scholarly journals Upregulation of Connexin43 Gap Junctions Between Smooth Muscle Cells After Balloon Catheter Injury in the Rat Carotid Artery

1997 ◽  
Vol 17 (11) ◽  
pp. 3174-3184 ◽  
Author(s):  
Hung-I Yeh ◽  
Florea Lupu ◽  
Emmanuel Dupont ◽  
Nicholas J. Severs
Keyword(s):  
Smooth Muscle ◽  
Carotid Artery ◽  
Smooth Muscle Cells ◽  
Gap Junctions ◽  
Balloon Catheter ◽  
Muscle Cells ◽  
Connexin43 Gap Junctions ◽  
Balloon Catheter Injury

RAPID AND STRONG PLATELET REACTIONS AND COAGULATION CAUSED BY INJURY OF PROLIFERATING INTIMAL SMOOTH MUSCLE CELLS

1987 ◽  
Author(s):  
L Jϕrgensen ◽  
A G Grϕthe ◽  
H M Groves ◽  
M Richardson
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Balloon Catheter ◽  
Muscle Cells ◽  
Luminal Surface ◽  
Sem And Tem ◽  
Balloon Catheter Injury ◽  
Fibrin Thrombi

We have shown that while one balloon catheter injury to rabbit aortae results in formation of a monolayer of platelets on the de-endothelialized surface, a second identical injury 7 days later gives rise to platelet-fibrin thrombi as observed at 30 minutes after the reinjury. The enhanced thrombogenicitythe second time was related to damage of theneointima which had formed during the intervening days. It was unclear whether it was due to damage of the cells or of the interstitum. In order to further explore the mechanisms of the enhanced thrombogenicity followingreinjury we observed by SEM and TEM the sequence of reactions before and during the first seconds and minutes after the second injury. The neointima was distributed around and opposite the branch orifices; the remainder of the luminal surface consisted of uncovered subendothelium. Within 10-30 seconds afterthe reinjury some of the neointimal cells were partly detached, and a few platelets and fibrin-like strands were in contact with them. Within 1-5 minutes many platelets, both single and in groups, with or without fibrin strands, had gathered in association with injured smooth muscle cells. The reinjured subendothelium remained uncovered the first 10-30 seconds; at 1-5 minutes an incomplete monolayer of swollen platelets had formed, but no fibrin was observed.These observations confirm that injury to neointima causes increased thrombogenicity. Since the first platelet reactionsand coagulation are associated with injured neointimal cells, it is likely that injury to these cells precipitates these reactions.

Upregulation of connexin43 gap junctions between neointimal smooth muscle cells

2004 ◽  
Vol 83 (10) ◽  
pp. 521-530 ◽  
Author(s):  
Gabriele Plenz ◽  
Yu-Shien Ko ◽  
Hung-I Yeh ◽  
Heike Eschert ◽  
Jürgen R. Sindermann ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Gap Junctions ◽  
Muscle Cells ◽  
Connexin43 Gap Junctions

Isolation of smooth muscle cells from swine carotid artery by digestion with papain

1986 ◽  
Vol 251 (3) ◽  
pp. C474-C481 ◽  
Author(s):  
S. P. Driska ◽  
R. Porter
Keyword(s):  
Smooth Muscle ◽  
Carotid Artery ◽  
Smooth Muscle Cells ◽  
Single Cells ◽  
Calcium Ionophore ◽  
Muscle Cells ◽  
Ionophore A23187 ◽  
Free Solution ◽  
Isolated Cells ◽  
Viable Cells

A new method is described for the preparation of viable, elongated smooth muscle cells from the swine carotid artery. Cells were prepared by papain digestion of pressurized arteries in calcium-free solution. After digestion, the arteries were everted, and fine strips were teased from the intimal surface of the media in calcium-free solution, releasing single cells. Viability was assessed by exclusion of trypan blue and by appearance under phase-contrast microscopy. By these criteria, approximately 20% of the isolated cells were viable. The most distinguishing and unexpected characteristic of these cells was their length. Mean length of the relaxed viable cells was 240.4 +/- 47.4 microns (SD, n = 76), which is much longer than previously reported for arterial smooth muscle cells. Calcium (1.6 mM) caused most of the viable cells to contract slightly, and the mean cell length in calcium was 194.4 +/- 57.7 microns. Cells in 1.6 mM calcium contracted substantially in response to 10 microM histamine or the calcium ionophore A23187 (10 microM), demonstrating that histamine receptors and the contractile apparatus were still functional.

scholarly journals Tamoxifen Accelerates Endothelial Healing by Targeting ERα in Smooth Muscle Cells

2020 ◽  
Vol 127 (12) ◽  
pp. 1473-1487 ◽  
Author(s):  
Rana Zahreddine ◽  
Morgane Davezac ◽  
Natalia Smirnova ◽  
Melissa Buscato ◽  
Emeline Lhuillier ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Endothelial Cells ◽  
Smooth Muscle ◽  
Carotid Artery ◽  
Smooth Muscle Cells ◽  
Mouse Models ◽  
Expression Profiles ◽  
Protective Action ◽  
Muscle Cells ◽  
17Β Estradiol

Rationale: Tamoxifen prevents the recurrence of breast cancer and is also beneficial against bone demineralization and arterial diseases. It acts as an ER (estrogen receptor) α antagonist in ER-positive breast cancers, whereas it mimics the protective action of 17β-estradiol in other tissues such as arteries. However, the mechanisms of these tissue-specific actions remain unclear. Objective: Here, we tested whether tamoxifen is able to accelerate endothelial healing and analyzed the underlying mechanisms. Methods and Results: Using 3 complementary mouse models of carotid artery injury, we demonstrated that both tamoxifen and estradiol accelerated endothelial healing, but only tamoxifen required the presence of the underlying medial smooth muscle cells. Chronic treatment with 17β-estradiol and tamoxifen elicited differential gene expression profiles in the carotid artery. The use of transgenic mouse models targeting either whole ERα in a cell-specific manner or ERα subfunctions (membrane/extranuclear versus genomic/transcriptional) demonstrated that 17β-estradiol-induced acceleration of endothelial healing is mediated by membrane ERα in endothelial cells, while the effect of tamoxifen is mediated by the nuclear actions of ERα in smooth muscle cells. Conclusions: Whereas tamoxifen acts as an antiestrogen and ERα antagonist in breast cancer but also on the membrane ERα of endothelial cells, it accelerates endothelial healing through activation of nuclear ERα in smooth muscle cells, inviting to revisit the mechanisms of action of selective modulation of ERα.

Platelet And Smooth Muscle Cell Responses After Endothelial Desquamation

1981 ◽  
Author(s):  
M B Stemerman
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Abdominal Aorta ◽  
Vessel Wall ◽  
Balloon Catheter ◽  
Muscle Cells ◽  
Mechanical Removal ◽  
Cell Counts ◽  
Old Rats

Although compromise of endothelial integrity occurs through many mechanisms, mechanical removal by balloon catheter is an excellent experimental method to study vascular responsiveness after injury. The interaction of platelets with the vessel wall, as well as proliferation of vascular smooth muscle cells can be assessed in this model. Following platelet attachment to the subendothelium, platelets release materials from their alpha granules. Using an antibody raised against platelet factor 4, a protein stored in alpha granules, we have demonstrated that material released from platelets do enter the vessel wall. A large amount of PF 4 antigen enters the wall shortly after endothelial removal, permeating the wall completely by 30 minutes, but little trace of the antigen can be found four hours after injury. Using infusions of PGI2 to a level of 850 ng/kg/min in rabbits, in vivo platelet adhesion to the exposed subendothelium can be greatly reduced and release of PF4 antigen into the vessel wall markedly diminished. Growth of smooth muscle cells (SMC) after endothelial removal has also been measured by 3H-Thymidine labeling of SMC DNA. As measured by this method as well as direct cell counts, SMC proliferation in the abdominal aorta is significantly greater than the thoracic. Reinjury of only the abdominal aorta by balloon catheter 4 days after the initial total aortic injury causes a proliferative spurt in the thoracic aortic SMC, thus demonstrating that a humoral signal can initiate SMC proliferation. In addition, the response of SMC from 21 month old rats when compared with 3 month old rats is much greater. These studies demonstrate in vivo methods for examining the response of platelets and SMC following endothelial injury. Further, these studies indicate that the response to injury hypothesis of atherosclerosis progression should now be broadened to the concept of a response to signal view of atherogenesis.

Characterization of Ca2+ channels involved in ET-1-induced transactivation of EGF receptors

2002 ◽  
Vol 283 (6) ◽  
pp. H2671-H2675 ◽  
Author(s):  
Yoshifumi Kawanabe ◽  
Nobuo Hashimoto ◽  
Tomoh Masaki
Keyword(s):  
Smooth Muscle ◽  
Carotid Artery ◽  
Internal Carotid Artery ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Internal Carotid ◽  
Specific Inhibitor ◽  
Muscle Cells ◽  
Receptor Protein

The purpose of this study was to demonstrate the involvement of Ca2+ influx through voltage-independent Ca2+ channels (VICCs) in endothelin-1 (ET-1)-induced transactivation of epidermal growth factor receptor protein tyrosine kinase (EGFR PTK) using the Ca2+ channel blockers LOE-908 and SK&F-96365 in rabbit internal carotid artery vascular smooth muscle cells. ET-1-induced EGFR PTK transactivation was completely inhibited by AG-1478, which is a specific inhibitor of EGFR PTK. In the absence of extracellular Ca2+, the magnitude of EGFR PTK transactivation was near the basal level. Based on sensitivity to nifedipine, which is a specific blocker of voltage-operated Ca2+ channels (VOCCs), VOCCs have minor roles in EGFR PTK transactivation. In contrast, Ca2+ influx through VICCs plays an important role in EGFR PTK transactivation. Moreover, based on the sensitivity of VICCs to SK&F-96365 and LOE-908, VICCs were shown to consist of two types of Ca2+-permeable nonselective cation channels (NSCCs), which are designated NSCC-1 and NSCC-2, and a store-operated Ca2+ channel. In summary, Ca2+influx through VICCs plays an essential role in ET-1-induced EGFR PTK transactivation in rabbit internal carotid artery vascular smooth muscle cells.

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