D Delbro

Örebro universitet, Örebro, Örebro, Sweden

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Publications (106)253.92 Total impact

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    ABSTRACT: Nitric oxide (NO) production from the bladder wall in patients with Bladder Pain Syndrome (BPS) Type 3C is increased compared to undetectable NO levels in non-Hunner BPS patients and healthy controls. However, the underlying mechanism/s of the increased NO production is largely unknown. Our aim was to compare mRNA expression of a selected group of cytokines in BPS/IC Type 3C patients versus pain-free controls. Cold cup biopsies from seven BPS Type 3C patients and six healthy subjects were analysed; mRNA expressions of IL-4, IL-6, IL-10, IL-17A, iNOS, TNF-α, TGF-β and IFN-γ were estimated by real time PCR. The protein expression of IL-17 was determined with immunohistochemistry. Mast cell tryptase labelling was used to evaluate the appearance and count of mast cells. The mRNA levels of IL-6, IL-10, IL-17A and iNOS, as well as the numbers of mast cells infiltrating the bladder mucosa, were significantly increased in BPS Type 3C patients as compared with healthy subjects. TNF-α, TGF-β and IFN-γ mRNA were similar in patients and controls. The expression of IL-17A at the protein level was up-regulated and localised to inflammatory cells and urothelium in the BPS Type 3C patients. BPS/IC patients had increased mRNA levels of IL-17A, IL-10, IL-6 and iNOS. IL-17A might be an important player in the inflammatory process. The increase in IL-17A is a novel finding that may have new treatment implications.
    The Journal of urology 05/2014; 192(5). DOI:10.1016/j.juro.2014.04.099 · 3.75 Impact Factor
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    ABSTRACT: Interstitial cystitis is regarded as a heterogenous syndrome with two distinguishable forms: the non-ulcer and the classic form of interstitial cystitis, the latter with Hunner's lesions; or bladder pain syndrome type 3C and non-Hunner bladder pain syndrome, respectively. A cohort of 379 patients diagnosed with interstitial cystitis was studied. Nitric oxide release from the bladder was measured using a chemiluminescence nitric oxide analyzer. Bladder biopsies from the patients and healthy controls were analyzed by routine histopathological examination. Biopsies from a subset of patients and controls were also analyzed by immunohistochemistry and cytokine gene expression by real-time polymerase chain reaction. Patients with bladder pain syndrome type 3C/classic interstitial cystitis had considerably higher levels of nitric oxide as compared with non-Hunner bladder pain syndrome/non-ulcer interstitial cystitis patients and healthy individuals, and showed histologically a chronic inflammation in the bladder mucosa, with abundant mast cell infiltration in all layers of the bladder wall. No inflammation was noted in non-Hunner bladder pain syndrome/non-ulcer interstitial cystitis patients. The isoenzymes inducible nitric oxide synthase, the catalyst in the nitric oxide production, was strongly expressed in the inflammatory cells in the bladder mucosa of bladder pain syndrome type 3C/classic interstitial cystitis patients. In addition, the expression of the pro-inflammatory cytokines interleukin-6 and interleukin-17A messenger ribonucleic acid, and of anti-inflammatory interleukin-10 messenger ribonucleic acid showed significantly increased levels in bladder pain syndrome type 3C/classic interstitial cystitis compared with healthy controls. Bladder pain syndrome type 3C/classic interstitial cystitis is a distinct inflammatory disease and in many aspects shares features of inflammatory autoimmune diseases. These findings could open up novel research avenues with expectations for new targets for pharmacological treatment.
    International Journal of Urology 04/2014; 21 Suppl S1:75-78. DOI:10.1111/iju.12370 · 1.80 Impact Factor
  • European Urology Supplements 03/2013; 12(1):e664. DOI:10.1016/S1569-9056(13)61146-X · 3.37 Impact Factor
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    ABSTRACT: Abstract Objective. Bladder pain syndrome/interstitial cystitis (BPS/IC) includes a heterogeneous collection of underlying pathological conditions. Compared to the classic IC with a Hunner lesion, now denominated ESSIC type 3C, the non-Hunner type of BPS/IC appears different in a number of respects. In a previous study, measuring luminal nitric oxide (NO) in the bladder of patients with BPS/IC, it was reported that all patients with ESSIC type 3C had high levels of NO. The aim of the present study was to investigate the source of inducible nitric oxide synthase (iNOS) and thereby the cellular origin of NO production via iNOS. Material and methods. Immunohistochemistry, with two different anti-iNOS antibodies, was used to study10 patients with BPS/IC ESSIC type 3C who expressed high levels of intraluminal NO. These results were compared with four patients with non-Hunner BPS/IC. To substantiate further the involvement of iNOS in this condition, the protein expression of nitrotyrosine, a marker for iNOS activation, was also assessed. Results. On routine histopathology, the tissues of type 3C patients exhibited inflammatory infiltrates of varying intensity. Strong immunoreactivity for both iNOS and nitrotyrosine was noted within the urothelium but also within the inflammatory infiltrates in the lamina propria of these subjects. Conclusions. The findings of a clearly detectable protein expression of iNOS in both the urothelium and the inflammatory infiltrates in bladder biopsies from patients with BPS/IC ESSIC type 3C suggest that the production of NO, in this entity, may occur in different tissue compartments.
    Scandinavian Journal of Urology and Nephrology 07/2012; DOI:10.3109/00365599.2012.699100 · 1.06 Impact Factor
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    ABSTRACT: Ischemic preconditioning (IPC) of an organ may induce protection against the injury caused by longer duration of ischemia and subsequent reperfusion. In a standardized model of such injury in the rat liver, we used the following protocol to investigate whether adenosine played a role in IPC by preventing its enzymatic degradation by dipyridamole pretreatment according to the following protocol: group 1, nonischemic control rats; group 2, ischemic control rats subjected to 60 minutes of ischemia by clamping of the common hepatic artery followed by 60 minutes of reperfusion; group 3, IPC with 10 minutes of ischemia followed by 15 minutes of reperfusion, prior to the ischemia/reperfusion period as in group 2; group 4, pharmacologic preconditioning with administration of dipyridamole prior to the ischemia/reperfusion period as in group 2. Peripheral liver blood flow was significantly reduced during clamping (groups 2 to 4). After unclamping, blood flow was still reduced in the ischemic rats (group 2) but had returned to preclamp values in the animals that had been subjected to ischemic (group 3) or pharmacologic (group 4) preconditioning. Liver cell injury was significantly increased in the ischemia group (group 2) only. In our experimental model of ischemia/reperfusion injury in the rat liver, we found an equally beneficial effect with ischemic and pharmacologic preconditioning. Adenosine appears to be a crucial factor in IPC.
    Journal of Gastrointestinal Surgery 04/2012; 4(1):44-9. DOI:10.1016/S1091-255X(00)80031-1 · 2.39 Impact Factor
  • Dick S Delbro
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    ABSTRACT: Various markers of the cholinergic system (like e.g. choline acetyltransferase) were demonstrated by immunohistochemistry in, seemingly, β-cells of rat pancreas. The findings may suggest an autocrine role of acetylcholine for the β-cells.
    Autonomic neuroscience: basic & clinical 04/2012; 167(1-2):75-7. DOI:10.1016/j.autneu.2011.11.006 · 1.82 Impact Factor
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    Dick S. Delbro
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    ABSTRACT: Signaling molecules in the gastrointestinal (GI) tract, as released from intrinsic, or extrinsic neurons, or from local endocrine cells may serve as positive or negative growth factors, and it has been suggested that such could participate also in colorectal carcinogenesis/cancer progression. Sporadic colorectal cancer arises from an initially benign adenoma, which, in turn, develops from the stem cell compartment, located in the bottom of the crypts of the colorectal mucosa. It was recently demonstrated in rat that intrinsic denervation of the colon appeared to be protective against chemically induced carcinogenesis. Of the various GI signaling molecules, noradrenaline (NA) and substance P (SP) may be of particular importance as growth factors involved in colorectal cancer. In the current issue of Neurogastroenterology and Motility, Graf et al. demonstrate that in benign, human colon polyps, there was a loss of innervation compared with adjacent mucosa, affecting efferent, noradrenergic, as well as sensory, SP‐ergic fibers, while there was an increase in SP‐immunoreactive non‐neuronal cells in the polyps. The results obtained could suggest that loss of mucosal innervation, due to e.g. luminal, pro‐inflammatory stimuli, could result in unbalanced pro‐tumorigenic stimulation of the stem cell region by non‐neuronal SP. The current findings may be important for the further understanding of the development of sporadic colorectal cancer.
    Neurogastroenterology and Motility 02/2012; 24(2). DOI:10.1111/j.1365-2982.2011.01854.x · 3.42 Impact Factor
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    ABSTRACT: Non-neuronal acetylcholine (ACh) has been suggested to be a mediator for the development of various types of cancer. We analyzed a possible role for this molecule in carcinogenesis and/or progression of human colon cancer, in patient biopsies harvested from the colon during surgery. We addressed whether ACh synthesis (by choline acetyltransferase) and/or degradation (by ACh esterase), as well as the expression of the α7-subtype of the nicotinic ACh receptors, and the peptide ligand at the α7 receptors, secreted mammalian Ly6/urokinase-type plasminogen activator receptor-related protein-1, respectively, are deranged in tumor tissue as compared with macroscopically tumor-free colon tissue. A total of 38 patients were grouped for analysis based on their respective Dukes stage (either Dukes A + B or C + D). A mucosal tissue sample was harvested from macroscopically tumor-free colon tissue (i.e. control tissue), as well as from the tumor, and protein lysates were prepared for quantitative Western blotting. Full-thickness specimens were taken for immunohistochemistry. For all the above named markers, there was a significant difference between control and tumor tissue with regard to protein levels, and there was, in addition, a significant difference in protein levels between the Dukes A + B and C + D groups. The current findings may suggest a role for ACh in colon carcinogenesis/cancer progression; the data obtained could have prognostic and/or therapeutic significance for this disease.
    Scandinavian Journal of Gastroenterology 04/2011; 46(4):446-55. DOI:10.3109/00365521.2010.539252 · 2.33 Impact Factor
  • Apmis 03/2011; 119(3):227-8. DOI:10.1111/j.1600-0463.2011.02719.x · 1.92 Impact Factor
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    ABSTRACT: Urokinase-type plasminogen activator (uPA) is an important factor for tumour cell invasion and metastasis. We recently showed that acetylcholine is an autocrine/paracrine growth factor for the human colon cancer cell line, HT-29, in part via the α7 subtype of the nicotinic acetylcholine receptors. In the current study, we investigated whether acetylcholine participates in the regulation of the protein expressions of also uPA and its receptor (uPAR) in the HT-29 cell line. Such were investigated by immunocytochemistry and Western blotting, and quantitation of uPA secretion was undertaken by ELISA. Stimulation of the cells for 24h with nicotine caused increased uPA secretion with peak effect (78% above the control) occurring at a nicotine concentration of 10nM. This effect was markedly inhibited by α-Bungarotoxin, thus showing the involvement of α7 nicotinic acetylcholine receptors. Basal uPA secretion was found to be partly dependent on ongoing activation of nicotinic receptors, suggesting tonic production of acetylcholine. Conversely, there was no cholinergic influence on the expression of uPAR. The current findings demonstrate novel aspects of receptor-mediated regulation of tumour metastatic potential via uPA secretion. This may suggest future pharmaceutical strategies in treatment of colorectal cancer.
    European journal of pharmacology 11/2010; 646(1-3):22-30. DOI:10.1016/j.ejphar.2010.08.004 · 2.59 Impact Factor
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    ABSTRACT: Secretion from the lacrimal gland is an important part of the well-being of the eye, and a central part in the search for treatment of dry eye syndrome. Adenosine has stimulatory effects on the lacrimal gland, and can potentiate the effect of the cholinergic agonist carbachol (Cch). The aim of the present study is to investigate the presence of the adenosine A(2) receptor subtypes A(2A) and A(2B) in the rabbit lacrimal gland, and to characterize their role in regulated acinar cell secretion. Expression of the receptors was investigated using reverse transcriptase-PCR (RT-PCR) and immunofluorescence, and secretion effects were studied using a secretion assay in isolated lacrimal gland acinar cells. Presence of both receptors was detected by RT-PCR and immunofluorescence. The secretion assay revealed a minor effect of stimulation of the A(2) receptors, and a strong synergistic effect with the cholinergic agonist Cch. The synergistic effect was significantly reduced by the A(2B) antagonist PSB 1115, but not by the A(2A) antagonist SCH 58261, indicating that A(2B) is the receptor responsible for this potentiation. The study reveals the presence of the adenosine A(2) receptor subtypes as well as a role for them in lacrimal gland secretion, and especially in the synergy with purinergic and cholinergic stimulation.
    Current eye research 06/2010; 35(6):466-74. DOI:10.3109/02713681003602667 · 1.51 Impact Factor
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    ABSTRACT: Morphiceptin (Tyr-Pro-Phe-Pro-NH(2)), a tetrapeptide present in the enzymatic digest of bovine beta-casein, is a selective ligand of the mu-opioid receptor. In the present study, we describe the synthesis of a series of novel morphiceptin analogs modified in positions 1-3. Two of the obtained analogs, [Dmt(1), D-Ala(2), D-1-Nal(3)]morphiceptin and [Dmt(1), D-NMeAla(2), D-1-Nal(3)]morphiceptin (Dmt-2',6'-dimethyltyrosine and d-1-Nal-3-(1-naphthyl)-D-alanine)) displayed very high mu-receptor affinity, resistance to enzymatic degradation, and remarkable supraspinally mediated analgesia, as shown in the hot-plate test after intracerebroventricular but not intravenous administration, which indicated that they could not cross the blood-brain barrier. Therefore, these two analogs were further tested in vitro and in vivo towards their possible peripheral analgesic activity and inhibitory effect on gastrointestinal (GI) motility. We report that both peptides showed strong antinociceptive effect in the writhing test after intraperitoneal administration, inhibited smooth muscle contractility in vitro and GI motility in vivo. Taken together, these findings indicate that the novel morphiceptin analogs which induce peripheral, but not central antinociception, inhibit GI transit, and possess exceptional metabolic stability, may provide an interesting approach to the development of peripherally restricted agents for the treatment of GI motility disorders, such as diarrhea or diarrhea-predominant irritable bowel syndrome.
    Peptides 04/2010; 31(8):1617-24. DOI:10.1016/j.peptides.2010.04.018 · 2.61 Impact Factor
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    ABSTRACT: 1 Possibly acting via mu-opioid receptors (MORs), morphine inhibits the formation of experimentally induced postoperative abdominal adhesions in rats. Mesothelial cells may participate in adhesion formation by secreting mediators that interfere negatively with fibrinolysis. Morphine may prevent adhesions by inhibiting the release of pro-adhesion mediators from mesothelial cells. This study aimed to investigate whether human mesothelial cells express MOR-1; if so, such could constitute a site of action for morphine in adhesion prevention. 2 Cells from Met-5A, a human mesothelial cell line were seeded and prepared for immunocytochemistry and Western blotting. 3 Immunocytochemistry showed MOR-1 expression in mesothelial cells, predominantly in the nuclei. Western blotting showed two bands (c. 35 and 50 kDa) which correspond to those obtained with a control lysate from cells known to express MORs. In addition, we found MOR-1 expression with nuclear and cytoplasmatic localization in biopsies from human abdominal adhesions. 4 The current findings may suggest that morphine could interact directly with mesothelial cells via MOR-1 receptors, and thereby modulate adhesion formation, possibly by interfering with the release of pro-adhesion factors from these cells.
    Autonomic &amp Autacoid Pharmacology 11/2009; 29(4):165-70. DOI:10.1111/j.1474-8665.2009.00444.x
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    ABSTRACT: Urokinase plasminogen activator plays a key role in tumor-associated processes, increasing cancer cell invasion and metastasis, and is therefore used as a marker in cancer prognosis. In this study, we have determined the effect of mu-opioid receptor agonists and antagonists on the urokinase plasminogen activator secretion in MCF-7 cell line. It was shown that mu-opioid receptor agonists, such as morphine and endomorphins, greatly stimulate urokinase plasminogen activator secretion, while naloxone and MOR-selective antagonists elicit the opposite effect. The same tendency was observed also on the urokinase plasminogen activator mRNA level. However, neither agonists nor antagonists had any effect on proliferation of MCF-7 cells. The findings reported in this study may be useful in designing further experiments aimed at elucidating the role of the opioid system in cancer cells.
    Chemical Biology &amp Drug Design 09/2009; 74(4):390-6. DOI:10.1111/j.1747-0285.2009.00875.x · 2.51 Impact Factor
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    ABSTRACT: Pyrrolidine dithiocarbamate has been shown to be a potent inducer of haemeoxygenase-1. This study investigated its in-vivo effects on systemic and hepatic microcirculatory perfusion. Male Sprague-Dawley rats (n=12) were administered intravenously with pyrrolidine dithiocarbamate (10, 20 and 50 mg/kg body weight) or vehicle (0.2 ml physiological saline) served as control. Systemic and hepatic haemodynamics including arterial oxygen saturation, heart rate, mean arterial blood pressure and portal blood flow were monitored. Microcirculation in skeletal muscle and liver was measured by laser Doppler flowmetry and intravital fluorescence microscopy, whereas hepatic tissue oxyhaemoglobin and cytochrome oxidase CuA redox state, which is an indicative of extracellular and intracellular oxygenation were measured by near infrared spectroscopy. Pyrrolidine dithiocarbamate induced a dose-dependent increase in mean arterial blood pressure and skeletal muscle microcirculation. The hepatic parenchymal microcirculation was significantly improved and an increase in sinusoidal diameter and reduction in RBC velocity were observed. Pyrrolidine dithiocarbamate also showed beneficial effect on hepatic tissue oxygenation showed by an increase in oxyhaemoglobin and cytochrome oxidase CuA redox state as well. Pyrrolidine dithiocarbamate improves hepatic parenchymal microcirculation and tissue oxygenation, suggesting that it may be used as a potential agent in pharmacological preconditioning in the liver.
    European journal of gastroenterology & hepatology 06/2009; 21(10):1184-90. DOI:10.1097/MEG.0b013e32831d28cc · 1.66 Impact Factor
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    ABSTRACT: The secreted mammalian Ly-6/urokinase plasminogen activator receptor-related protein-1 (SLURP-1) is an endogenous ligand at the alpha 7 subunit of the nicotinic acetylcholine receptor (nAChR). SLURP-1 has anti-tumourigenic properties. In the current study, we demonstrate that the challenge of HT-29 human colon cancer cells with nicotine for 24 h to increase cell growth via the alpha 7nAChRs, caused a marked reduction of the protein expression of SLURP-1. We suggest that there is an interplay between acetylcholine and SLURP-1 in the HT-29 cells, both molecules serving as autocrine growth controlling ligands at the alpha 7nAChR, where acetylcholine regulates the release of SLURP-1.
    Autonomic neuroscience: basic & clinical 05/2009; 148(1-2):97-100. DOI:10.1016/j.autneu.2009.03.002 · 1.82 Impact Factor
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    ABSTRACT: We investigated whether sympathetic, noradrenergic nerves participate in experimental acute ischemia-reperfusion injury of the rat liver. Female Wistar rats (200-250 g body weight) were anesthetized with pentobarbital. After tracheotomy, we cannulated a carotid artery and jugular vein. The rats were divided in 2 groups (n = 8 per group). The control group received NaCl IV and the test group received the sympatholytic agent, guanethidine (3 mg/kg, IV). After 30 minutes of drug equilibration, laparotomy was performed to arrange the liver for temporary occlusion (by a ligature) of its vascular supply, corresponding with 70% reduction in hepatic blood flow. The rats were then allowed 60 minutes of equilibration. Thereafter, regional ischemia was induced for 30 minutes. The animals were then monitored for 2 hours of reperfusion. Blood samples for alanine aminotransferase (ALT) estimation (as a measure of injury to the parenchyma) were drawn immediately before ischemia, as well as 60 and 120 minutes after reperfusion. Readings of mean arterial pressure were taken during these times. After 2 hours of reperfusion, there were no significant differences between the groups with regard to ALT or mean arterial pressure. Sympathetic, noradrenergic nerves did not affect experimental ischemia-reperfusion injury of rat liver in the current model.
    Transplantation Proceedings 04/2009; 41(2):743-5. DOI:10.1016/j.transproceed.2009.01.035 · 0.95 Impact Factor
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    ABSTRACT: We used immunochemistry to demonstrate expression of acetylcholine's nicotinic alpha7-receptor subtype in human colon cancer cell line HT-29. Moreover, RT-PCR and immunochemistry showed that choline acetyltransferase and acetylcholine esterase, the enzymes responsible for acetylcholine synthesis and degradation, respectively, localise in HT-29 cells. Bromoacetylcholine bromide, an inhibitor of choline acetyltransferase, significantly attenuated basal cell growth. Our findings suggest that acetylcholine might serve as an autocrine/paracrine-or speculatively, even intracrine-signalling molecule in cell line HT-29, thus contributing to carcinogenesis/cancer progression.
    European journal of pharmacology 04/2009; 609(1-3):27-33. DOI:10.1016/j.ejphar.2009.03.002 · 2.59 Impact Factor
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    ABSTRACT: The aim of this study was to investigate whether nicotine acetylcholine receptors (nAChRs) are expressed in a more pronounced way in astrocytes co-cultured with microvascular endothelial cells from adult rat brain, compared with monocultured astrocytes, as a sign of a more developed signal transduction system. Also investigated was whether nicotine plays a role in the control of neuroinflammatory reactivity in astrocytes. Ca(2+) imaging experiments were performed using cells loaded with the Ca(2+) indicator Fura-2/AM. Co-cultured astrocytes responded to lower concentrations of nicotine than did monocultured astrocytes, indicating that they are more sensitive to nicotine. Co-cultured astrocytes also expressed a higher selectivity for alpha7nAChR and alpha4/beta2 subunits and evoked higher Ca(2+) transients compared with monocultured astrocytes. The Ca(2+) transients referred to are activators of Ca(2+)-induced Ca(2+) release from intracellular stores, both IP(3) and ryanodine, triggered by influx through receptor channels. The nicotine-induced Ca(2+) transients were attenuated after incubation with the inflammatory mediator lipopolysaccharide (LPS), but were not attenuated after incubation with the pain-transmitting peptides substance P and calcitonin-gene-related peptide, nor with the infection and inflammation stress mediator, leptin. Furthermore, LPS-induced release of interleukin-1beta (IL-1beta) measured by enzyme-linked immunosorbent assay (ELISA) was more pronounced in co-cultured versus monocultured astrocytes. Incubation with both LPS and IL-1beta further attenuated nicotine-induced Ca(2+) response. We also found that LPS and IL-1beta induced rearrangement of the F-actin filaments, as measured with an Alexa488-conjugated phalloidin probe. The rearrangements consisted of increases in ring formations and a more dispersed appearance of the filaments. These results indicate that there is a connection between a dysfunction of nicotine Ca(2+) signaling in inflammatory reactive astrocytes and upregulation of IL-1beta and the rearrangements of actin filaments in the cells.
    Neuroscience 02/2009; 159(2):770-9. DOI:10.1016/j.neuroscience.2009.01.005 · 3.33 Impact Factor
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    ABSTRACT: 1. Secreted mammalian Ly-6/urokinase plasminogen activator receptor-related protein-1 (SLURP-1) is a recently discovered endogenous ligand at the alpha7 subunit of the nicotinic acetylcholine receptors. Previous reports have shown that SLURP-1 is expressed in normal human keratinocytes seemingly with a pro-apoptotic function. Conversely, such expression was markedly attenuated in transformed cells and it was suggested that the molecule could convey protection against malignant transformation. 2. In this study, we demonstrated the mRNA expression (by RT-PCR) and protein expression (by Western blotting and immunocytochemistry) of SLURP-1 in the human colon cancer cell line, HT-29. 3. Furthermore, we demonstrated the expression of SLURP-1 (by immunohistochemistry) in tumour cells of human colon cancer tissue, and, to a greater extent, in immune and smooth muscle cells of adjacent, macroscopically tumour-free colon tissue. 4. The current findings suggest that SLURP-1 participates in the regulation of gut immune functions and motility, as well as possibly playing a role in colon carcinogenesis/cancer progression.
    Autonomic &amp Autacoid Pharmacology 09/2008; 28(4):109-16. DOI:10.1111/j.1474-8673.2008.00424.x

Publication Stats

1k Citations
253.92 Total Impact Points


  • 2012–2014
    • Örebro universitet
      • School of Health and Medical Sciences
      Örebro, Örebro, Sweden
  • 2011–2012
    • Karlstads universitet
      Karlstad, Värmland, Sweden
  • 1996–2012
    • Sahlgrenska University Hospital
      • • Department of Cardiology
      • • Department of Urology
      Goeteborg, Västra Götaland, Sweden
  • 1982–2011
    • University of Gothenburg
      • • Department of Surgery
      • • Department of Physiology
      Goeteborg, Västra Götaland, Sweden
  • 2010
    • Linnaeus University
      Kalmar, Kalmar, Sweden
  • 2005–2009
    • University College of Kalmar
      • • School of Pure and Applied Natural Sciences
      • • Department of Chemistry and Biomedical Sciences
      Kalmar, Kalmar, Sweden
  • 2006
    • Kungälv sjukhus
      Kungälv, Västra Götaland, Sweden