| 1. |
- Peter, Hannes, 1982-
(författare)
-
Diversity and Ecosystem Functioning : Redundancy and Resilience in Freshwater Bacterial Communities
- 2011
-
Doktorsavhandling (övrigt vetenskapligt/konstnärligt)abstract
- Bacteria are immensely diverse and hold key-positions in essentially all biogeochemical cycles. In freshwater ecosystems, bacteria degrade and mineralize organic compounds, linking the pool of dissolved organic matter to higher trophic levels. Aware of the global biodiversity loss, ecologists have started identifying the relationship of diversity and ecosystem functioning. Central to this is the question if species can functionally replace other species, hence being functionally redundant. Functional redundancy might allow communities to maintain functioning when diversity is lost. Due to their large numbers and great diversity, bacterial communities have been suspected to harbor large amounts of redundancy. The central aim of this thesis is to investigate the coupling of diversity and ecosystem functioning of bacterial communities and to understand how environmental perturbation affects this relationship. I manipulated the diversity of complex communities by a dilution technique, and measured the performance of bacterioplankton and biofilm-forming communities at different diversities. Reduction of bacterial diversity differently affected different functions, and that the presence or absence of certain species might be causing this pattern. However, for ecosystems to function, the interplay of multiple functions, i.e. multifunctionality, has to be sustained over long periods of time. In bacterial biofilm communities reduced diversity affected multifunctionality, as reflected by extracellular enzyme activities. A continuous cultivation system was used to address the importance of diversity for resistance and resilience upon environmental perturbation. The analysis of co-occurrence of bacterial taxa showed that the communities form a dense network before the perturbation and that these patterns are disturbed by the environmental perturbation. The final chapter of the thesis presents experimental evidence for the positive effects of temporal and spatial refuges for bacterial communities and the functions they provide. Overall, I found several indications for a lower amount of functional redundancy as previously assumed and it becomes apparent from this thesis that a multifunctional perspective and the consideration of environmental heterogeneity is pivotal.
|
|
| 2. |
- Svensson Holm, Ann-Charlotte B., et al.
(författare)
-
Platelet membranes induce airway smooth muscle cell proliferation
- 2011
-
Ingår i: Platelets. - : Informa Healthcare. - 0953-7104 .- 1369-1635. ; 22:1, s. 45-55
-
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.
|
|
| 3. |
- Svensson Holm, Ann-Charlotte, et al.
(författare)
-
Hyaluronic acid influence on platelet-induced airway smooth muscle cell proliferation
- 2012
-
Ingår i: Experimental Cell Research. - San Diego, USA : Elsevier. - 0014-4827 .- 1090-2422. ; 318:5, s. 632-640
-
Tidskriftsartikel (refereegranskat)abstract
- Hyaluronic acid (HA) is one of the main components of the extracellular matrix (ECM) and is expressed throughout the body including the lung and mostly in areas surrounding proliferating and migrating cells. Furthermore, platelets have been implicated as important players in the airway remodelling 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 HA, the HA-binding surface receptor CD44 and focal adhesion kinase (FAK) in platelet-induced ASMC proliferation. Proliferation of ASMC was measured using the MTS-assay, and we found that the CD44 blocking antibody and the HA synthase inhibitor 4-Methylumbelliferone (4-MU) significantly inhibited platelet-induced ASMC proliferation. The interaction between ASMC and platelets was studied by fluorescent staining of F-actin. In addition, the ability of ASMC to synthesise HA was investigated by fluorescent staining using biotinylated HA-binding protein and a streptavidin conjugate. We observed that ASMC produced HA and that a CD44 blocking antibody and 4-MU significantly inhibited platelet binding to the area surrounding the ASMC. Furthermore, the FAK-inhibitor PF 573228 inhibited platelet-induced ASMC proliferation. Co-culture of ASMC and platelets also resulted in increased phosphorylation of FAK as detected by Western blot analysis. In addition, 4-MU significantly inhibited the increased FAK-phosphorylation. In conclusion, our findings demonstrate that ECM has the ability to influence platelet-induced ASMC proliferation. Specifically, we propose that HA produced by ASMC is recognised by platelet CD44. The platelet/HA interaction is followed by FAK activation and increased proliferation of co-cultured ASMC. We also suggest that the mitogenic effect of platelets represents a potential important and novel mechanism that may contribute to airway remodelling. (C) 2011 Elsevier Inc. All rights reserved.
|
|
