Ograniczanie wyników

Czasopisma help
Autorzy help
Lata help
Preferencje help
Widoczny [Schowaj] Abstrakt
Liczba wyników

Znaleziono wyników: 25

Liczba wyników na stronie
Pierwsza strona wyników Pięć stron wyników wstecz Poprzednia strona wyników Strona / 2 Następna strona wyników Pięć stron wyników wprzód Ostatnia strona wyników

Wyniki wyszukiwania

Wyszukiwano:
w słowach kluczowych:  smooth muscle cell
help Sortuj według:

help Ogranicz wyniki do:
Pierwsza strona wyników Pięć stron wyników wstecz Poprzednia strona wyników Strona / 2 Następna strona wyników Pięć stron wyników wprzód Ostatnia strona wyników
We have performed a study about the incidence of the atherosclerotic phenomenon in the human facial artery, having observed an increase with aging. We also have researched the role of the smooth muscle cells in its genesis, with morphological, ultrastructural and immunohistochemical techniques.
Previously we have shown that aldolase (ALD; EC 4.1.2.13) is present in cardiomyocyte nuclei. Now, we focused our attention on ALD localization in smooth muscle cells. Immunocytochemical methods were used to study the subcellular localization of ALD. Aldolase was localized in the cytoplasm as well as in the nuclei. Within the nuclei ALD was located in the heterochromatin region. Native polyacrylamide gel electrophoresis followed by aldolase activity staining in gel was used to study the ALD isoenzyme pattern in porcine smooth muscle cells. Two ALD isoenzymes, A and C, were found in these cells but in the nuclei only the muscle isoenzyme was detected. To support the nuclear localization of ALD, measurement of aldolase activity in the smooth muscle cell nuclei isolated from porcine stomach was performed. The ALD activity in the isolated nuclei was detectable only after preincubation of the nuclear fraction with Triton X-100 and high concentration of KCl.
We investigated the effects of the selective inhibitor of Na+/Ca2+ exchanger (NCX), 2',4'- and 3',4'-dichlorobenzamil (DCB), on large-conductance Ca2+-activated K+ (BKCa) channels in cultured human umbilical vein endothelial cells (HUVECs) and fresh isolated mouse aortic smooth muscle cells (MASMCs) using the patch clamp techniques. Both kinds of DCB reversibly activated BKCa currents in whole-cell clamped HUVECs or MASMCs. The EC50 of 2',4'-DCB for BKCa current activation in HUVECs was 2.64 ± 0.10 µM. In inside-out and outside-out patches, 2',4'-DCB remarkably increased BKCa channels activity. 2',4'-DCB increased open frequency, but had no significant effect on mean open time. In inside-out patches, 2',4'-DCB shifted the relationship curve between [Ca2+]i and open probability (NPo) to the left; the [Ca2+]i required to evoke half-maximal activation changed from 1087.45 ± 142.91 nM to 500.24 ± 66.83 nM by 10 µM 2',4'-DCB. In addition, 2',4'-DCB shifted the relationship curve between membrane potential and NPo to the left; the membrane potential to evoke half-maximal activation changed from 81.1 ± 2.4 to 64.7 ± 3.1 mV by 10 µM 2',4'-DCB. 3',4'-DCB also increased BKCa channels activity. There was no significant difference in the effect of DCB on BKCa channels between both excised patches. These results suggested that 2',4'- and 3',4'-DCB activate BKCa channels activity in HUVECs and MASMCs by increasing the sensitivity of BKCa channels to cytosolic free Ca2+ and membrane potential. Our report would provide a consideration if they are used as NCX blocker in vascular endothelial cells or smooth muscle cells.
9
Content available remote

Mechanisms of vascular dysfunction after subarachnoid hemorrhage

63%
The main consequence of subarachnoid hemorrhage, for those who survive bleeding, is delayed, persistent vasospasm of intracranial conduit arteries which occurs between the third and seventh day after the insult and results in symptomatic brain ischemia in about 40% of cases. This vasospasm is considered to be a major cause of disability of post-SAH patients. Despite extensive experimental and clinical research, mechanisms of vasospasm are not fully understood. Dysfunction of the endothelium resulting in enhanced production of vasoconstrictors, phenotypic changes of the receptors in endothelium and smooth muscle cells, increased sensitivity of vascular smooth muscle cells to vasoconstrictors, release of spasmogens from lysed blood clot and inflammatory response of the vascular wall have been demonstrated and discussed as pathological mechanisms participating in the development of spasm. In recent years more attention is paid to the functional and structural changes in microcirculation and a concept of microvascular spasm is evolving. Our experimental studies in rat model of SAH strongly suggest that microcirculatory dysfunction and delayed vasospasm are related to the severity of acute, transient ischemia caused by critical decrease of perfusion pressure and active vasoconstriction immediately after the bleeding.
Hypertension alters expression of connexin-43 (Cx43) in cardiovascular system. The aim of the study was to investigate the effect of omega-3 polyunsaturated fatty acids (30 mg/day for 2 months) on expression of Cx43 in the aorta of 1-year-old male spontaneously hypertensive rats (SHR). Spatial distribution and expression of Cx43 in aortic wall of SHR and age-matched Lewis rats were determined by immunofluorescent method and Western blot. NO synthase (NOS) activity and endothelium-dependent relaxation of the aorta were measured as well. Immunofluorescent pattern of Cx43 was identified in endothelial and smooth muscle cells of the aorta of all experimental groups studied. However, local decrease in the number and intensity of fluorescent spots and reduced phosphorylation of Cx43 were observed in SHR in contrast to normotensive LEW. Omega-3 fatty acid diet increased Cx43 immunolabeling in endothelium and media of SHR comparing to untreated ones. Parallel, 3-fatty acids significantly elevated phosphorylation of Cx43 in the aorta of SHR (p<0.001). Despite the omega-3 fatty acids reduced blood pressure and stimulated aortic NOS activity in SHR, endothelium-dependent relaxation of the aorta did not significantly change. Results indicate that the aorta of old SHR might partially benefit from 3-PUFA supplementation due to increased Cx43 phosphorylation, NOS activity and decreased blood pressure.
Computational approaches for spatial modeling of dynamics of the intercellular distribution of molecules can parse, simplify, classify and organize the spatiotemporal richness of any biochemical pathway and demonstrate its impact on the cells function by simply coupling it with the downstream effecters. One such online system biology modeling package is Virtual cell that provides a unique open source software and it’s used for making mathematical models to simulate the cytoplasmic control of molecule that interact to produce certain cellular behavior. In our present study, a spatial model for time dependent acetylcholine induced relaxation of vascular endothelial cells lining the lumen of blood vessel that regulate the contractility of the arteries was generated. The time-dependent action of neurotransmitter acetylcholine for total time period for 1 second was studied on the endothelial cell at an interval of every 0.05 seconds. Such time simulated spatial models may be useful for testing and developing new hypotheses, interpretation of results and understand the dynamic behavior of cells.
Background: Smooth muscle cells (SMC) constitute the major contractile cell population of blood vessels and inner organs. SMC contraction depends on energy provided by adenosine triphosphate (ATP) catabolism, which can be generated through oxidative phosphorylation in mitochondria or by anaerobic glycolysis. Mitochondrial activity may also modulate smooth muscle tone by biotransformation of vasoactive mediators. Here, we study the role of mitochondrial DNA gene expression for vascular function in vivo. Methods: Since loss of functional mitochondria in SMC may not be compatible with normal development, we generated mice with inducible SMC-specific abrogation of the mitochondrial transcription factor A (Tfam). Deletion of this gene leads to dysfunctional mitochondria and prevents aerobic ATP production in affected cells. Results: Invasive blood pressure monitoring in live animals demonstrated that SMC specific Tfam deletion results in lower blood pressure and a defective blood-pressure response to stress, changes that were not compensated by increased heart rate. The contractility to agonists was reduced in arterial and gastric fundus strips from Tfam-deficient mice. Endothelium-dependent relaxation of arterial strips in response to ACh was also blunted. Conclusion: Our data show that mitochondrial function is needed for normal gastric contraction, vascular tone, and maintenance of normal blood pressure.
Pierwsza strona wyników Pięć stron wyników wstecz Poprzednia strona wyników Strona / 2 Następna strona wyników Pięć stron wyników wprzód Ostatnia strona wyników
JavaScript jest wyłączony w Twojej przeglądarce internetowej. Włącz go, a następnie odśwież stronę, aby móc w pełni z niej korzystać.