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  • 1. Aspelund, Aleksanteri
    et al.
    Tammela, Tuomas
    Antila, Salli
    Nurmi, Harri
    Leppanen, Veli-Matti
    Zarkada, Georgia
    Stanczuk, Lukas
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology.
    Francois, Mathias
    Mäkinen, Taija
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology, Vascular Biology.
    Saharinen, Pipsa
    Immonen, Ilkka
    Alitalo, Kari
    Therapeutic Insights to Lymphangiogenic Growth Factors2015In: Journal of Vascular Research, ISSN 1018-1172, E-ISSN 1423-0135, Vol. 52, no S1, p. 19-19Article in journal (Other academic)
  • 2.
    Claesson-Welsh, Lena
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology, Vascular Biology.
    New Frontiers in VEGF/VEGFR Biology2015In: Journal of Vascular Research, ISSN 1018-1172, E-ISSN 1423-0135, Vol. 52, p. 79-79Article in journal (Other academic)
  • 3.
    Dias, Mariana
    et al.
    Theodor Kocher Inst, Bern, Switzerland..
    Coisne, Caroline
    Theodor Kocher Inst, Bern, Switzerland..
    Baden, Pascale
    Theodor Kocher Inst, Bern, Switzerland..
    Lazarevic, Ivana
    Theodor Kocher Inst, Bern, Switzerland..
    Francisco, David
    Univ Bern, Bern, Switzerland..
    Lyck, Ruth
    Theodor Kocher Inst, Bern, Switzerland..
    Enzmann, Gaby
    Theodor Kocher Inst, Bern, Switzerland..
    Deutsch, Urban
    Theodor Kocher Inst, Bern, Switzerland..
    Bruggmann, Remy
    Univ Bern, Bern, Switzerland..
    Betsholtz, Christer
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology, Vascular Biology. Karolinska Inst, Uppsala, Sweden..
    Furuse, Mikio
    Natl Inst Physiol Sci, Okazaki, Aichi, Japan..
    Engelhardt, Britta
    Theodor Kocher Inst, Bern, Switzerland..
    Claudin 3-Deficient C57BL/6 Mice Display Intact Brain Barriers2017In: Journal of Vascular Research, ISSN 1018-1172, E-ISSN 1423-0135, Vol. 54, p. 63-63Article in journal (Other academic)
  • 4. Gidlöf, Andreas C.
    et al.
    Ocaya, Pauline
    Olofsson, Peder S.
    Törmä, Hans
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Dermatology and Venereology.
    Sirsjö, Allan
    Differences in retinol metabolism and proliferative response between neointimal and medial smooth muscle cells2006In: Journal of Vascular Research, ISSN 1018-1172, E-ISSN 1423-0135, Vol. 43, no 4, p. 392-398Article in journal (Refereed)
    Abstract [en]

    Vascular disease is multifactorial and smooth muscle cells (SMCs) play a key role. Retinoids have been shown to influence many disease-promoting processes including proliferation and differentiation in the vessel wall. Phenotypic heterogeneity of vascular SMCs is a well-known phenomenon and phenotypic modulation of SMCs precedes intimal hyperplasia. The SMCs that constitute the intimal hyperplasia demonstrate a distinct phenotype and differ in gene expression compared to medial SMCs. Cellular retinol-binding protein-1 (CRBP-I), involved in retinoid metabolism, is highly expressed in intimal SMCs, indicating altered retinoid metabolism in this subset of cells. The aim of this study was to evaluate the metabolism of all-trans ROH (atROH), the circulating prohormone to active retinoids, in vascular SMCs of different phenotypes. The results show an increased uptake of atROH in intimal SMCs compared to medial SMCs as well as increased expression of the retinoid-metabolizing enzymes retinol clehydrogenase-5 and retinal dehydrogenase-1 and, in conjunction with this gene expression, increased production of all-trans retinoic acid (atRA). Furthermore, the retinoic acid-catabolizing enzyme CYP26A1 is expressed at higher levels in medial SMCs compared to intimal SMCs. Thus, both retinoid activation and deactivation processes are in operation. To analyze if the difference in ROH metabolism was also correlated to differences in the biological response to retinol, the effects of ROH on proliferation of SMCs with this phenotypic heterogeneity were studied. We found that intimal SMCs showed a dose- and time-dependent growth inhibition when treated with atROH in contrast to medial SMCs, in which atROH had a mitogenic effect. This study shows, for the first time, that (1) vascular SMCs are able to synthesize biologically active atRA from the prohormone atROH, (2) intimal SMCs have a higher capacity to internalize atROH and metabolize atROH into atRA compared to medial SMCs and (3) atROH inhibits growth of intimal SMCs, but induces medial SMC growth.

  • 5. Laine, M
    et al.
    Björck, Martin
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Vascular Surgery.
    Beiles, B
    Szeberin, Z
    Thomson, I
    Altreuther, M
    Debus, S
    Mani, Kevin
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Surgical Sciences, Vascular Surgery.
    Menyhei, G
    Venermo, M
    Few Internal Iliac artery Aneurysms Rupture under 4 cm2017In: Journal of Vascular Research, ISSN 1018-1172, E-ISSN 1423-0135, Vol. 65, no 1, p. 76-81Article in journal (Refereed)
    Abstract [en]

    Objective

    This 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.

    Methods

    This 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.

    Results

    Sixty-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%).

    Conclusions

    IIAA 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 6

    IAAs 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.10

    The 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.

  • 6.
    Lyons, Oliver
    et al.
    Kings Coll London, London, England..
    Saha, Prakash
    St Thomas Hosp, Kings Coll London, BHF Ctr Res Excellence, Acad Dept Vasc Surg,Cardiovasc Div, London, England..
    Seet, Christopher
    St Thomas Hosp, Kings Coll London, BHF Ctr Res Excellence, Acad Dept Vasc Surg,Cardiovasc Div, London, England..
    Kuchta, Adam
    Guys & St Thomas Fdn Trust, Dept Ultrason Angiol, London, England..
    Arnold, Andrew
    Guys & St Thomas Fdn Trust, Dept Ultrason Angiol, London, England..
    Grover, Steven
    Beth Israel Deaconess Med Ctr, Div Hemostasis & Thrombosis, Boston, MA 02215 USA.;Harvard Med Sch, Boston, MA USA..
    Rashbrook, Victoria
    St Thomas Hosp, Kings Coll London, BHF Ctr Res Excellence, Acad Dept Vasc Surg,Cardiovasc Div, London, England..
    Sabine, Amelie
    CHU Vaudois, Dept Fundamental Oncol, Epalinges, Switzerland.;Univ Lausanne, Epalinges, Switzerland..
    Vizcay-Barrena, Gema
    Kings Coll London, Ctr Ultrastructural Imaging, London, England..
    Patel, Ashish
    St Thomas Hosp, Kings Coll London, BHF Ctr Res Excellence, Acad Dept Vasc Surg,Cardiovasc Div, London, England..
    Ludwinski, Francesca
    St Thomas Hosp, Kings Coll London, BHF Ctr Res Excellence, Acad Dept Vasc Surg,Cardiovasc Div, London, England..
    Padayachee, Soundrie
    Guys & St Thomas Fdn Trust, Dept Ultrason Angiol, London, England..
    Kume, Tsutomu
    Northwestern Univ, Sch Med, Feinberg Cardiovasc Res Inst, Evanston, IL 60208 USA..
    Kwak, Brenda
    Univ Geneva, Dept Pathol & Immunol, Geneva, Switzerland..
    Brice, Glen
    St George Hosp, SW Thames Reg Genet Serv, London, England..
    Mansour, Sahar
    St George Hosp, SW Thames Reg Genet Serv, London, England..
    Ostergaard, Pia
    St Georges Univ London, Cardiovasc & Cell Sci Inst, London, England..
    Mortimer, Peter
    St Georges Univ London, Cardiovasc & Cell Sci Inst, London, England..
    Jeffery, Steve
    St Georges Univ London, Cardiovasc & Cell Sci Inst, London, England..
    Brown, Nigel
    St Georges Univ London, Inst Med Biomed Educ, London, England..
    Mäkinen, Taija
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology, Vascular Biology.
    Petrova, Tatiana
    CHU Vaudois, Dept Fundamental Oncol, Epalinges, Switzerland.;Univ Lausanne, Epalinges, Switzerland..
    Modarai, Bijan
    St Thomas Hosp, Kings Coll London, BHF Ctr Res Excellence, Acad Dept Vasc Surg,Cardiovasc Div, London, England..
    Smith, Alberto
    St Thomas Hosp, Kings Coll London, BHF Ctr Res Excellence, Acad Dept Vasc Surg,Cardiovasc Div, London, England..
    Human Venous Valve Disease Caused by Mutations in FOXC2 and GJC22017In: Journal of Vascular Research, ISSN 1018-1172, E-ISSN 1423-0135, Vol. 54, p. 62-62Article in journal (Other academic)
  • 7. Mellor, Russell H
    et al.
    Tate, Naomi
    Stanton, Anthony W B
    Hubert, Charlotte
    Mäkinen, Taija
    Smith, Alberto
    Burnand, Kevin G
    Jeffery, Steve
    Levick, J Rodney
    Mortimer, Peter S
    Mutations in FOXC2 in humans (lymphoedema distichiasis syndrome) cause lymphatic dysfunction on dependency.2011In: Journal of Vascular Research, ISSN 1018-1172, E-ISSN 1423-0135, Vol. 48, no 5Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Human lymphoedema distichiasis syndrome (LDS) results from germline mutations in transcription factor FOXC2. In a mouse model, lack of lymphatic and venous valves is observed plus abnormal smooth muscle cell recruitment to initial lymphatics. We investigated the mechanism of lymphoedema in humans with FOXC2 mutations, specifically the effect of gravitational forces on dermal lymphatic function.

    METHODS: We performed (1) quantitative fluorescence microlymphangiography (FML) on the skin of the forearm (non-swollen region) at heart level, and the foot (swollen region) below heart level (dependent) and then at heart level, and (2) immunohistochemical staining of microlymphatics in forearm and foot skin biopsies, using antibodies to podoplanin, LYVE-1 and smooth muscle actin.

    RESULTS: FML revealed a marked reduction in fluid uptake by initial lymphatics in the LDS foot during dependency, yet normal uptake (similar to controls) in the same foot at heart level and in LDS forearms. In control subjects, dependency did not impair initial lymphatic filling. Immunohistochemical microlymphatic density in forearm and foot did not differ between LDS and controls.

    CONCLUSIONS: FOXC2 mutations cause a functional failure of dermal initial lymphatics during gravitational stress (dependency), but not hypoplasia. The results reveal a pathophysiological mechanism contributing to swelling in LDS.

  • 8.
    Mäkinen, Taija
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology, Vascular Biology.
    Organ-Specific Origins of Lymphatic Vasculature2015In: Journal of Vascular Research, ISSN 1018-1172, E-ISSN 1423-0135, Vol. 52, no S1, p. 18-19Article in journal (Other academic)
  • 9. Ocaya, Pauline Ajok
    et al.
    Elmabsout, Ali Ateia
    Olofsson, Peder Stefan
    Törmä, Hans
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Dermatology and Venereology.
    Gidlöf, Andreas Carl
    Sirsjö, Allan
    CYP26B1 Plays a Major Role in the Regulation of All-trans-Retinoic Acid Metabolism and Signaling in Human Aortic Smooth Muscle Cells2011In: Journal of Vascular Research, ISSN 1018-1172, E-ISSN 1423-0135, Vol. 48, no 1, p. 23-30Article in journal (Refereed)
    Abstract [en]

    Aim: The cytochrome P450 enzymes of the CYP26 family are involved in the catabolism of the biologically active retinoid all-trans-retinoic acid (atRA). Since it is possible that an increased local CYP26 activity would reduce the effects of retinoids in vascular injury, we investigated the role of CYP26 in the regulation of atRA levels in human aortic smooth muscle cells (AOSMCs). Methods: The expression of CYP26 was investigated in cultured AOSMCs using real-time PCR. The metabolism of atRA was analyzed by high-performance liquid chromatography, and the inhibitor R115866 or small interfering RNA (siRNA) was used to suppress CYP26 activity/expression. Results: AOSMCs expressed CYP26B1 constitutively and atRA exposure augmented CYP26B1 mRNA levels. Silencing of the CYP26B1 gene expression or reduction of CYP26B1 enzymatic activity by using siRNA or the inhibitor R115866, respectively, increased atRA-mediated signaling and resulted in decreased cell proliferation. The CYP26 inhibitor also induced expression of atRA-responsive genes. Therefore, atRA-induced CYP26 expression accelerated atRA inactivation in AOSMCs, giving rise to an atRA-CYP26 feedback loop. Inhibition of this loop with a CYP26 inhibitor increased retinoid signaling. Conclusion: The results suggest that CYP26 inhibitors may be a therapeutic alternative to exogenous retinoid administration.

  • 10.
    Sarabi, Mahziar
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences.
    Vessby, Bengt
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Public Health and Caring Sciences.
    Basu, Samar
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Public Health and Caring Sciences.
    Millgård, Jonas
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences.
    Lind, Lars
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences.
    Relationships between Endothelium-Dependent Vasodilation, Serum Vitamin E and Plasma Isoprostane 8-Iso-PGF2alpha Levels in Healthy Subjects1999In: Journal of Vascular Research, ISSN 1018-1172, E-ISSN 1423-0135, Vol. 36, no 6, p. 486-491Article in journal (Refereed)
    Abstract [en]

    Due to the reported associations between a low intake of vitamin E and atherosclerosis on one hand, and between endothelial dysfunction and atherosclerosis on the other hand, we investigated the relationship between endothelium-dependent vasodilation and serum levels of vitamin E (alpha- and gamma-tocopherol) as well as the lipid peroxidation markers malondialdehyde and 8-iso-PGF(2alpha) in a healthy population. Healthy subjects (31 men and 25 women), aged between 20 and 69 years, underwent measurements of forearm blood flow (FBF) at rest and during local infusion of 2 and 4 microg/min of methacholine (Mch, to evaluate endothelium-dependent vasodilation) and 5 and 10 microg/min of sodium nitroprusside (SNP, to evaluate endothelium-independent vasodilation, and during reactive hyperemia using venous occlusion plethysmography. Serum alpha-tocopherol concentration was significantly related to the index of endothelial function (r = 0.46, p < 0.01), defined as the ratio between the maximal dilatations during Mch and SNP infusions. Serum gamma-tocopherol levels were positively related to the maximal FBF during reactive hyperemia (r = 0.54, p < 0.01) in women only. Furthermore, in women only, plasma 8-iso-PGF(2alpha) levels were inversely related to the relative increases in FBF during both Mch and SNP infusions (r = -0.58 and r = -0.59, p < 0.01 for both). The results show a relationship between the levels of alpha-tocopherol and endothelial vasodilatory function, suggesting a beneficial role for this potent lipid-soluble antioxidant also in a population sample of apparently healthy subjects. Furthermore, in women, the accumulation of lipid peroxidation products such as 8-iso-PGF(2alpha) seems to be associated with an impaired vasodilation in general.

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