Angiomyofibroblastoma is a recently described mesenchymal tumor characterized by unique morphologic features, a propensity to arise in the vulva, and a non-aggressive beni-gn biologic behavior. It is typically well circumscribed and superficially located tumor and its cellularity is variable with hypercellular and hypocellular areas composed of bland-looking, pump stromal cells showing the immunophenotype of vimentin-/desmin - positive, and muscle specific actin(MSA)-/alpha-smooth muscle actin(ASMA) - negative. Spindle or plasm-acytoid cells are the characteristic cell types of most tumors. It is similar to an aggressive pelvic angiomyxoma in histology. Because of histologic similarity and differences in the clinical course and treatment, distinction from aggressive angiomyxoma was needed. It rep-resents new type in the expanding spectrum of tumors of which myofibroblasts constitute an integral component. We experienced a case of angiomyofibroblastoma of the vulva occuring in a 42 years old woman. The lesion was relatively well encapsulated mass(3 X 1.5 X 0.9 cm in dimension), showing intimate admixture of hypercellular and hypocellular area. The tumor contained prominent, somewhat ectatic vessels surrounded by smooth muscle cells, some of which blend or fan out from the muscular walls of the vessels. The margin was relatively free from tumor cells. At immunohistochemical stain, vimentin and desmin was diffuse and weak positive, smooth muscle actin was very a few and weak positive in tumor cells.
Actins ; Adult ; Desmin ; Female ; Humans ; Muscle, Smooth ; Myocytes, Smooth Muscle ; Myofibroblasts ; Myxoma ; Stromal Cells ; Vimentin ; Vulva*

No abstract available.
Angiotensins ; Muscle, Smooth ; Myocytes, Smooth Muscle

This study is performed to reveal the changes of the arterial wall, especially, tunica intima and tunica media, after endothelial denudation and the effects of dexamethasone sodium on intimal hyperplasia morphologically in the rat. After arterial denudation by modified air drying technique, dexamethasone 1, 200 mg/kg/day was administered intramuscularly daily from the day of operation for 14 days. At 5 DAT (days after treatment) and 14 DAT, tunica intima was greatly thickened in control groups compared with normal group, but not in the dexamethasone-treated groups. Light microscopically, greatly increased cells and intercellular matrix in the tunica intima are observed in control group, but not in the dexamethasone-treated group. In the TEM observation, the cells considered as myofibroblasts and extracellular matrix were greatly increased in both tunica intima and tunica media just below the internal elastic lamina in the control group. Myofibroblasts and extracellular matrix migrated through the apertures of internal elastic lamina into the endothelial layer. Characteristic false internal elastic lamina also found. In dexamethasone-treated group, myofibroblasts and extracellular matrix decreased significantly, and apoptotic electron-dense cells, fragmented nucleus and autophagic vacuoles are observed. Through the apertures of internal elastic lamina, comma-shaped fragmented nuclei migrated into the tunica intima. These results suggest that dexamethasone inhibits the myofibroblast-transformation and proliferation of smooth muscle cells, migration of myofibroblasts and matrix synthetic activity, and induces the apoptosis of smooth muscle cells under the internal elastic lamina.
Animals ; Apoptosis ; Dexamethasone* ; Extracellular Matrix ; Hyperplasia* ; Myocytes, Smooth Muscle ; Myofibroblasts ; Rats ; Sodium ; Tunica Intima ; Tunica Media ; Vacuoles

Infantile myofibromatosis is an uncornmon, benign, self-limiting, localized or generalized process, probably of hamartomatous origin, which consists to a large degree of cells having the characteristics of myofibroblasts and sometimes of pericytes. Both solitary and multicentric forms occur. Most lesions are present at birth or in early infancy, and some are familial in origin. A female newborn presented with a firm, round, red colored, 3 x 3 cm sized tumor with central necrosis on the left chest. Histological examination revealed well-circumscribed nodules consisting of short bundles of plump, spindle shaped cells displaying staining characteristics intermediate between fibroblasts and smooth muscle cells. The tumor was immunoreactive for actin but did not stain for desmin. A Follow-up examination at the age of 3 months revealed a moderate degree of spontaneous regressior of the lesion.
Actins ; Desmin ; Female ; Fibroblasts ; Follow-Up Studies ; Humans ; Infant, Newborn ; Myocytes, Smooth Muscle ; Myofibroblasts ; Myofibromatosis* ; Necrosis ; Parturition ; Pericytes ; Thorax

Glomus tumors are benign neoplasms that are derived from modified smooth muscle cells known as glomus cells. Histologically, it can be subdivided as glomus tumor proper, glomangioma, and glomangiomyoma according to relative proportions of components. Glomangiomyomas are the least frequent type and their overall architectural pattern may resemble glomus tumor proper or glomangioma, but there is a gradual transition from glomus cells to elongated mature smooth muscle cells. This transition is most obvious in the region surrounding large vessels. We present a case of glomangiomyoma of the left upper arm and the left fourth finger, in which ten-year history of two painful, bluish-colored subcutaneous nodules. On histologic examination, this case showed marked smooth muscle cell proliferation around large vessles and mucinous stromal change.
Arm ; Fingers ; Glomus Tumor ; Mucins* ; Muscle, Smooth* ; Myocytes, Smooth Muscle*

Humans ; MicroRNAs ; Muscle, Smooth, Vascular ; Myocytes, Smooth Muscle ; Phenotype

We demonstrated the effect of nortriptyline, a tricyclic antidepressant drug and serotonin reuptake inhibitor, on voltage-dependent K⁺ (Kv) channels in freshly isolated rabbit coronary arterial smooth muscle cells using a whole-cell patch clamp technique. Nortriptyline inhibited Kv currents in a concentration-dependent manner, with an apparent IC₅₀ value of 2.86±0.52 µM and a Hill coefficient of 0.77±0.1. Although application of nortriptyline did not change the activation curve, nortriptyline shifted the inactivation current toward a more negative potential. Application of train pulses (1 or 2 Hz) did not change the nortriptyline-induced Kv channel inhibition, suggesting that the effects of nortiprtyline were not use-dependent. Preincubation with the Kv1.5 and Kv2.1/2.2 inhibitors, DPO-1 and guangxitoxin did not affect nortriptyline inhibition of Kv channels. From these results, we concluded that nortriptyline inhibited Kv channels in a concentration-dependent and state-independent manner independently of serotonin reuptake.
Coronary Vessels ; Muscle, Smooth* ; Myocytes, Smooth Muscle* ; Nortriptyline* ; Serotonin

In this study, we demonstrated the inhibitory effect of the Class Ic antiarrhythmic agent propafenone on voltage-dependent K⁺ (Kv) channels using freshly isolated coronary artery smooth muscle cells from rabbits. The Kv current amplitude was progressively inhibited by propafenone in a dose-dependent manner, with an apparent IC₅₀ value of 5.04±1.05 µM and a Hill coefficient of 0.78±0.06. The application of propafenone had no significant effect on the steady-state activation and inactivation curves, indicating that propafenone did not affect the voltage-sensitivity of Kv channels. The application of train pulses at frequencies of 1 or 2 Hz progressively increased the propafenone-induced inhibition of the Kv current. Furthermore, the inactivation recovery time constant was increased after the application of propafenone, suggesting that the inhibitory action of propafenone on Kv current is partially use-dependent. Pretreatment with Kv1.5, Kv2.1 or Kv7 inhibitor did not change the inhibitory effect of propafenone on the Kv current. Together, these results suggest that propafenone inhibits the vascular Kv channels in a dose- and use-dependent manner, regardless of Na⁺ channel inhibition.
Coronary Vessels ; Muscle, Smooth* ; Myocytes, Smooth Muscle* ; Propafenone* ; Rabbits

We investigated the inhibitory effect of escitalopram, a selective serotonin reuptake inhibitor (SSRI), on voltage-dependent K⁺ (Kv) channels in freshly separated from rabbit coronary arterial smooth muscle cells. The application of escitalopram rapidly inhibited vascular Kv channels. Kv currents were progressively inhibited by an increase in the concentrations of escitalopram, suggesting that escitalopram inhibited vascular Kv currents in a concentration-dependent manner. The IC₅₀ value and Hill coefficient for escitalopram-induced inhibition of Kv channels were 9.54±1.33 µM and 0.75±0.10, respectively. Addition of escitalopram did not alter the steady-state activation and inactivation curves, suggesting that the voltage sensors of the channels were not affected. Pretreatment with inhibitors of Kv1.5 and/or Kv2.1 did not affect the inhibitory action of escitalopram on vascular Kv channels. From these results, we concluded that escitalopram decreased the vascular Kv current in a concentration-dependent manner, independent of serotonin reuptake inhibition.
Citalopram* ; Coronary Vessels ; Muscle, Smooth* ; Myocytes, Smooth Muscle* ; Serotonin*

BACKGROUND: Midazolam has a direct relaxing effect on vascular smooth muscle, but the mechanisms that this agent produces muscle relaxation are not fully understood. The current study was performed to identify the effects of the midazolam on K+ channels current in rabbit cerebral arterial smooth muscle cells. METHODS: Whole cell patch-clamp recording technique was used to evaluate the effects of midazolam (0.1 to 100micrometer) on outward K+ channel currents in dispersed rabbit cerebral arterial smooth muscle cells. RESULTS: Outward K+ currents of rabbit cerebral artery smooth muscle cells were voltage-dependent. Midazolam (10, 100micrometer) tested significantly inhibited outward K+ currents in a dose-dependent manner and half-blocking concentration (IC50) was 15.94micrometer at 60 mV. CONCLUSIONS: Midazolam inhibit outward K+ currents of rabbit cerebral arterial smooth muscle cells. Further study will be needed to determine the effect of midazolam on calcium channel current because it is unclear if the inhibitory effect of midazolam on outward K+current induces vasoconstriction.
Calcium Channels ; Cerebral Arteries ; Midazolam* ; Muscle Relaxation ; Muscle, Smooth* ; Muscle, Smooth, Vascular ; Myocytes, Smooth Muscle* ; Vasoconstriction