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  • 1.
    Cavallini, Nicola
    et al.
    Gothenburg University.
    Delbro, Dick
    Karlstad University, Faculty of Technology and Science, Department of Chemistry and Biomedical Sciences. Sahlgrens Univ Hosp, Dept Surg, Gothenburg, Sweden.;Univ Karlstad, Sch Pure & Appl Nat Sci, Karlstad, Sweden..
    Tobin, Gunnar
    Gothenburg University.
    Braide, Magnus
    Gothenburg University.
    Neuropeptide release augments serum albumin loss and reduces ultrafiltration in peritoneal dialysis2012In: Peritoneal Dialysis International, ISSN 0896-8608, E-ISSN 1718-4304, Vol. 32, no 2, p. 168-176Article in journal (Refereed)
    Abstract [en]

    Background: The triggers of the acute local inflammatory response to peritoneal dialysis (PD) fluid exposure remain unknown. In the present study, we investigated the effects of neurogenic inflammation and mast cell degranulation on water and solute transport in experimental PD. Methods: Single 2-hour dwells in rats with PD catheters were studied. Histamine and the neuropeptides substance P and calcitonin gene-related peptide (CGRP) were measured in PD fluid samples by ELISA. Radiolabeled albumin (I-125 and I-131 respectively) was used as an intraperitoneal (IP) and intravascular tracer. Glucose and urea concentrations were measured in plasma and PD fluid. The effects of varying the volume and osmolarity of a lactate-buffered PD fluid were compared and related to the effects of pharmacologic intervention. Results: Application of 20 mL 3.9% glucose PD fluid induced an IP histamine release during the first 30 minutes, blockable by the mast cell stabilizer doxantrazole and the substance P neurokinin-1 receptor (NK1R)-blocker spantide. Histamine release was also inhibited at a reduced PD volume (14 mL), but was not affected by normalizing the PD fluid osmolarity. Blockade of NK1R also reduced plasma albumin leakage to the peritoneal cavity. Inhibition of CGRP receptors by CGRP8-37 improved osmotic (transcapillary) and net ultrafiltration and reduced the dialysate urea concentration. Neuropeptide release was not clearly related to activation of the TrpV1 receptor, the classic trigger of neurogenic inflammation. Conclusions: Neuropeptide release exaggerated albumin loss and reduced ultrafiltration in this rat PD model. Intervention aimed at the neuropeptide action substantially improved PD efficiency.

  • 2.
    Delbro, Dick
    Karlstad University, Faculty of Technology and Science, Department of Chemistry and Biomedical Sciences. Sahlgrens Univ Hosp, Dept Surg, Gothenburg, Sweden..
    Do neuro-humoral signaling molecules participate in colorectal carcinogenesis/cancer progression?2012In: Neurogastroenterology and Motility, ISSN 1350-1925, E-ISSN 1365-2982, Vol. 24, no 2, p. 96-99Article in journal (Refereed)
    Abstract [en]

    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.

  • 3.
    Delbro, Dick
    et al.
    Karlstad University, Faculty of Technology and Science, Department of Chemistry and Biomedical Sciences.
    Carlsson, Stina K
    Edman, Maria C
    Gierow, J. Peter
    Adenosine A2 receptor presence and synergy with cholinergic stimulation in rabbit lacrimal gland2010In: Current Eye Research, ISSN 0271-3683, Vol. 35, no 6, p. 466-474Article in journal (Refereed)
    Abstract [en]

    PURPOSE: 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.METHODS: 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.RESULTS: 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.CONCLUSIONS: 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.

  • 4.
    Delbro, Dick
    et al.
    Karlstad University, Faculty of Technology and Science, Department of Chemistry and Biomedical Sciences.
    Gach, K
    Szemraj, J
    Fichna, J
    Piestrzeniewicz, M
    Janecka, A
    The influence of opioids on urokinase plasminogen activator on protein and mRNA level in MCF-7 breast cancer cell line2009In: Chemical Biology and Drug Design, ISSN 1747-0277, E-ISSN 1747-0285, Vol. 74, no 4, p. 390-396Article in journal (Refereed)
    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

  • 5.
    Delbro, Dick
    et al.
    Karlstad University, Faculty of Technology and Science, Department of Chemistry and Biomedical Sciences.
    Gach, Katarzyna
    do-Rego, Jean Claude
    Fichna, Jakub
    Storr, Martin
    Toth, Geza
    Janecka, Anna
    Synthesis and biological evaluation of novel peripherally active morphiceptin analogs2010In: Peptides, ISSN 0196-9781, Vol. 31, no 8, p. 1617-1624Article in journal (Refereed)
    Abstract [en]

    Morphiceptin (Tyr-Pro-Phe-Pro-NH2), 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 13. Two of the obtained analogs, [Dmt1, d-Ala2, d-1-Nal3]morphiceptin and [Dmt1, d-NMeAla2, d-1-Nal3]morphiceptin (Dmt2,6-dimethyltyrosine andd-1-Nal3-(1-naphthyl)-d-alanine)) displayed very high -receptor affinity, resistance to enzymaticdegradation, and remarkable supraspinally mediated analgesia, as shown in the hot-plate test afterintracerebroventricular but not intravenous administration, which indicated that they could not cross the bloodbrain 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.Wereport 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

  • 6.
    Delbro, Dick
    et al.
    Karlstad University, Faculty of Technology and Science, Department of Chemistry and Biomedical Sciences.
    Khorram-Manesh, A
    Nordlander, S
    Novotny, A
    Bengtsson, C
    Nylund, G
    Levin, M
    Nordgren, S
    Nuclear expression of mu-opioid receptors in a human mesothelial cell line2009In: Autonomic & Autacoid Pharmacology, ISSN 1474-8665, E-ISSN 1474-8673, Vol. 29, no 4, p. 165-170Article in journal (Refereed)
    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

  • 7.
    Delbro, Dick
    et al.
    Karlstad University, Faculty of Technology and Science, Department of Chemistry and Biomedical Sciences.
    Lång, P
    Lange, S
    Andersson, G
    Induction and cellular expression of tartrate resistant acid phosphatase during dextran sodium sulphate induced colitis in rats2009In: Histochemistry and Cell Biology, ISSN 0948-6143, E-ISSN 1432-119X, Vol. 132, no 6, p. 599-612Article in journal (Refereed)
    Abstract

    The aim of this study was to investigate the

    cellular and molecular expression of tartrate resistant acid phosphatase (TRAP) as a marker of activated macrophages in macrophage dependent dextran sulphate sodium (DSS)-induced colitis in rats. In normal colon, TRAP+/CX3CR1+ macrophages were located in the upper part of the lamina propria. In the early stage (day 13) of acute colitis prior to

    histopathological changes, induction of the cytokines

    TNF, IL-12 and IFNgamma occurred concomitant with

    increased mRNA and enzyme activity of TRAP along with

    a slight increase of TRAP immunolabelling in macrophages of the upper lamina propria, suggesting induction of TRAP in resident macrophages. Among these cytokines,TNFalpha up-regulated TRAP expression in the RAW 264.7 monocyte/macrophage cell line. In a later phase (day 7) with fulminant colitis, a massive infiltration of macrophages including recruited TRAP+/CCR2+ cells was observed also in the lower part of the lamina propria as well as in the submuscular layer. Additionally, diVerentiated cellular

    expression of pro- and mature TRAP also suggest that

    mucosal macrophages in the lower part of lamina propria

    bordering the sub-mucosa provide a source of replenishment of macrophages situated in the upper lamina propria.

    In conclusion, induction of TRAP provides an early sign of macrophage responsiveness in DSS induced colitis

  • 8.
    Delbro, Dick
    et al.
    Karlstad University, Faculty of Technology and Science, Department of Chemistry and Biomedical Sciences.
    Novotny, Ann
    Edsparr, Karin
    Nylund, Gunnar
    Khorram-Manesh, Amir
    Albertsson, Per
    Nordgren, Svante
    A pharmacological analysis of the cholinergic regulation of urokinase-type plasminogen activator secretion in the human colon cancer cell line, HT-292010In: European Journal of Pharmacology, ISSN 0014-2999, Vol. 646, no 1,2,3, p. 22-30Article in journal (Refereed)
    Abstract [en]

    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 7 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 -Bungarotoxin, thus showing the involvement of 7 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.

  • 9.
    Delbro, Dick
    et al.
    Karlstad University, Faculty of Technology and Science, Department of Chemistry and Biomedical Sciences.
    Pettersson, A
    Nilsson, L
    Nylund, G
    Khorram-Manesh, A
    Nordgren, S
    Is acetylcholine an autocrine/paracrine growth factor via the nicotinic α-receptor subtype in the human colon cancer cell line HT-29?2009In: European Journal of Pharmacology, ISSN 0014-2999, E-ISSN 1879-0712, Vol. 609, no 1-3, p. 27-33Article in journal (Refereed)
    Abstract

    We used immunochemistry to demonstrate expression of acetylcholine's nicotinic 7-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/paracrineor speculatively, even intracrinesignalling molecule in cell line HT-29, thus

    contributing to carcinogenesis/cancer progression

  • 10.
    Delbro, Dick
    et al.
    Karlstad University, Faculty of Technology and Science, Department of Chemistry and Biomedical Sciences.
    Pettersson, A
    Nylund, G
    Khorram-Manesh, A
    Nordgren, S
    Nicotine induced modulation of SLURP-1 expression in human colon cancer cells2009In: Autonomic Neuroscience, ISSN 1566-0702, Vol. 148, no 1-2, p. 97-100Article in journal (Refereed)
    Abstract [en]

    The secreted mammalian Ly-6urokinase plasminogen activator receptor-related protein-1 (SLURP-1) is anendogenous ligand at the 7 subunit of the nicotinic acetylcholine receptor (nAChR). SLURP-1 has antitumourigenic properties. In the current study, we demonstrate that the challenge of HT-29 human coloncancer cells with nicotine for 24 h to increase cell growth via the 7nAChRs, caused a marked reduction ofthe protein expression of SLURP-1. We suggest that there is an interplay between acetylcholine and SLURP-1in the HT-29 cells, both molecules serving as autocrine growth controlling ligands at the 7nAChR, where acetylcholine regulates the release of SLURP-1

  • 11.
    Delbro, Dick S.
    Karlstad University, Faculty of Technology and Science, Department of Chemistry and Biomedical Sciences.
    Expression of the non-neuronal cholinergic system in rat beta-cells2012In: Autonomic Neuroscience: Basic & Clinical, ISSN 1566-0702, E-ISSN 1872-7484, Vol. 167, no 1-2, p. 75-77Article in journal (Refereed)
    Abstract [en]

    Various markers of the cholinergic system (like e.g. choline acetyltransferase) were demonstrated by immunohistochemistry in, seemingly, beta-cells of rat pancreas. The findings may suggest an autocrine role of acetylcholine for the beta-cells. (C) 2011 Elsevier B.V. All rights reserved.

  • 12.
    Delbro, Dick S.
    et al.
    Univ Gothenburg, Dept Surg, Inst Clin Sci, Sahlgrenska Acad, Gothenburg, Sweden.;Karlstad Univ, Dept Chem & Biomed Sci, Karlstad, Sweden..
    Hallsberg, Lena
    Univ Gothenburg, Dept Surg, Inst Clin Sci, Sahlgrenska Acad, Gothenburg, Sweden..
    Wallin, Monica
    Univ Gothenburg, Dept Surg, Inst Clin Sci, Sahlgrenska Acad, Gothenburg, Sweden..
    Gustafsson, Bengt I.
    Univ Gothenburg, Dept Surg, Inst Clin Sci, Sahlgrenska Acad, Gothenburg, Sweden.;Sahlgrens Univ Hosp, Sahlgrenska Transplant Inst, Gothenburg, Sweden..
    Friman, Styrbjorn
    Univ Gothenburg, Dept Surg, Inst Clin Sci, Sahlgrenska Acad, Gothenburg, Sweden.;Sahlgrens Univ Hosp, Sahlgrenska Transplant Inst, Gothenburg, Sweden..
    Expression of the non-neuronal cholinergic system in rat liver2011In: Acta Pathologica, Microbiologica et Immunologica Scandinavica (APMIS), ISSN 0903-4641, E-ISSN 1600-0463, Vol. 119, no 3, p. 227-228Article in journal (Refereed)
  • 13.
    Engström, Alexander
    et al.
    Karlstad University, Faculty of Health, Science and Technology (starting 2013), Department of Health Sciences (from 2013).
    Erlandsson, Ann
    Karlstad University, Faculty of Health, Science and Technology (starting 2013), Department of Health Sciences (from 2013).
    Delbro, Dick
    Örebro universitet.
    Wijkander, Jonny
    Karlstad University, Faculty of Health, Science and Technology (starting 2013), Department of Health Sciences (from 2013).
    Conditioned media from M1 but not M2 macrophage phenotype inhibits proliferation of thr colon cancer cell lines HT29 and CACO-22013Conference paper (Refereed)
    Abstract [en]

    Background

    Tumor associated macrophages (TAMs) are often present at a high level in colorectal cancer (CRC) but whether the presence of TAMs in CRC is good or bad is unclear. Macrophages can be categorized into two main subgroups, M1 or M2, that display pro – and anti-inflammatory properties respectively. An improved knowledge of the different macrophage phenotypes will broaden the understanding of their involvement in CRC. We have used an in vitro model to study the effects of human M1 and M2 macrophages on the growth and cell cycle of colon cancer cell lines.

     

    Method

    Human monocytes were differentiated into M1 or M2 macrophages and conditioned media was collected. Effects of the conditioned media were measured on the colon cancer cell lines HT-29 and CACO-2 in regards to proliferation, cell cycle distribution and apoptosis. A protein array was used to analyze the released amount of 42 different cytokines from M1 and M2 macrophages into the collected conditioned media.

     

    Results

    Growth arrest was induced in HT-29 and CACO-2 by M1 conditioned media, while M2 conditioned media had no major effect. Analysis of cell cycle distribution and apoptosis in HT-29 cells revealed that treatment with M1 conditioned media on these cells increased apoptosis and caused a disturbed cell cycle with accumulation in G0/G1 and G2/M and a corresponding reduction in S-phase. The protein array revealed several cytokines expressed in M1 with potential inhibitory growth effects. We treated HT-29 cells with two of the candidates, TNF-a and CXCL9, but neither induced growth arrest.

     

    Conclusion

    M1 – but not M2-macrophages had a major inhibitory effect on the growth of the colon cancer cell lines HT-29 and CACO-2 and suggest a role for M1 macrophages in anti-tumor activity and possible favorable outcome for CRC patients.

  • 14.
    Engström, Alexander
    et al.
    Karlstad University, Faculty of Health, Science and Technology (starting 2013), Department of Health Sciences (from 2013).
    Erlandsson, Ann
    Karlstad University, Faculty of Health, Science and Technology (starting 2013), Department of Health Sciences (from 2013).
    Delbro, Dick
    School of Health and Medical Sciences, Örebro University.
    Wijkander, Jonny
    Karlstad University, Faculty of Health, Science and Technology (starting 2013), Department of Health Sciences (from 2013).
    Conditioned media from macrophages of M1, but not M2 phenotype, inhibit the proliferation of the colon cancer cell lines HT-29 and CACO-22014In: International Journal of Oncology, ISSN 1019-6439, Vol. 44, p. 385-392Article in journal (Refereed)
    Abstract [en]

    Solid tumors are infiltrated by stroma cells including macrophages and these cells can affect tumor growth, metastasis and angiogenesis. We have investigated the effects of conditioned media (CM) from different macrophages on the proliferation of the colon cancer cell lines HT-29 and CACO-2. CM from THP-1 macrophages and monocyte-derived human macrophages of the M1 phenotype, but not the M2 phenotype, inhibited proliferation of the tumor cells in a dose-dependent manner. Lipopolysaccaharide and interferon γ was used for differentiation of macrophages towards the M1 phenotype and CM were generated both during differentiation (M1DIFF) and after differentiation (M1). M1 and M1DIFF CM as well as THP-1 macrophage CM resulted in cell cycle arrest in HT-29 cells with a decrease of cells in S phase and an increase in G2/M phase. Treatment of HT-29 cells with M1DIFF, but not M1 or THP-1 macrophage CM, resulted in apoptosis of about 20% of the tumor cells and this was accompanied by lack of recovery of cell growth after removal of CM and subsequent culture in fresh media. A protein array was used to identify cytokines released from M1 and M2 macrophages. Among the cytokines released by M1 macrophages, tumor necrosis factor α and CXCL9 were tested by direct addition to HT-29 cells, but neither affected proliferation. Our results indicate that M1 macrophages inhibit colon cancer cell growth and have the potential of contributing to reducing tumor growth in vivo.

  • 15.
    Esguerra, Maricris
    et al.
    Sahlgrens Univ Hosp, Vasc Engn Ctr, Gothenburg, Sweden..
    Fink, Helen
    Sahlgrens Univ Hosp, Vasc Engn Ctr, Gothenburg, Sweden..
    Laschke, Matthias W.
    Univ Saarland, Inst Clin & Expt Surg, D-6650 Homburg, Saarland, Germany..
    Jeppsson, Anders
    Sahlgrens Univ Hosp, Dept Cardiothorac Surg, Gothenburg, Sweden..
    Delbro, Dick
    Karlstad University, Faculty of Technology and Science, Department of Chemistry and Biomedical Sciences. Sahlgrens Univ Hosp, Dept Surg, Gothenburg, Sweden.;Univ Karlstad, Sch Pure & Appl Nat Sci, Karlstad, Sweden..
    Gatenholm, Paul
    Chalmers, Dept Biol & Chem Engn, S-41296 Gothenburg, Sweden..
    Menger, Michael D.
    Univ Saarland, Inst Clin & Expt Surg, D-6650 Homburg, Saarland, Germany..
    Risberg, Bo
    Sahlgrens Univ Hosp, Vasc Engn Ctr, Gothenburg, Sweden..
    Intravital fluorescent microscopic evaluation of bacterial cellulose as scaffold for vascular grafts2010In: Journal of Biomedical Materials Research. Part A, ISSN 1549-3296, E-ISSN 1552-4965, Vol. 93A, no 1, p. 140-149Article in journal (Refereed)
    Abstract [en]

    Although commonly used synthetic vascular grafts perform satisfactorily in large caliber blood vessels, they are prone to thrombosis in small diameter vessels. Therefore, small vessels might benefit from tissue engineered vascular grafts. This study evaluated bacterial cellulose (BC) as a potential biomaterial for biosynthetic blood vessels. We implanted the dorsal skinfold chambers in three groups of Syrian golden hamsters with BC (experimental group), polyglycolic acid, or expanded polytetrafluorethylane (control groups). Following implantation, we used intravital fluorescence microscopy, histology, and immunochemistry to analyze the biocompatibility, neovascularization, and incorporation of each material over a time period of 2 weeks. Biocompatibility was good in all groups, as indicated by the absence of leukocyte acti-vation upon implantation. All groups displayed angiogenic response in the host tissue, but that response was highest in the polyglycolic acid group. Histology revealed vascularized granulation tissue Surrounding all three biomaterials, with many proliferating cells and a lack of apoptotic cell death 2 weeks after implantation. In conclusion, BC offers good biocompatibility and material incorporation compared with commonly used materials in vascular surgery. Thus, BC represents a promising new biomaterial for tissue engineering of vascular grafts. (C) 2009 Wiley Periodicals, Inc. J Biomed Mater Res 93A: 140-149, 2010

  • 16.
    Hedbrant, Alexander
    et al.
    Karlstad University, Faculty of Health, Science and Technology (starting 2013), Department of Health Sciences (from 2013).
    Erlandsson, Ann
    Karlstad University, Faculty of Health, Science and Technology (starting 2013), Department of Health Sciences (from 2013).
    Delbro, Dick
    Örebro university.
    Wijkander, Jonny
    Karlstad University, Faculty of Health, Science and Technology (starting 2013), Department of Health Sciences (from 2013).
    Conditioned media from human macrophages of M1 phenotype attenuate the cytotoxic effect of 5‑fluorouracil on the HT‑29 colon cancer cell line2015In: International Journal of Oncology, ISSN 1019-6439, Vol. 46, no 1, p. 37-46Article in journal (Refereed)
    Abstract [en]

    Resistance of tumor cells to chemotherapy, such as 5‑fluorouracil (5‑FU), is an obstacle for successful treatment of cancer. As a follow‑up of a previous study we have investigated the effect of conditioned media (CM) from macrophages of M1 or M2 phenotypes on 5‑FU cytotoxicity on the colon cancer cell lines HT‑29 and CACO‑2. HT‑29 cells, but not CACO‑2 cells, having been treated with a combination of M1 CM and 5‑FU recovered their cell growth to a much larger extent compared to cells having been treated with 5‑FU alone when further cultured for 7 days in fresh media. M1 CM treatment of HT‑29, but not CACO‑2 cells, induced cell cycle arrest in the G0/G1 and G2/M phases. 5‑FU treatment induced accumulation of cells in S‑phase in both HT‑29 and CACO‑2 cells. This accumulation of cells in S‑phase was attenuated by combined M1 CM and 5‑FU treatment in HT‑29 cells, but not in CACO‑2 cells. The mRNA expression of cell cycle regulatory proteins and 5‑FU metabolic enzymes were analyzed in an attempt to find possible mechanisms for the M1 CM induced attenuation of 5‑FU cytotoxicity in HT‑29. Thymidylate synthetase (TS) and thymidine phosphorylase (TP) were found to be substantially downregulated and upregulated, respectively, in HT‑29 cells treated with M1 CM, making them unlikely as mediators of reduced 5‑FU cytotoxicity. Among cell cycle regulating proteins, p21 was induced in HT‑29 cells, but not in CACO‑2 cells, in response to M1 CM treatment. However, small interfering RNA (siRNA) knockdown of p21 had no effect on the M1 CM induced cell cycle arrest seen in HT‑29 and neither did it change the growth recovery after combined treatment of HT‑29 cells with M1 CM and 5‑FU. In conclusion, treatment of HT‑29 cells with M1 CM reduces the cytotoxic effect of 5‑FU and this is mediated by a M1 CM induced cell cycle arrest in the G0/G1 and G2/M phases. So far, we lack an explanation why this action is absent in the CACO‑2 cells. The current findings may be important for optimization of chemotherapy in colon cancer.

  • 17.
    Hedbrant, Alexander
    et al.
    Karlstad University, Faculty of Health, Science and Technology (starting 2013), Department of Health Sciences (from 2013).
    Wijkander, Jonny
    Karlstad University, Faculty of Health, Science and Technology (starting 2013), Department of Health Sciences (from 2013).
    Seidal, Tomas
    Karlstad University, Faculty of Health, Science and Technology (starting 2013), Department of Health Sciences (from 2013).
    Delbro, Dick
    Örebro University.
    Erlandsson, Ann
    Karlstad University, Faculty of Health, Science and Technology (starting 2013), Department of Health Sciences (from 2013).
    Macrophages of M1 phenotype have properties that influence lung cancer cell progression.2015In: Tumor Biology, ISSN 1010-4283, E-ISSN 1423-0380, Vol. 36, no 11, p. 8715-8725Article in journal (Refereed)
    Abstract [en]

    Stromal macrophages of different phenotypes can contribute to the expression of proteins that affects metastasis such as urokinase-type plasminogen activator (uPA), its receptor uPAR, and plasminogen activator inhibitor-1 (PAI-1), but knowledge of how essential their contribution is in comparison to the cancer cells in small cell lung cancer (SCLC) and lung squamous cell carcinoma (SCC) is lacking. The expression of uPA, uPAR, and PAI-1 and of the matrix metalloproteinases (MMP)-2 and MMP-9 were studied in human macrophages of M1 and M2 phenotype and compared to a lung SCC (NCI-H520) and a SCLC (NCI-H69) cell line. Effects of treatment with conditioned media (CM) from M1 and M2 macrophages on the expression of these genes in H520 and H69 cells as well as effects on the cell growth were investigated. In addition, data on the stromal macrophages immunoreactivity of uPAR, MMP-2, and MMP-9 in a few SCC and SCLC biopsies was included. uPAR, MMP-2, and MMP-9 were confirmed in stromal cells including macrophages in the SCC and SCLC biopsies. In vitro, both macrophage phenotypes expressed considerably higher mRNA levels of uPA, uPAR, PAI-1, and MMP-9 compared to the cancer cell lines, and regarding uPAR, the highest level was found in the M1 macrophage phenotype. Furthermore, M1 CM treatment not only induced an upregulation of PAI-1 in both H520 and H69 cells but also inhibited cell growth in both cell lines, giving M1 macrophages both tumor-promoting and tumor-killing potential.

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