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| 2. |
- Claesson-Welsh, Lena
(author)
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New Frontiers in VEGF/VEGFR Biology
- 2015
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In: Journal of Vascular Research. - 1018-1172 .- 1423-0135. ; 52, s. 79-79
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Journal article (other academic/artistic)
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| 3. |
- Dahan, Diana, et al.
(author)
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MicroRNA-Dependent Control of Serotonin-Induced Pulmonary Arterial Contraction
- 2017
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In: Journal of Vascular Research. - : S. Karger AG. - 1018-1172 .- 1423-0135. ; 54:4, s. 246-256
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Journal article (peer-reviewed)abstract
- Background: Serotonin (5-HT) is considered to play a role in pulmonary arterial hypertension by regulating vascular remodeling and smooth muscle contractility. Here, arteries from mice with inducible and smooth muscle-specific deletion of Dicer were used to address mechanisms by which microRNAs control 5-HT-induced contraction. Methods: Mice were used 5 weeks after Dicer deletion, and pulmonary artery contractility was analyzed by wire myography. Results: No change was seen in right ventricular systolic pressure following dicer deletion, but systemic blood pressure was reduced. Enhanced 5-HT-induced contraction in Dicer KO pulmonary arteries was associated with increased 5-HT2A receptor mRNA expression whereas 5-HT1B and 5-HT2B receptor mRNAs were unchanged. Contraction by the 5-HT2A agonist TCB-2 was increased in Dicer KO as was the response to the 5-HT2B agonist BW723C86. Effects of Src and protein kinase C inhibition were similar in control and KO arteries, but the effect of inhibition of Rho kinase was reduced. We identified miR-30c as a potential candidate for 5-HT2A receptor regulation as it repressed 5-HT2A mRNA and protein. Conclusion: Our findings show that 5-HT receptor signaling in the arterial wall is subject to regulation by microRNAs and that this entails altered 5-HT2A receptor expression and signaling.
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| 4. |
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| 5. |
- Eriksson, L, et al.
(author)
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Glucagon-Like Peptide-1 Receptor Activation Does not Affect Re-Endothelialization but Reduces Intimal Hyperplasia via Direct Effects on Smooth Muscle Cells in a Nondiabetic Model of Arterial Injury
- 2015
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In: Journal of vascular research. - : S. Karger AG. - 1423-0135 .- 1018-1172. ; 52:1, s. 41-52
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Journal article (peer-reviewed)abstract
- Diabetic patients have an increased risk of restenosis and late stent thrombosis after angioplasty, i.e. complications that are related to a defective re-endothelialization. Exendin-4, a stable glucagon-like peptide (GLP)-1 receptor agonist, has been suggested to influence the formation of intimal hyperplasia and to increase endothelial cell proliferation in vitro. Thus, the aim of this study was to investigate the mechanisms by which treatment with exendin-4 could influence re-endothelialization and intimal hyperplasia after vascular injury. <b><i>Methods:</i></b> Sprague-Dawley rats were subjected to balloon injury of the left common carotid artery and treated for 4 weeks with exendin-4 or vehicle. Intimal hyperplasia and vessel wall elasticity were monitored noninvasively by high-frequency ultrasound, and re-endothelialization was evaluated upon sacrifice using Evans blue dye. <b><i>Results and Conclusion:</i></b> Exendin-4 selectively reduced the proliferation of smooth muscle cells (SMCs) and intimal hyperplasia in vivo without affecting the re-endothelialization process, but treatment with exendin-4 improved arterial wall elasticity. Our data also show that exendin-4 significantly decreased the proliferation and increased the apoptosis of SMCs in vitro, effects that appear to be mediated through cAMP signaling and endothelial nitric oxide synthase following GLP-1 receptor activation. Together, these effects of exendin-4 are highly desirable and may lead to an improved outcome for patients undergoing vascular interventions.
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| 6. |
- Gabrielson, Marike, et al.
(author)
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Altered PPARγ coactivator-1 alpha expression in abdominal aortic aneurysm : Possible effects on mitochondrial biogenesis
- 2016
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In: Journal of Vascular Research. - : S. Karger. - 1018-1172 .- 1423-0135. ; 53:1-2, s. 17-26
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Journal article (peer-reviewed)abstract
- Introduction: Abdominal aortic aneurysm (AAA) is a complex and deadly vascular disorder. The pathogenesis of AAA includes destruction and phenotypic alterations of the vascular smooth muscle cells (VSMCs) and aortic tissues. PPARγ coactivator-1 alpha (PGC1α) regulates VSMC migration and matrix formation and is a major inducer of mitochondrial biogenesis and function, including oxidative metabolism. Methods: Protein and gene expression of PGC1α and markers for mitochondria biogenesis and cell type-specificity were analysed in AAA aortas from humans and mice and compared against control aortas. Results: Gene expression of PPARGC1A was decreased in human AAA and angiotensin (Ang) II-induced AAA in mice when compared to control vessels. However, high expression of PGC1α was detected in regions of neovascularisation in the adventitia layer. In contrast, the intima/media layer of AAA vessel exhibited defective mitochondrial biogenesis as indicated by low expression of PPARGC1A, VDAC, ATP synthase and citrate synthase. Conclusion: Our results suggest that mitochondrial biogenesis is impaired in AAA in synthetic SMCs in the media, with the exception of newly formed supporting vessels in the adventitia where the mitochondrial markers seem to be intact. To our knowledge, this is the first study investigating PGC1α and mitochondria biogenesis in AAA.
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| 7. |
- Gidlöf, Olof, et al.
(author)
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Extracellular Uridine Triphosphate and Adenosine Triphosphate Attenuate Endothelial Inflammation through miR-22-Mediated ICAM-1 Inhibition.
- 2015
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In: Journal of Vascular Research. - : S. Karger AG. - 1423-0135 .- 1018-1172. ; 52:2, s. 71-80
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Journal article (peer-reviewed)abstract
- Adenosine and uridine triphosphate (ATP and UTP) can act as extracellular signalling molecules, playing important roles in vascular biology and disease. ATP and UTP acting via the P2Y2-receptor have, for example, been shown to regulate endothelial dilatation, inflammation and angiogenesis. MicroRNAs (miRNAs), a class of regulatory, short, non-coding RNAs, have been shown to be important regulators of these biological processes. In this study, we used RNA deep-sequencing to explore changes in miRNA expression in the human microvascular endothelial cell line HMEC-1 upon UTP treatment. The expression of miR-22, which we have previously shown to target ICAM-1 mRNA in HMEC-1, increased significantly after stimulation. Up-regulation of miR-22 and down-regulation of cell surface ICAM-1 were confirmed with qRT-PCR and flow cytometry, respectively. siRNA-mediated knockdown of the P2Y2-receptor abolished the effect of UTP on miR-22 transcription. Leukocyte adhesion was significantly inhibited in HMEC-1 following miR-22 overexpression and treatment with UTP/ATP. In conclusion, extracellular UTP and ATP can attenuate ICAM-1 expression and leukocyte adhesion in endothelial cells through miR-22. © 2015 S. Karger AG, Basel.
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| 8. |
- Laine, M, et al.
(author)
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Few Internal Iliac artery Aneurysms Rupture under 4 cm
- 2017
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In: Journal of Vascular Research. - : Elsevier BV. - 1018-1172 .- 1423-0135 .- 0741-5214. ; 65:1, s. 76-81
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Journal article (peer-reviewed)abstract
- ObjectiveThis study investigated the diameter of internal iliac artery (IIA) aneurysms (IIAAs) at the time of rupture to evaluate whether the current threshold diameter for elective repair of 3 cm is reasonable. The prevalence of concomitant aneurysms and results of surgical treatment were also investigated.MethodsThis was a retrospective analysis of patients with ruptured IIAA from seven countries. The patients were collected from vascular registries and patient records of 28 vascular centers. Computed tomography images taken at the time of rupture were analyzed, and maximal diameters of the ruptured IIA and other aortoiliac arteries were measured. Data on the type of surgical treatment, mortality at 30 days, and follow-up were collected.ResultsSixty-three patients (55 men and 8 women) were identified, operated on from 2002 to 2015. The patients were a mean age of 76.6 years (standard deviation, 9.0; range 48-93 years). A concomitant common iliac artery aneurysm was present in 65.0%, 41.7% had a concomitant abdominal aortic aneurysm, and 36.7% had both. IIAA was isolated in 30.0%. The mean maximal diameter of the ruptured artery was 68.4 mm (standard deviation, 20.5 mm; median, 67.0 mm; range, 25-116 mm). One rupture occurred at <3 cm and four at <4 cm (6.3% of all ruptures). All patients were treated, 73.0% by open repair and 27.0% by endovascular repair. The 30-day mortality was 12.7%. Median follow-up was 18.3 months (interquartile range, 2.0-48.3 months). The 1-year Kaplan-Meier estimate for survival was 74.5% (standard error, 5.7%).ConclusionsIIAA is an uncommon condition and mostly coexists with other aortoiliac aneurysms. Follow-up until a diameter of 4 cm seems justified, at least in elderly men, although lack of surveillance data precludes firm conclusions. The mortality was low compared with previously published figures and lower than mortality in patients with ruptured abdominal aortic aneurysm.Abdominal aortic aneurysm (AAA) is the most common and studied aneurysm. Aneurysms of the iliac arteries are found considerably less often, and epidemiologic data on these do not exist. In many cases iliac artery aneurysms coexist with aortic aneurysms: ∼10% to 20% of patients with AAA also have a concomitant aneurysm in the iliac arteries.1 The artery most often affected is the common iliac artery (CIA), followed by the internal iliac artery (IIA), also called the hypogastric artery. In the case of isolated aneurysms in the iliac arteries, without involvement of the aorta, the most common location is the IIA.2 Aneurysms of the external iliac artery are extremely rare, possibly because these arteries originate later in development from a different cell population than the distal aorta and the CIA and IIA. Studies on IIA aneurysms (IIAAs) are scarce owing to the rarity of the condition. The existing literature consists primarily of case reports and small patient series. No prospective studies on IAAs exist.According to the literature, IAAs have a high rupture and mortality rate even in elective cases, possibly because of their deep location in the pelvis.3 The etiology and risk factors of IAA seem to be the same as AAA.4 Iliac aneurysms are mostly degenerative but can also be mycotic or caused by genetic disorders such as Marfan or Ehlers-Danlos syndromes. Traumatic aneurysms in the iliac arteries have also been described; for example, caused by iatrogenic trauma from hip, lumbar, or gynecologic operations. A mainly historical subpopulation of young women with IIAA caused by trauma from pregnancy and delivery has been described.5 and 6IAAs cause symptoms more often than AAA because of compression of pelvic structures such as ureters, bladder, veins, or lumbar nerves. Wilhelm et al7 reported that 53% of published isolated IIAA cases were symptomatic, not including the ruptured ones (31%). The high proportion of symptomatic patients in these older reports may partly be explained, however, by the fact that most of these cases were from time before widespread use of modern imaging. IIAA are not easily discovered with clinical examination because of their location8 but are detected increasingly often as a result of imaging and screening programs.Because the studies on IIAAs are scarce, the natural history is virtually unknown. A widely used threshold for elective repair is 3 cm, originally suggested by McCready et al9 because their series did not include any ruptures under that diameter. However, only seven ruptures were included in that report. The reference list of this article illustrates that most of the papers on this subject were published when open repair was the only treatment option. Nowadays endovascular treatment is the first option in many centers.10The aim of this study was to investigate at what diameter IIAAs tend to rupture and whether the current operative threshold of 3 cm is rational. Secondary aims were to assess the prevalence of concomitant aortoiliac aneurysms, treatment patterns, and the results of treatment.
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| 9. |
- Laskowski, Marta, 1991, et al.
(author)
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Potassium-Channel-Independent Relaxing Influence of Adipose Tissue on Mouse Carotid Artery
- 2017
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In: Journal of Vascular Research. - : S. Karger AG. - 1018-1172 .- 1423-0135. ; 54:1, s. 51-57
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Journal article (peer-reviewed)abstract
- Since the cardiovascular consequences of obesity reportedly vary in different types of obesity, we investigated the influence of adipose tissue from different locales on the phenylephrine- induced tone of the mouse carotid artery. Vessels were mounted in a Mulvany-Halpern-type wire myograph, and adipose tissue, from the back (brown) or mesenteric or inguinal subcutaneous (white), was placed around the artery. Contractile responses to phenylephrine were not affected by brown adipose tissue but were reduced (p < 0.001) by either type of white adipose tissue, with no difference between the 2 locales. The relaxing effect persisted in the presence of the Kv7 channel inhibitor XE991 (10,10-bis(4pyridinylmethyl)- 9(10H)-anthracenone), the K-ATP channel inhibitor glibenclamide (1 mu M), or the K-V channel inhibitor 4-amino pyridine (1 mM), as well as after elevation of the extracellular potassium concentration to 30 mM. Contractions of rat carotid artery were equally reduced by mouse and rat subcutaneous adipose tissue. Thus, white, but not brown, adipose tissue reduces the adrenergic contractions of the carotid artery with no differences between the locales of origin, and the effect appears largely independent of potassium channels.
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