scholarly journals The effect of endothelial progenitor cell transplantation on neointimal hyperplasia and reendothelialisation after balloon catheter injury in rat carotid arteries

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Wei Wang ◽  
Yingqian Zhang ◽  
Hui Hui ◽  
Wei Tong ◽  
Zechen Wei ◽  
...  
Keyword(s):  
Cell Culture ◽  
Endothelial Cells ◽  
Carotid Arteries ◽  
Neointimal Hyperplasia ◽  
Balloon Catheter ◽  
Enzyme Linked Immunosorbent Assay ◽  
Sham Operation ◽  
Luminal Surface ◽  
Endothelial Progenitor ◽  
Culture Supernatants

Abstract Background Reendothelialisation is the natural pathway that inhibits neointimal hyperplasia and in-stent restenosis. Circulating endothelial progenitor cells (EPCs) derived from bone marrow (BM) might contribute to endothelial repair. However, the temporal and spatial distributions of reendothelialisation and neointimal hyperplasia after EPC transplantation in injured arteries are currently unclear. Methods A carotid balloon injury (BI) model was established in Sprague-Dawley rats, and PKH26-labelled BM-derived EPCs were transplanted after BI. The carotid arteries were harvested on the first, fourth, seventh, and 14th day post-injury and analysed via light-sheet fluorescence microscopy and pathological staining (n = 3). EPC and human umbilical vein endothelial cell culture supernatants were collected, and blood samples were collected before and after transplantation. The paracrine effects of VEGF, IGF-1, and TGF-β1 in cell culture supernatants and serum were analysed by enzyme-linked immunosorbent assay (n = 4). Results Transplanted EPCs labelled with PKH26 were attached to the injured luminal surface the first day after BI. In the sham operation group, the transplanted EPCs did not adhere to the luminal surface. From the fourth day after BI, the mean fluorescence intensity of PKH26 decreased significantly. However, reendothelialisation and inhibition of neointimal hyperplasia were significantly promoted by transplanted EPCs. The degree of reendothelialisation of the EPC7d and EPC14d groups was higher than that of the BI7d and BI14d groups, and the difference in neointimal hyperplasia was observed between the EPC14d and BI14d groups. The number of endothelial cells on the luminal surface of the EPC14d group was higher than that of the BI14d group. The number of infiltrated macrophages in the injured artery decreased in the EPC transplanted groups. Conclusions Transplanted EPCs had chemotactic enrichment and attached to the injured arterial luminal surface. Although decreasing significantly after the fourth day at the site of injury after transplantation, transplanted EPCs could still promote reendothelialisation and inhibit neointimal hyperplasia. The underlying mechanism is through paracrine cytokines and not differentiation into mature endothelial cells.

scholarly journals Effect of Endothelial Progenitor Cells Transplantation on Neointimal Hyperplasia and Reendothelialization after Balloon Catheter Injury in Rat Carotid Arteries

2020 ◽  
Author(s):  
WEI WANG ◽  
Yingqian Zhang ◽  
Hui Hui ◽  
Wei Tong ◽  
Zechen Wei ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Spatial Distribution ◽  
Progenitor Cells ◽  
Carotid Arteries ◽  
Neointimal Hyperplasia ◽  
Luminal Surface ◽  
Balloon Injury ◽  
Post Injury ◽  
Temporal And Spatial Distribution ◽  
Temporal And Spatial

Abstract Background: Reendothelialization is a natural pathway to inhibit neointimal hyperplasia and in-stent restenosis. Circulating endothelial progenitor cells (EPCs) derived from bone marrow might contribute to endothelial repair. However, the temporal and spatial distribution of injured vascular reendothelialization and neointimal hyperplasia in the presence of transplanted EPCs is not quite clear. Methods: We performed a carotid balloon injury model and treated by transplantation of bone marrow-derived EPCs. To evaluate the temporal and spatial distribution of neointimal hyperplasia and reendothelialization after injury, the carotid arteries were harvested at different time points after transplantation. Results: Transplanted EPCs labeled by PKH26 were clearly observed attaching on the injured luminal surface at day 1 post-injury. For the undamaged arteries, the transplanted EPCs never adhered to the luminal surface. From day 4 post-injury, the average value of PKH26 fluorescence decreased significantly. Although transplanted EPCs were decreased significantly at the site of injury on day 4 after transplantation, reendothelialization at the site of the injury and inhibition of neointimal hyperplasia were significantly promoted by transplanted EPCs. The degree of reendothelialization of EPC7d (group of EPCs transplantation after balloon injury and harvested at day 7 post-transplantation)/EPC14d was significantly better than that of the BI7d (group of medium injection after balloon injury and harvested at day 7 post-injection)/BI14d, and the statistical difference of neointimal hyperplasia began to appear between EPC14d and BI14d. The number of endothelial cells on the lumen surface of EPC14d increased than that of BI14d, and the number of infiltrated macrophages at the injury site decreased.Conclusions: Transplanted EPCs had chemotactic enrichment and attached to the injured arterial intima after transplantation. Although decreased significantly at the site of injury over time after transplantation, transplanted EPCs could still promote the reendothelialization at the site of the injury and inhibition of neointimal hyperplasia.

scholarly journals Diabetes-Induced Oxidative Stress in Endothelial Progenitor Cells May Be Sustained by a Positive Feedback Loop Involving High Mobility Group Box-1

2016 ◽  
Vol 2016 ◽  
pp. 1-9 ◽  
Author(s):  
Han Wu ◽  
Ran Li ◽  
Zhong-Hai Wei ◽  
Xin-Lin Zhang ◽  
Jian-Zhou Chen ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Culture ◽  
Positive Feedback ◽  
Feedback Loop ◽  
High Mobility ◽  
High Mobility Group ◽  
Dependent Manner ◽  
Endothelial Progenitor ◽  
Positive Feedback Loop ◽  
Culture Supernatants

Oxidative stress is considered to be a critical factor in diabetes-induced endothelial progenitor cell (EPC) dysfunction, although the underlying mechanisms are not fully understood. In this study, we investigated the role of high mobility group box-1 (HMGB-1) in diabetes-induced oxidative stress. HMGB-1 was upregulated in both serum and bone marrow-derived monocytes from diabetic mice compared with control mice. In vitro, advanced glycation end productions (AGEs) induced, expression of HMGB-1 in EPCs and in cell culture supernatants in a dose-dependent manner. However, inhibition of oxidative stress with N-acetylcysteine (NAC) partially inhibited the induction of HMGB-1 induced by AGEs. Furthermore, p66shc expression in EPCs induced by AGEs was abrogated by incubation with glycyrrhizin (Gly), while increased superoxide dismutase (SOD) activity in cell culture supernatants was observed in the Gly treated group. Thus, HMGB-1 may play an important role in diabetes-induced oxidative stress in EPCs via a positive feedback loop involving the AGE/reactive oxygen species/HMGB-1 pathway.

scholarly journals Detection of Cell Wall Mannoprotein Mp1p in Culture Supernatants of Penicillium marneffei and in Sera of Penicilliosis Patients

1999 ◽  
Vol 37 (4) ◽  
pp. 981-986 ◽  
Author(s):  
Liang Cao ◽  
King-Man Chan ◽  
Daliang Chen ◽  
Nongnuch Vanittanakom ◽  
Cindy Lee ◽  
...  
Keyword(s):  
Cell Culture ◽  
Cell Wall ◽  
Western Blotting ◽  
Predictive Value ◽  
Culture Supernatant ◽  
Pathogenic Fungus ◽  
Penicillium Marneffei ◽  
Cell Culture Supernatant ◽  
Enzyme Linked Immunosorbent Assay ◽  
Culture Supernatants

Mannoproteins are important and abundant structural components of fungal cell walls. The MP1 gene encodes a cell wall mannoprotein of the pathogenic fungus Penicillium marneffei. In the present study, we show that Mp1p is secreted into the cell culture supernatant at a level that can be detected by Western blotting. A sensitive enzyme-linked immunosorbent assay (ELISA) developed with antibodies against Mp1p was capable of detecting this protein from the cell culture supernatant of P. marneffei at 104 cells/ml. The anti-Mp1p antibody is specific since it fails to react with any protein-form lysates of Candida albicans, Histoplasma capsulatum, or Cryptococcus neoformans by Western blotting. In addition, this Mp1p antigen-based ELISA is also specific for P. marneffei since the cell culture supernatants of the other three fungi gave negative results. Finally, a clinical evaluation of sera from penicilliosis patients indicates that 17 of 26 (65%) patients are Mp1p antigen test positive. Furthermore, a Mp1p antibody test was performed with these serum specimens. The combined antibody and antigen tests for P. marneffeicarry a sensitive of 88% (23 of 26), with a positive predictive value of 100% and a negative predictive value of 96%. The specificities of the tests are high since none of the 85 control sera was positive by either test.

scholarly journals Expression of Heparin-Binding Epidermal Growth Factor–Like Growth Factor in Neointimal Cells Induced by Balloon Injury in Rat Carotid Arteries

1996 ◽  
Vol 16 (12) ◽  
pp. 1524-1531 ◽  
Author(s):  
Takumi Igura ◽  
Sumio Kawata ◽  
Jun-ichiro Miyagawa ◽  
Yoshiaki Inui ◽  
Shinji Tamura ◽  
...  
Keyword(s):  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Carotid Arteries ◽  
Balloon Catheter ◽  
Arterial Injury ◽  
Luminal Surface ◽  
Heparin Binding ◽  
Neointimal Formation ◽  
Epidermal Growth

Balloon catheter injury of rat carotid arteries induces migration and proliferation of smooth muscle cells (SMCs), with subsequent neointimal formation. Several growth factors, such as platelet-derived growth factor and basic fibroblast growth factor, have been shown to be involved in this process, but the mechanisms that modulate the growth and/or migratory properties of SMCs remain unclear. In this study, we investigated whether heparin-binding epidermal growth factor–like growth factor (HB-EGF), which is known to be a potent SMC stimulator from in vitro study, is associated with the proliferative response of SMCs to arterial injury. Northern blot analysis showed that the transcript levels of HB-EGF increased rapidly approximately 12-fold within 2 hours after injury and declined by 2 days but remained 3-fold at 14 days. In situ hybridization analysis demonstrated that the transcript of HB-EGF remained strongly expressed in the neointima, especially near the luminal surface, at 14 days after injury. Immunohistochemical staining showed that HB-EGF protein was positive in the endothelium and only faintly visible in medial SMCs in uninjured vessels. In contrast, 2 days after injury, positive HB-EGF immunostaining was detected in the medial SMCs along the luminal surface. At 7 days, the neointimal SMCs exhibited strong immunostaining for HB-EGF, and at 14 days, they exhibited a gradient of HB-EGF expression with strong immunoreactivity in the most luminal cells. SMCs labeled with 5-bromo-2′-deoxyuridine in their nuclei showed strong immunostaining for HB-EGF protein. Furthermore, the epidermal growth factor receptor to which HB-EGF can bind was also immunostained positively in neointimal SMCs. These data suggest that HB-EGF may play an important role of the proliferation and migration of SMCs in the process of neointimal accumulation induced by arterial injury, probably in an autocrine, paracrine, and/or juxtacrine manner.

The Basement Membrane Underlying the Vascular Endothelium Is Not Thrombogenic: In Vivo and In Vitro Studies with Rabbit and Human Tissue

1987 ◽  
Vol 58 (02) ◽  
pp. 698-704 ◽  
Author(s):  
M R Buchanan ◽  
M Richardson ◽  
T A Haas ◽  
J Hirsh ◽  
J A Madri
Keyword(s):  
Endothelial Cells ◽  
Basement Membrane ◽  
Carotid Arteries ◽  
Platelet Adhesion ◽  
Balloon Catheter ◽  
Ammonium Hydroxide ◽  
Platelet Accumulation ◽  
Scanning Electron

SummaryStudies examining the interaction of platelets with exposed subendothelium in vivo have reported conflicting results, lo examine possible explanations for the apparently discrepant findings, we measured the platelet reactivity of subendothelium prepared by a number of methods both in vivo and in vitro. In addition, we examined the possibility that 13-hydroxyoc-tadecadinoic acid (13-HODE), an endothelial cell-derived chemorepellant, modulates the reactivity of the subendothelium to platelets. In vivo, the subendothelium of segments of rabbit carotid arteries was exposed by removing the endothelial cells by air perfusion or by balloon catheter stripping. Platelet accumulation onto the dc-cndothelialized segments was assessed by 3H-radioaclivily uptake, using 3H-adenine-labelled platelets, and by scanning electron microscopy. In vitro, 3H-adenine-labelled platelet adhesion was measured onto plain plastic discs and onto plastic discs coated with the following purified basement membrane components: collagens type I, III, IV, V, laminin, or fibronectin. In addition, 3H-adenine-labelled platelet adhesion was measured onto plastic discs coveredwith human endothelial cells or onto the basement membrane underlying the endothelial cells. In vivo, there was marked 3H-platelet accumulation onto the ballon catheter carotid arteries one hour after injury. In contrast, there was no platelet accumulation onto the subendothelium of carotid arteries de-endothelialized by air perfusion. These differences were confirmed by scanning electron microscopy. Transmission electron microscopic examination demonstrated that the extracellular matrix was intact following the air perfusion injury whereas the majority of it was removed by the balloon catheter injury. In vitro, the accumulation of 3H-platelets onto plain discs and onto discs coated with any of the four collagens, fibronectin or laminin was significantly greater than the adhesion of 3H-platelets onto intact endothelial cells or the basement membrane prepared by cellulose acetate stripping. In contrast, 3H-platelet adhesion onto the basement membrane prepared by ammonium hydroxide treatment was significantly increased. An HPLC analysis of methanol extracts obtained from the two basement membranes and the cultured endothelial in vitro demonstrated that there was significant amounts of 13-HODE present in the endothelial cells and in the basement membrane prepared by the mechanical stripping, but there was no detectable 13-HODE in the basement membrane prepared by ammonium hydroxide treatment.We conclude that platelets do not adhere to subendothelium immediately beneath the endothelium and that this thromboresistance is contributed to by 13-HODE. We also suggest that the observed thrombogeneicity of subendothelium following balloon-induced injury is due to the mechanical removal of sub-endothelial structures including 13-HODE, exposing deeper more thrombogenic vascular wall structures.

Alterations in Vascular Endothelial Cell-related Plasma Proteins In Thalassaemic Patients and their Correlation with Clinical Symptoms

1995 ◽  
Vol 74 (04) ◽  
pp. 1045-1049 ◽  
Author(s):  
P Butthep ◽  
A Bunyaratvej ◽  
Y Funahara ◽  
H Kitaguchi ◽  
S Fucharoen ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Immunosorbent Assay ◽  
Plasma Proteins ◽  
Clinical Symptoms ◽  
Vascular Endothelial Cells ◽  
Vascular Endothelial Cell ◽  
Enzyme Linked Immunosorbent Assay ◽  
Vascular Endothelial ◽  
Leg Ulcers

SummaryAn increased level of plasma thrombomodulin (TM) in α- and β- thalassaemia was demonstrated using an enzyme-linked immunosorbent assay (ELISA). Nonsplenectomized patients with β-thalassaemia/ haemoglobin E (BE) had higher levels of TM than splenectomized cases (BE-S). Patients with leg ulcers (BE-LU) were found to have the highest increase in TM level. Appearance of larger platelets in all types of thalassaemic blood was observed indicating an increase in the number of younger platelets. These data indicate that injury of vascular endothelial cells is present in thalassaemic patients.

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