Wyniki wyszukiwania - Biblioteka Nauki

1

Facial artery and atherosclerosis

100%

Alconchel M. D. , Whyte J. , Torres A. , Cisneros A. , Sarrat R.

Folia Morphologica

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1999

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tom 58

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nr 3

EN

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.

2

The role of external Ca2plus in the action of Ca2plus-channel agonists and antagonists on isolated human thoracic arteries

88%

Garaliene V. , Barsys V. , Giedraitis S. , Benetis R. , Krauze A.

Journal of Physiology and Pharmacology

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2014

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tom 65

|

nr 1

3

Beta3-integrin cytoplasmic binding proteins

88%

Zhao R. , Pathak A. S. , Stouffer G. A.

Archivum Immunologiae et Therapiae Experimentalis

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2004

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tom 52

|

nr 5

4

Physiology and pathophysiology of vascular signaling controlled by guanosine 3',5'-cyclic monophosphate-dependent protein kinase.

75%

Birschmann I. , Walter U.

Acta Biochimica Polonica

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2004

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tom 51

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nr 2

397-404

EN

Recent medical advances suggest that the cellular natriuretic peptide/cGMP and NO/cGMP effector systems represent important signal transduction pathways especially in the cardiovascular system. These pathways also appear to be very interesting targets for the possible prevention of cardiovascular diseases. Exciting candidates for prevention include cGMP-dependent signaling networks initiated by natriuretic peptides (NP) and nitric oxide (NO) which are currently explored for their diagnostic and therapeutic potential. cGMP signaling contributes to the function and interaction of several vascular cell types, and its dysfunction is involved in the progression of major cardiovascular diseases such as atherosclerosis, hypertension and diabetic complications. This review will take a focussed look at key elements of the cGMP signaling cascade in vascular tissue. Recent advances in our knowledge of cGMP-dependent protein kinases (cGK, also known as PKG), the potential for assessing the functional status of cGMP signaling and the possible cross talk with insulin signaling will be reviewed.

5

Iatrogenic Chlamydia infection-associated damage in the basilar arterial wall of the rat

75%

Chrapusta S. J. , Walski M.

Folia Histochemica et Cytobiologica

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2002

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tom 40

|

nr 4

6

Phosphodiesterase 3A expression is modulated by nitric oxide in rat pulmonary artery smooth muscle cells

63%

Busch C. J. , Graveline A. R. , Jiramongkolchai K. , Liu H. , Sanchez L. S. , Bloch K. D.

Journal of Physiology and Pharmacology

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2010

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tom 61

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nr 6

7

Selected aspects of endothelial dysfunction and their influence on the atherosclerosis process modeled and analyzed by Petri net based approach

63%

Formanowicz D. , Kozak A. , Formanowicz P.

BioTechnologia. Journal of Biotechnology Computational Biology and Bionanotechnology

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2011

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tom 92

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nr 4

8

Time-dependent model to mimic acetylcholine induced vasodilatation in arterial smooth muscle cells

63%

Sahrawat T. R. , Chatterjee D.

International Letters of Natural Sciences

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2016

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tom 52

EN

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.

9

Aldolase A is present in smooth muscle cell nuclei

63%

Mamczur P. , Dzugaj A.

Acta Biochimica Polonica

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2008

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tom 55

|

nr 4

799-805

EN

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.

10

Potentially positive ageing-related variations of medial smooth muscle cells in the saphenous veins used as aortocoronary bypass grafts

63%

Perek B. , Malinska A. , Gasowski J. , Ostalska-Nowicka D. , Perek A. , Jemielity M. , Zabel M. , Nowicki M.

Folia Histochemica et Cytobiologica

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2016

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tom 54

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nr 2

11

Mechanisms of vascular dysfunction after subarachnoid hemorrhage

63%

Kozniewska E. , Michalik R. , Rafalowska J. , Gadamski R. , Walski M. , Frontczak-Baniewicz M. , Piotrowski P. , Czernicki Z.

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tom 57

|

nr 11

145-160

EN

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.

12

Modulation of connexin-43 by omega-3 fatty acids in the aorta of old spontaneously hypertensive rats

63%

Dlugosova K. , Okruhlicova L. , Mitasikova M. , Sotnikova R. , Bernatova I. , Weismann P. , Slezak J. , Tribulova N.

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nr 3

63-69

EN

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.

13

Stimulation of large-conductance Ca2plus-activated Kplus channels by the Naplus-Ca2plus exchanger inhibitor dichlorobenzamil in cultured human umbilical vein endothelial cells and mouse aortic smooth muscle cells

63%

Liang G. H. , Park S. , Kim J. A. , Choi S. , Suh S. H.

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tom 60

|

nr 1

43-50

EN

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.

14

Cross talk between NO and cyclic nucleotide phosphodiesterases in the modulation of signal transduction in blood vessel

63%

Lugnier C. , Keravis T. , Eckly-Michel A.

Journal of Physiology and Pharmacology

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1999

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tom 50

|

nr 4

15

Abrogation of mitochondrial transcription in smooth muscle cells impairs smooth muscle contractility and vascular tone

63%

Jawien J. , Bian Z. , Sheikine Y. , Olofsson P. S. , Pang Y. , Edholm T. , Dou Y. , Metzger D. , Hellstrom P. M. , Feil R. , Hansson G. K.

Journal of Physiology and Pharmacology

|

2008

|

tom 59

|

nr 2

EN

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.

16

Mechanism of collagen biosynthesis up-regulation in cultured leiomyoma cells

51%

Zbucka M. , Miltyk W. , Bielawski T. , Surazynski A. , Palka J. , Wolczynski S.

Folia Histochemica et Cytobiologica. Supplement

|

2007

|

tom 45

|

nr 1

181-185

17

Assessment of S100 protein expression in the epididymis of juvenile and adult European bison

51%

Czykier E. , Zabel M. , Surdyk-Zasada J. , Lebelt A. , Klim B.

Folia Histochemica et Cytobiologica

|

2010

|

tom 48

|

nr 3

18

Different expression of cyclooxygenase-2 (COX-2) in selected nonmelanocytic human cutaneous lesions

51%

Kuzbicki L. , Lange D. , Stanek-Widera A. , Chwirot B. W.

Folia Histochemica et Cytobiologica

|

2011

|

tom 49

|

nr 3

19

Immunohistochemical localization of selected pro-inflammatory factors in uterine myomas and myometrium in women of various ages

51%

Plewka A. , Madej P. , Plewka D. , Kowalczyk A. , Miskiewicz A. , Wittek P. , Leks T. , Bilski R.

Folia Histochemica et Cytobiologica

|

2013

|

tom 51

|

nr 1

20

A poly[ADP-ribose] synthetase inhibitor, benzamide protects smooth muscle cells but not endothelium against ischemia-reperfusion injury in isolated guinea-pig heart

51%

Jakubowski A. , Lomnicka M.

Acta Biochimica Polonica

|

2007

|

tom 54

|

nr 1

EN

Activation of the nuclear enzyme poly(ADP-ribose) synthethase (PARS) is important in the cellular response to oxidative stress. During ischemia and reperfusion (I/R) increased free radical production leads to DNA breakage that stimulates PARS which in turn results in an energy-consuming metabolic cycle and initiation of the apoptotic process. Previous studies have reported that PARS inhibition confers protection in various models of I/R-induced cardiovascular damage. The purpose of this study was to determine the role of PARS inhibition in I/R-induced injury of smooth muscle cells and endothelium in the coronary circulation of the isolated guinea-pig heart. Control hearts and those treated with a PARS inhibitor — benzamide (100 µmol L-1), were subjected to 30 min of subglobal ischemia and subsequent reperfusion (90 min). To analyze the functional integrity of smooth muscle cells and endothelium, one-minute intracoronary infusions of endothelium-independent (sodium nitroprusside, NaNP; 3 µmol L-1) and endothelium-dependent (substance P, SP; 10 nmol L-1) vasodilators were used before ischemia and at the reperfusion time. The degree of the injury of coronary smooth muscle and endothelial cells induced by I/R was estimated in terms of diminished vasodilator responses to NaNP (at 55 min and 85 min of reperfusion) and to SP (at 70 min of reperfusion), respectively, and expressed as the percentage of preischemic response. I/R reduced vasorelaxant responses to both vasodilators by half (to 54.1 ± 5.1% and to 53.6 ± 4.9% of preischemic value for NaNP at 55 min and 85 min of reperfusion, respectively and to 45.9 ± 6.5% for SP at 70 min of reperfusion). PARS inhibition provided complete restoration of vasorelaxation induced by NaNP (107.6 ± 13.3% and 104 ± 14.4% of preischemic response at the two time points of reperfusion, respectively). However, there was no effect on the SP-induced response (48+12.1% of preischemic response). We conclude that pharmacological PARS inhibition with benzamide protects coronary smooth muscle cells but not endothelium against I/R-induced reperfusion injury in the coronary circulation of the guinea-pig heart.