| 1. |
- Jönsson, Daniel, et al.
(author)
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Immunocytochemical demonstration of estrogen receptor beta in human periodontal ligament cells.
- 2004
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In: Archives of Oral Biology. - 1879-1506 .- 0003-9969. ; 49:1, s. 85-88
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Journal article (peer-reviewed)abstract
- Two transcription associated estrogen receptor (ER) subtypes have been identified and named ERα and ERβ. In the present study we investigate the expression of these ER subtypes in cultured human periodontal ligament (PDL) cells by immunocytochemistry. ERβ immunoreactivity was observed in the nuclei of about 40% of the PDL cells, while no ERα immunoreactivity was detected. In human breast cancer MCF-7 cells, serving as positive controls, both ERα and ERβ immunoreactivities were demonstrated. No immunoreactivity was observed after omission of the primary antibodies. This study suggests that estrogen acts on gene transcription preferentially via ERβ in human PDL cells.
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| 2. |
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| 3. |
- Voss, Ulrikke, et al.
(author)
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Enteric neuropathy can be induced by high fat diet in vivo and palmitic Acid exposure in vitro.
- 2013
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In: PLoS ONE. - : Public Library of Science (PLoS). - 1932-6203. ; 8:12
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Journal article (peer-reviewed)abstract
- Obese and/or diabetic patients have elevated levels of free fatty acids and increased susceptibility to gastrointestinal symptoms. Since the enteric nervous system is pivotal in regulating gastrointestinal functions alterations or neuropathy in the enteric neurons are suspected to occur in these conditions. Lipid induced intestinal changes, in particular on enteric neurons, were investigated in vitro and in vivo using primary cell culture and a high fat diet (HFD) mouse model.
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| 4. |
- Ekblad, Eva, et al.
(author)
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Innervation of the small intestine.
- 2002
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In: Biology of the Intestine in Growing Animals. - 9780444509284 - 0444509283 ; , s. 235-235
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Book chapter (other academic/artistic)abstract
- Intestinal activities are controlled and co-ordinated by way of neuronal reflexes involving both extrinsic and intramural neurones, the enteric nervous system (ENS). This review focuses on the organisation, development and functional properties of the intestinal innervation and of the neurotransmitters utilised.
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| 5. |
- Sand, Elin, et al.
(author)
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Expression and distribution of GnRH, LH, and FSH and their receptors in gastrointestinal tract of man and rat.
- 2013
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In: Regulatory Peptides. - : Elsevier BV. - 1873-1686 .- 0167-0115. ; 187, s. 24-28
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Journal article (peer-reviewed)abstract
- Gonadotropin-releasing hormone (GnRH), luteinizing hormone (LH), and follicle-stimulating hormone (FSH) regulate the reproductive axis. Their analogs have been found to influence gastrointestinal activity and enteric neuronal survival. The aims of the study were to investigate expression and cellular distribution of GnRH, LH, and FSH and their receptors in human and rat gastrointestinal tract.
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| 6. |
- Lindqvist, A, et al.
(author)
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Platelet-derived growth factor receptors expressed in response to injury of differentiated vascular smooth muscle in vitro: effects on Ca2+ and growth signals
- 2001
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In: Acta Physiologica Scandinavica. - 0001-6772. ; 173:2, s. 175-175
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Journal article (peer-reviewed)abstract
- Vascular smooth muscle cells (VSMCs) in the intact vascular wall are differentiated for contraction, whereas the response to vascular injury involves transition towards a synthetic phenotype, with increased tendency for proliferation. Platelet-derived growth factor (PDGF) is thought to be important for this process. We investigated expression and functional coupling of PDGF receptors (PDGFRs) alpha and beta in rat tail arterial rings kept in organ culture, in order to capture early events in the phenotypic transition. In freshly dissected rings no PDGFR immunoreactivity was found in medial VSMCs, whereas PDGFR alpha was detected in nerve fibres. After organ culture for 1-4 days PDGFR alpha and beta as well as phospholipase Cgamma2 (PLCgamma2), known to couple to PDGFR, were expressed in VSMCs within 100 microm of the cut ends. Calponin, a marker for the contractile phenotype, was decreased near the injured area, suggesting that cells were in transition towards synthetic phenotype. In these cells, which showed functional Ca2+-release from the sarcoplasmic reticulum, PDGF-AB (100 ng x mL(-1)) had no effect on [Ca2+]i, whereas cultured VSMCs obtained from explants of rat tail arterial rings responded to PDGF-AB with an increase in [Ca2+]i. However, PDGFR within the cultured rings coupled to growth signalling pathways, as PDGF-AB caused a tyrphostin AG1295-sensitive activation of extracellular signal-regulated kinases 1 and 2 and of [3H]-thymidine incorporation. Thus, early expression of PDGFR in VSMC adjacent to sites of vascular injury coincides with signs of dedifferentiation. These receptors couple to growth signalling, but do not activate intracellular Ca2+ release.
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| 7. |
- Sand, Elin, et al.
(author)
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Buserelin treatment to rats causes enteric neurodegeneration with moderate effects on CRF-immunoreactive neurons and Enterobacteriaceae in colon, and in acetylcholine-mediated permeability in ileum
- 2015
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In: BMC Research Notes. - : Springer Science and Business Media LLC. - 1756-0500. ; 8:1
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Journal article (peer-reviewed)abstract
- Background: The gonadotropin-releasing hormone (GnRH) analog buserelin causes enteric neuronal loss. Acute stress or injection of corticotropin-releasing factor (CRF) affects motility, secretion, and barrier function of the gastrointestinal tract. The aim of the study was to characterize the CRF immunoreactivity in enteric neurons after buserelin treatment, and to evaluate possible effects of enteric neuropathy on gut microbiota, intestinal permeability, and stress response behavior. Results: Sixty rats were given buserelin (20 μg) or saline subcutaneously for 5 days, repeated four times with 3 weeks in-between. At the study end, enteric neuronal density, enteric expression of CRF, gut microbial composition, and plasma levels of adrenocorticotropic hormone (ACTH) and CRF were analyzed. Intestinal permeability was examined in Ussing chambers and the reaction to stressful events was measured by behavior tests. Buserelin treatment reduced the number of neurons along the entire gastrointestinal tract, with increased relative numbers of CRF-immunoreactive submucosal and myenteric neurons in colon (p < 0.05 and p < 0.01, respectively). The overall microbial diversity and relative abundance did not differ between groups, but Enterobacteriaceae was decreased in colon in buserelin-treated rats (p = 0.020). Basal intestinal permeability did not differ between groups, whereas carbachol stimulation increased ileum permeability in controls (p < 0.05), but not in buserelin-treated rats. Buserelin did not affect stress behavior. Conclusions: Although buserelin treatment leads to enteric neuronal loss along the gastrointestinal tract with an increased percentage of CRF-immunoreactive neurons in colon, the physiology is well preserved, with modest effects on colon microbiota and absence of carbachol-induced permeability in ileum as the only observed changes. © 2015 Sand et al.
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| 8. |
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| 9. |
- Andersson, Amelie, et al.
(author)
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Expression and motor effects of secretin in small and large intestine of the rat
- 2000
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In: Peptides. - : Elsevier BV. - 0196-9781. ; 21:11, s. 94-1687
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Journal article (peer-reviewed)abstract
- Immunocytochemistry and in situ hybridization revealed abundant secretin expressing cells on duodenal villi with a gradual decrease throughout the small intestines of the rat. They were absent in pancreas, stomach and colon. Secretin caused relaxation of rat intestinal longitudinal muscle in vitro. Studies on colon revealed that the secretin-evoked response was unaffected by apamin, tetrodotoxin, L-NAME, VIP or PACAP pretreatment; secretin itself caused desensitization. Addition of VIP or PACAP when the secretin-evoked relaxation was maximal evoked a further relaxation suggesting the presence of distinct receptors. Secretin causes relaxation via activation of secretin receptors located on the smooth muscle and not via any of the related VIP/PACAP receptors.
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| 10. |
- Arciszewski, Marcin, et al.
(author)
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Lipopolysaccharide induces cell death in cultured porcine myenteric neurons.
- 2005
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In: Digestive Diseases and Sciences. - : Springer Science and Business Media LLC. - 1573-2568 .- 0163-2116. ; 50:9, s. 1661-1668
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Journal article (peer-reviewed)abstract
- Enteric bacteria execute, via lipopolysaccharide (LPS), a pathogenic role in intestinal inflammation. The effects of LPS on survival and neurotransmitter expression in cultured porcine myenteric neurons were investigated. Myenteric neurons were isolated and cultured for 6 days in medium, in LPS (100 ng/ml) with or without α-ketoglutarate or the nitric oxide synthase (NOS) inhibitor L-NAME, in α-ketoglutarate or in the NO donor SNAP. Neuronal survival and expression of vasoactive intestinal peptide (VIP) and NOS were evaluated by immunocytochemistry. Addition of LPS significantly decreased neuronal survival; only 40% survived, compared to controls run in parallel. The LPS-induced neurotoxic effect was not counteracted by the simultaneous presence of α-ketoglutarate or L-NAME. Either SNAP or α-ketoglutarate influenced neuronal survival. Culturing, particularly in the presence of LPS, markedly increased the proportion of VIP-immunoreactive neurons; NOS-immunoreactive neurons were unchanged. The reported LPS-induced neurotoxicity indicates loss of enteric neurons as a consequence of intestinal inflammation.
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