerebrovascular disease (p < 0.05). The serum level of TGFβ1 was also significantly higher in patients with moyamoya disease than in controls (p < 0.0005). Conclusions. Taking into account the functional roles of TGFβ1 in the expression of connective tissue genes and angiogenesis, these investigators suggest that TGFβ1 is associated with the pathogenesis of moyamoya disease, including abundant neovascularization, although their findings do not necessarily mean that TGFβ1 is a causative factor in this disease.

Sign in / Sign up

Export Citation Format

Share Document