12 results on '"Anton Razuvaev"'
Search Results
2. Effects of Linagliptin on Vessel Wall Healing in the Rat Model of Arterial Injury Under Normal and Diabetic Conditions
- Author
-
Malin Kronqvist, Samuel Röhl, Claes-Göran Östenson, Robert Saxelin, Kenneth Caidahl, Mariette Lengquist, Anton Razuvaev, and Linnéa Eriksson
- Subjects
Blood Glucose ,Male ,Neointima ,medicine.medical_specialty ,medicine.medical_treatment ,Linagliptin ,030209 endocrinology & metabolism ,030204 cardiovascular system & hematology ,Pharmacology ,Random Allocation ,03 medical and health sciences ,chemistry.chemical_compound ,0302 clinical medicine ,Restenosis ,In vivo ,Angioplasty ,Animals ,Hypoglycemic Agents ,Medicine ,Rats, Wistar ,Cell Proliferation ,Evans Blue ,Wound Healing ,Dose-Response Relationship, Drug ,business.industry ,medicine.disease ,Rats ,Surgery ,Treatment Outcome ,Diabetes Mellitus, Type 2 ,chemistry ,Carotid Artery, External ,cardiovascular system ,Immunohistochemistry ,Carotid Artery Injuries ,Cardiology and Cardiovascular Medicine ,business ,Wound healing ,medicine.drug - Abstract
Diabetic patients suffer an increased risk of restenosis and late stent thrombosis after angioplasty, complications which are related to a defective reendothelialization. Dipeptidyl peptidase-4 inhibitors have been suggested to exert a direct effect on endothelial and smooth muscle cells (SMCs). Therefore, the objective was to study if the dipeptidyl peptidase-4 inhibitor linagliptin could influence vascular repair and accelerate reendothelialization after arterial injury in healthy and diabetic animals. Diabetic Goto-Kakizaki and healthy Wistar rats were subjected to arterial injury and treated with linagliptin or vehicle. Vessel wall healing was monitored noninvasively using ultrasound, and on sacrifice, with Evans blue staining and immunohistochemistry. The effect of linagliptin on SMCs was also studied in vitro. We found that linagliptin reduced the proliferation and dedifferentiation of SMCs in vitro, and modulated the inflammatory response in the SMCs after arterial injury in vivo. However, these effects of linagliptin did not affect the neointima formation or the reendothelialization under normal and diabetic conditions. Although linagliptin did not influence vessel wall healing, it seems to possess a desirable antiproliferative influence on SMCs in vitro and an antiinflammatory effect in vivo. These pharmacological properties might carry a potential significance for favorable outcome after vascular interventions in diabetic patients.
- Published
- 2017
3. Whole Genome Expression Profiling to Detect Novel Pathways in Restenosis of Peripheral Arteries
- Author
-
Anton Razuvaev, Ulf Hedin, Joy Roy, Elena Ignatieva, Boris Kox, Anna Kostareva, Ljubica Perisic Matic, and Anton Fedorov
- Subjects
Gene expression profiling ,Restenosis ,business.industry ,medicine ,Surgery ,Computational biology ,Cardiology and Cardiovascular Medicine ,medicine.disease ,business ,Genome ,Peripheral - Published
- 2019
4. Negative Remodelling Contributes to Impaired Arterial Healing in Diabetic Rat
- Author
-
Claes-Göran Östenson, Ulf Hedin, Samuel Röhl, Kenneth Caidahl, and Anton Razuvaev
- Subjects
medicine.medical_specialty ,Endocrinology ,business.industry ,Diabetic rat ,Internal medicine ,medicine ,Surgery ,Cardiology and Cardiovascular Medicine ,business - Published
- 2019
5. Natural History of the Impaired Arterial Wall Healing Under Diabetic Conditions in the Rat Carotid Artery Balloon Injury Model
- Author
-
Ulf Hedin, Kenneth Caidahl, Anton Razuvaev, Ljubica Perisic Matic, Claes-Göran Östenson, Samuel Röhl, and Valeriy Vavilov
- Subjects
Natural history ,medicine.medical_specialty ,business.industry ,Carotid arteries ,Internal medicine ,Cardiology ,medicine ,Surgery ,Arterial wall ,Cardiology and Cardiovascular Medicine ,business ,Balloon injury - Published
- 2020
6. Absence of Pro-Protein Convertase Subtilisin/Kexin 6 Increases Flow-Mediated Outward Remodeling in the Mouse Carotid Artery
- Author
-
Ljubica Perisic Matic, Samuel Röhl, Kenneth Caidahl, Anton Razuvaev, Ulf Hedin, and Anders Arner
- Subjects
business.industry ,Carotid arteries ,Subtilisin ,Medicine ,Kexin ,Surgery ,Cardiology and Cardiovascular Medicine ,Pro protein ,business ,Cell biology - Published
- 2019
7. Liver parenchyma access and lesion marker via the endovascular route
- Author
-
Staffan Holmin, Bengt Isaksson, Anton Razuvaev, Johan Lundberg, Stefan Jonsson, and Thorhallur Agustsson
- Subjects
medicine.medical_specialty ,Pathology ,Catheters ,Swine ,business.industry ,Colorectal cancer ,Endovascular Procedures ,Local ablation ,food and beverages ,Antineoplastic Agents ,Signal-To-Noise Ratio ,medicine.disease ,Lesion ,Hepatic Artery ,Liver ,Animals ,Hepatectomy ,Medicine ,Female ,Surgery ,Radiology ,medicine.symptom ,business ,Liver parenchyma ,Ultrasonography - Abstract
Neoadjuvant chemotherapeutic regimens for metastatic colorectal cancer are now so effective that they can cause "vanishing" lesions. With new advances such as local ablation, intra-arterial treatments in bolus with pumps or with beads, and isolation of hepatic perfusion, the need for a working channel to the liver may be warranted, ideally reducing the risk of spreading neoplastic cells.The endovascular trans-vessel wall Extroducer device makes it possible to gain direct access to the liver parenchyma. The distal tip is then detached, to act as both a marker and a securing plug in the vessel defect. We used ex vivo and in vivo tests to evaluate the device as a working channel for local administration of substances to the parenchyma and as a marker for detection with both transabdominal and intraoperative ultrasonography.We could deploy the Extroducer device without any hemorrhagic or thromboembolic complications in vivo, and we were able to detect all markers ex vivo and in vivo using both transabdominal and intraoperative ultrasonography. Furthermore, we found that it is possible to administer substances to the liver parenchyma using the catheter.The trans-vessel wall technique can be used to establish a working channel to the liver parenchyma for administration of any substance, such as chemotherapeutic agents or cells. The detached device can also be used as a marker for ultrasound-guided partial liver resection in "vanishing lesions." The technique should have a low risk of seeding of neoplastic cells. This study in large animals forms a strong basis for translation to clinical studies.
- Published
- 2015
8. Tissue factor pathway inhibitor-2 is induced by fluid shear stress in vascular smooth muscle cells and affects cell proliferation and survival
- Author
-
Ulf Hedin, Joy Roy, Lasse Folkersen, Anton Razuvaev, and Johan Ekstrand
- Subjects
Neointima ,DNA Replication ,Male ,Pathology ,medicine.medical_specialty ,Vascular smooth muscle ,Time Factors ,Cell Survival ,Myocytes, Smooth Muscle ,Apoptosis ,Muscle, Smooth, Vascular ,Rats, Sprague-Dawley ,Tissue factor ,Gene expression ,medicine ,Animals ,Humans ,RNA, Messenger ,education ,Cells, Cultured ,Cell Proliferation ,Glycoproteins ,Oligonucleotide Array Sequence Analysis ,education.field_of_study ,DNA synthesis ,business.industry ,Cell growth ,Caspase 3 ,Reverse Transcriptase Polymerase Chain Reaction ,Gene Expression Profiling ,Immunohistochemistry ,Tissue-factor-pathway inhibitor 2 ,Recombinant Proteins ,Cell biology ,Rats ,Up-Regulation ,Disease Models, Animal ,Real-time polymerase chain reaction ,cardiovascular system ,Surgery ,Stress, Mechanical ,business ,Carotid Artery Injuries ,Cardiology and Cardiovascular Medicine - Abstract
ObjectiveVascular smooth muscle cells (SMCs) are exposed to fluid shear stress (FSS) after interventional procedures such as balloon-angioplasty. Whereas the effects of hemodynamic forces on endothelial cells are explored in detail, the influence of FSS on smooth muscle cell function is poorly characterized. Here, we investigated the effect of FSS on SMC gene expression and function.MethodsLaminar FSS of arterial level (14 dynes/cm2) was applied to SMC cultures for 24 hours in a parallel-plate flow chamber. The effect of FSS on gene expression was first screened with microarray technology, and results further verified by real time polymerase chain reaction (RT-PCR) and immunoblotting. Tissue factor pathway inhibitor-2 (TFPI-2) and caspase-3 protein expression was studied in the rat carotid artery after balloon-injury, and the effect of TFPI-2 on SMC DNA synthesis and apoptosis was examined in vitro.ResultsMicroarrays identified TFPI-2 as one of the most differentially expressed gene by FSS in cultured SMCs (P < .001). Gene set enrichment analysis revealed significant regulation of genes linked to proliferation, apoptosis, and cell cycle regulation. TFPI-2 induction was confirmed by RT-PCR and immunoblotting demonstrating a more than 400-fold (P < .001) increase in TFPI-2 mRNA in SMCs exposed to FSS compared with static controls, and a consistent protein upregulation. Functionally, SMC proliferation was decreased by FSS (P < .001), and recombinant TFPI-2 was found to inhibit SMC proliferation (P < .001) and induce SMC apoptosis as indicated by activation of caspase-3 (P < .01). In vivo, TFPI-2 expression was found to be upregulated 5, 10, and 20 hours (P < .01) after rat carotid balloon injury, and immunohistochemistry demonstrated TFPI-2 protein in FSS-exposed luminal SMCs, co-localized with caspase-3 in the rat carotid neointima.ConclusionFSS influenced gene expression associated with cell growth and apoptosis in cultured SMCs and strongly induced expression of TFPI-2 mRNA and protein. TFPI-2 was expressed in luminal, FSS-exposed SMCs together with caspase-3 in the rat carotid neointima after balloon injury. Functionally, TFPI-2 may play a role in vessel wall repair by regulating SMC proliferation and survival. Further studies are needed to elucidate the mechanisms by which TFPI-2 controls SMC function.Clinical RelevanceIn the arterial wall, endothelial cells are exposed to fluid shear stress imposed by the flowing blood. However, after vascular interventions, where the endothelial layer is denuded and in intimal hyperplasia that develops, luminal smooth muscle cells are exposed to shear stress. We show that TFPI-2 expression is strongly augmented in smooth muscle cells exposed to shear stress and that TFPI-2 co-localizes with caspase-3 in vivo. In addition, TFPI-2 inhibits smooth muscle cell proliferation and induces apoptosis in vitro. The adaption of smooth muscle cells to shear stress is of interest in understanding the pathophysiology behind intimal hyperplasia and restenosis.
- Published
- 2010
- Full Text
- View/download PDF
9. Abstract 515: Effects of the Glucagon-Like Peptide-1 Analog Exendin-4 on Reendothelialization and Intimal Hyperplasia Formation in an Animal Model of Vascular Injury
- Author
-
Åke Sjöholm, Kenneth Caidahl, Robert Saxelin, Ulf Hedin, Anton Razuvaev, Linnéa Eriksson, Thomas Nyström, Joy Roy, and Samuel Röhl
- Subjects
medicine.medical_specialty ,Pathology ,Intimal hyperplasia ,business.industry ,medicine.medical_treatment ,medicine.disease ,Glucagon-like peptide-1 ,Surgery ,Endothelial stem cell ,Increased risk ,Animal model ,Restenosis ,Angioplasty ,medicine ,Stent thrombosis ,Cardiology and Cardiovascular Medicine ,business - Abstract
Background and aims: Diabetic patients have an increased risk of late stent thrombosis formation and restenosis, after angioplasty. It is hypothesized that delayed re-endothelization is a major underlying problem for late-stent thrombosis and also that rapid re-endothelization is essential for preventing restenosis. Exendin-4 is a stable GLP-1 receptor agonist, which is applied in clinical treatment of diabetes. Beside its insulinotropic action, it may also exert direct beneficial effects on endothelial function. We previously reported that exendin-4 is able to activate the GLP-1 receptor on human coronary artery endothelial cells, leading to increased cell proliferation and decreased apoptosis. Therefore, our aim was to study if exendin-4 can influence endothelialization and decrease neointima formation after vascular injury. Materials and Methods: Balloon injury of the left common carotid artery (LCCA) was performed on Sprague-Dawley rats. Rats were randomized into two groups and treated for four weeks with exendin-4 (1 nmol/day) or saline. Intimal hyperplasia and endothelialization was monitored non-invasively by high frequency ultrasound and upon sacrifice with Evans blue, respectively. The LCCA was then sectioned for subsequent morphometric and immunohistochemical analyses. To further investigate if and how smooth muscle cells (SMCs) are directly affected by exendin-4 treatment, we studied proliferation and apoptosis of SMCs in vitro . Results and conclusions: Our findings show that exendin-4 selectively reduces SMC proliferation and intimal hyperplasia through activation of cAMP signaling and endothelial nitric oxide synthase without influencing re-endothelialization. Treatment with exendin-4 did however improve arterial wall elasticity. Together, these effects of exendin-4 are highly desirable and may lead to improved outcome for patients undergoing vascular interventions
- Published
- 2014
10. PS238. Regulation of Endothelin-1 and Endothelin Receptors by Shear Stress in Vascular Smooth Muscle Cells
- Author
-
Anton Razuvaev, Joy Roy, Ulf Hedin, and Johan Ekstrand
- Subjects
medicine.medical_specialty ,Vascular smooth muscle ,Endocrinology ,business.industry ,Internal medicine ,Shear stress ,Medicine ,Surgery ,Cardiology and Cardiovascular Medicine ,business ,Endothelin receptor ,Endothelin 1 - Published
- 2010
11. PS206. A Specific Inhibitor of IGF-1 Receptor - Picropodophyllin Can Suppress Atheroma Progression and Has a Stabilizing Effect on Atherosclerotic Lesions in ApoE Deficient Mice
- Author
-
Magnus Axelson, Anton Razuvaev, Joy Roy, Olle Larsson, and Ulf Hedin
- Subjects
Apolipoprotein E ,Atheroma ,business.industry ,medicine ,Deficient mouse ,Cancer research ,Picropodophyllin ,Surgery ,Cardiology and Cardiovascular Medicine ,medicine.disease ,Receptor ,business - Full Text
- View/download PDF
12. Correlations Between Clinical Variables and Gene-expression Profiles in Carotid Plaque Instability
- Author
-
Johan Ekstrand, Joy Roy, Hanna E. Agardh, Anton Razuvaev, Gabrielle Paulsson-Berne, Anders Gabrielsen, D. Markus, Ulf Hedin, Göran K. Hansson, Lasse Folkersen, and Jesper Swedenborg
- Subjects
Male ,Pathology ,medicine.medical_treatment ,Statistics as Topic ,medicine.disease_cause ,Databases, Genetic ,Carotid Stenosis ,Cerebrovascular disease ,Oligonucleotide Array Sequence Analysis ,Endarterectomy ,Aged, 80 and over ,Medicine(all) ,Endarterectomy, Carotid ,biology ,Middle Aged ,Up-Regulation ,Phenotype ,Intracranial Embolism ,Matrix Metalloproteinase 9 ,Plaque healing ,Matrix Metalloproteinase 7 ,Female ,Collagen ,medicine.symptom ,Cardiology and Cardiovascular Medicine ,medicine.medical_specialty ,Antigens, Differentiation, Myelomonocytic ,Asymptomatic ,Antigens, CD ,medicine ,Humans ,Vulnerable plaque ,Aged ,Sweden ,Wound Healing ,business.industry ,Microarray analysis techniques ,Gene Expression Profiling ,RANK Ligand ,Atherosclerosis ,medicine.disease ,Elastin ,Gene expression profiling ,Embolism ,Gene chip analysis ,biology.protein ,Surgery ,Gene expression ,business - Abstract
Objective Strokes, a major cause of disability, are often caused by embolism from unstable carotid plaques. The aim of this study was to validate a biobank of human carotid endarterectomies as a platform for further exploration of pathways for plaque instability. For this purpose, we investigated the relationship between clinical parameters of plaque instability and expression of genes previously shown to be associated with either plaque instability or healing processes in the vessel wall. Methods A database of clinical information and gene-expression microarray data from 106 carotid endarterectomies were used. Results Expression of matrix metalloproteinase (MMP)-9 and MMP-7 was 100-fold higher in plaques than in normal artery. In general, genes associated with inflammation (such as RANKL and CD68) were overexpressed in symptomatic compared with asymptomatic plaques. Plaques obtained from patients undergoing surgery within 2 weeks after an embolic event showed up-regulation of genes involved in healing reactions in the vessel wall (including elastin and collagen). Statin treatment, as well as echodense lesions, were associated with a more stable phenotype. Conclusion Here, we demonstrate that gene-expression profiles reflect clinical parameters. Our results suggest that microarray technology and clinical variables can be used for the future identification of central molecular pathways in plaque instability.
- Full Text
- View/download PDF
Catalog
Discovery Service for Jio Institute Digital Library
For full access to our library's resources, please sign in.