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| 2. |
- Sauveroche, Mathilde, et al.
(författare)
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Hair cortisol in horses (Equus caballus) in relation to management regimes, personality and breed
- 2020
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Ingår i: Journal of Veterinary Behavior. - : Elsevier. - 1558-7878. ; 37
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Tidskriftsartikel (refereegranskat)abstract
- Hair cortisol is a promising biomarker to measure long-term stress since cortisol is incorporated into the hair shaft as it grows. However, few studies have previously assessed hair cortisol concentrations (HCC) in horses. In this study, HCC was evaluated in both mane hair from the neck and body hair from the withers in 153 horses of different breeds, from seven different stables with three different management regimes (Free-roaming horses, Riding school horses, Trotter horses). In addition, 4 hours of behavioral observations were performed at each stable, and for 43 of the horses, a personality survey was completed. Mane and withers HCC correlated moderately, but significantly (rs=0.48, p<0.001). Differences between the stables were found for both mane and withers hair (both p<0.01) and the stable with lowest HCC also showed highest occurrences of positive social and resting behaviors (both p<0.01). There were no significant differences in HCC between the management regimes even though Free-roaming horses showed less negative social behavior compared to Riding school horses (p=0.041) and Trotter horses (p=0.055). The personality traits Dominance, Anxiousness, and Excitability revealed weak to moderate correlations with mane HCC (rs=-0.34, p=0.027; rs=-0.46, p=0.002; rs=-0.31, p=0.043 respectively) which might suggest that personality could also be related to long-term stress levels in horses.
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| 3. |
- Svensson Holm, Ann-Charlotte B., et al.
(författare)
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Platelet membranes induce airway smooth muscle cell proliferation
- 2011
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Ingår i: Platelets. - : Informa Healthcare. - 0953-7104 .- 1369-1635. ; 22:1, s. 45-55
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Tidskriftsartikel (refereegranskat)abstract
- The role of platelets in airway disease is poorly understood although they have been suggested to influence on proliferation of airway smooth muscle cells (ASMC). Platelets have been found localized in the airways in autopsy material from asthmatic patients and have been implicated in airway remodeling. The aim of the present study was to investigate the effects of various platelet fractions on proliferation of ASMC obtained from guinea pigs (GP-ASMC) and humans (H-ASMC). Proliferation of ASMC was measured by the MTS assay and the results confirmed by measurements of the DNA content. A key observation was that the platelet membrane preparations induced a significant increase in the proliferation of both GP-ASMC (129.9 +/- 3.0 %) and H-ASMC (144.8 +/- 12.2). However, neither supernatants from lysed or filtrated thrombin stimulated platelets induced ASMC proliferation to the same extent as the membrane preparation. We have previously shown that platelet-induced proliferation is dependent on 5-lipoxygenase (5-LOX) and reactive oxygen species (ROS) pathways. In the present work we established that platelet membrane-induced ASMC proliferation was reduced in the presence of the NADPH oxidase inhibitor DPI and the 5-LOX inhibitor AA-861. In conclusion, our results showed that platelet membranes significantly induced ASMC proliferation, demonstrating that the mitogenic effect of platelets and platelet membranes on ASMC is mainly due to membrane-associated factors. The effects of platelet membranes were evident on both GP-ASMC and H-ASMC and involved 5-LOX and ROS. These new findings are of importance in understanding the mechanisms contributing to airway remodeling and may contribute to the development of new pharmacological tools in the treatment of inflammatory airway diseases.
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| 4. |
- Svensson Holm, Ann-Charlotte B.
(författare)
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Platelets and airway remodeling : Mechanisms involved in platelet-induced fibroblast and airway smooth muscle cell proliferation in vitro
- 2010
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Doktorsavhandling (övrigt vetenskapligt/konstnärligt)abstract
- Airway remodeling is a contributing cause to the pathological structural changes, such as increased cell proliferation, observed in asthma. Platelets have been found in autopsy lungmaterial obtained from asthmatic patients and are well known to induce proliferation in vitro of a variety of cells. However, the role of platelets in airway remodeling is far from understood. This thesis aims to clarify the involvement of platelets in fibroblast and airway smooth muscle cell (ASMC) proliferation in vitro and to elucidate the importance of HA, FAK, eicosanoid and ROS dependent signaling. The results demonstrate that platelets induce ASMC proliferation through NADPH-oxidase and 5-LOX dependent mechanisms. In addition, platelets also induce a 5-LOX dependent fibroblast proliferation. Furthermore, morphological analysis demonstrates that platelets bind to the extracellular matrix component HA through its receptor CD44 and thereby induce a FAK dependent ASMC proliferation. Taken together, the results obtained in this thesis suggest that platelet/HA interaction mediated through CD44 is of importance for platelets ability to induce cell proliferation. Moreover, the results propose that platelet-induced fibroblast proliferation is 5-LOX dependent and that platelets induce a HA, CD44, FAK, 5-LOX, and ROSdependent ASMC proliferation. This action of platelets represents a potential important and novel mechanism that may have an impact on the remodeling process and in the development of new pharmacological strategies in the treatment of inflammatory respiratory disease such as asthma.
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| 5. |
- Svensson Holm, Ann-Charlotte B., et al.
(författare)
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Platelets bind to hyaluronic acid through CD44 and induce a focal adhesion kinase dependent airway smooth muscle cell proliferation
- 2008
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Annan publikation (övrigt vetenskapligt/konstnärligt)abstract
- Platelets have been implicated as important players in the remodeling process, e.g. due to their ability to induce airway smooth muscle cell (ASMC) proliferation. The aim of the present study was to investigate the role of the extracellular matrix component hyaluronic acid (HA), the HA-binding surface receptor CD44 and focal adhesion kinase (FAK) in platelet-induced ASMC proliferation. The ability of ASMC to synthesize HA was investigated by fluorescent staining using biotinylated HA-binding protein and streptavidin conjugate. In addition, the interaction between ASMC and platelets was studied by fluorescent staining of the F-actin. We found that ASMC produced HA and that a CD44 blocking antibody and the hyaluronic acid synthase inhibitor 4-Methylumbelliferone (4-MU) inhibited platelet binding to the area surrounding the ASMC. Proliferation of ASMC was measured using the MTS-assay, and we found that the CD44 blocking antibody and 4-MU inhibited platelet-induced ASMC proliferation. We also found that co-culture of ASMC and platelets resulted in increased phosphorylation of FAK as detected by Western blot analysis. Furthermore, the FAKinhibitor PF 573228 inhibited platelet-induced ASMC proliferation. In conclusion, our findings demonstrate that HA, CD44 and FAK contribute to the increased ASMC proliferation caused by platelets. This event is initiated by an interaction between platelets CD44 and HA produced by the ASMC. These new findings may be important in understanding the interplay between ECM, platelets and ASMC in the remodeling process. In conclusion, our results demonstrate that FAK is phosphorylated and on that account activated during the CD44-dependent platelet/ASMC interaction and this contributes to proliferation of the ASMC. These new findings may be important in understanding the interplay between ECM, platelets and ASMC in the remodeling process.
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| 6. |
- Svensson Holm, Ann-Charlotte B., et al.
(författare)
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Platelets stimulate airway smooth muscle cell proliferation through mechanisms involving 5-lipoxygenase and reactive oxygen species
- 2008
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Ingår i: Platelets. - : Informa UK Limited. - 0953-7104 .- 1369-1635. ; 19:7, s. 528-536
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Tidskriftsartikel (refereegranskat)abstract
- Continuous recruitment and inappropriate activity of platelets in the airways may contribute to airway remodeling, a characteristic feature of inflammatory airway diseases that includes increased proliferation of the smooth muscle. The aim of the present investigation was to examine the effect of platelets on proliferation of airway smooth muscle cells (ASMC) in culture and to determine the possible role of 5-lipoxygenase (5-LOX) and reactive oxygen species (ROS) in this context. ASMC obtained from guinea pigs were cultured and co-incubated with washed platelets for 24 hours. Thereafter, the proliferation was measured with the MTS-assay; the results were also verified by using thymidine incorporation, DNA measurements and manual counting. The interaction between platelets and ASMC was visualized with fluorescence microscopy. We found that platelets bind to the ASMC and the presence of platelets caused a significant dose-dependent increase in ASMC proliferation. Co-incubation of ASMC with platelets also increased ROS-production, detected by the fluorescent probe DCFDA. Furthermore, the platelet-induced proliferation was reduced in the presence of the NADPH-oxidase inhibitors DPI and apocynin. A possible role of 5-LOX in platelet-induced proliferation and ROS-generation was evaluated by using the 5-LOX inhibitor AA-861 and the PLA2-inhibitor ATK. The results showed that inhibition of these enzymes significantly reduced the platelet-induced proliferation. Moreover, Western blot analysis revealed that the ASMC but not the platelets express 5-LOX. In addition, our experiments revealed that the presence of AA-861 and ATK significantly inhibited the ROS-production generated upon co-incubation of platelets and ASMC. In conclusion, we show that platelets have a marked capacity to induce ASMC proliferation. Furthermore, our study indicates that the interaction between platelets and ASMC leads to activation of 5-LOX in the ASMC followed by an increased ROS-production, events resulting in enhanced ASMC proliferation. The new findings are of importance in understanding possible mechanisms contributing to airway remodeling. © 2008 Informa UK Ltd.
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| 7. |
- Svensson Holm, Ann-Charlotte B, et al.
(författare)
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Thyroid hormone does not induce maturation of embryonicchicken cardiomyocytes in vitro
- 2014
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Ingår i: Physiological Reports. - : Wiley Periodicals, Inc.. - 2051-817X. ; 2:12, s. e12182-
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Tidskriftsartikel (refereegranskat)abstract
- Fetal cardiac growth in mammalian models occurs primarily by cell proliferation(hyperplasia). However, most cardiomyocytes lose the ability to proliferateclose to term and heart growth continues by increasing cell size(hypertrophy). In mammals, the thyroid hormone triiodothyronine (T3) is animportant driver of this process. Chicken cardiomyocytes, however, keep theirproliferating ability long after hatching but little information is available onthe mechanisms controlling cell growth and myocyte maturation in thechicken heart. Our aim was to study the role of T3 on proliferation and differentiationof embryonic chicken cardiomyocytes (ECCM), enzymaticallyisolated from 19-day-old embryos and to compare the effects to those of insulin-like growth factor-1 (IGF-1) and phenylephrine (PE). Hyperplasia wasmeasured using a proliferation assay (MTS) and hypertrophy/multinucleationwas analyzed morphologically by phalloidin staining of F-actin and nuclearstaining with DAPI. We show that IGF-1 induces a significant increase inECCM proliferation (30%) which is absent with T3 and PE. PE induced bothhypertrophy (61%) and multinucleation (41%) but IGF-1 or T3 did not. Inconclusion, we show that T3 does not induce maturation or proliferation ofcardiomyocytes, while IGF-1 induces cardiomyocyte proliferation and PEinduces maturation of cardiomyocytes.
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