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  • 1.
    Dimberg, J
    et al.
    Univ Coll Hlth Sci, Dept Nat Sci & Biomed, S-55111 Jonkoping, Sweden Fac Hlth Sci, Div Cell Biol, Dept Biomed & Surg, Linkoping, Sweden Ryhov Cty Hosp, Dept Surg, Jonkoping, Sweden Karolinska Hosp, Karolinska Inst, Ctr Mol Med, Stockholm, Sweden.
    Hugander, A
    Univ Coll Hlth Sci, Dept Nat Sci & Biomed, S-55111 Jonkoping, Sweden Fac Hlth Sci, Div Cell Biol, Dept Biomed & Surg, Linkoping, Sweden Ryhov Cty Hosp, Dept Surg, Jonkoping, Sweden Karolinska Hosp, Karolinska Inst, Ctr Mol Med, Stockholm, Sweden.
    Sirsjo, A
    Univ Coll Hlth Sci, Dept Nat Sci & Biomed, S-55111 Jonkoping, Sweden Fac Hlth Sci, Div Cell Biol, Dept Biomed & Surg, Linkoping, Sweden Ryhov Cty Hosp, Dept Surg, Jonkoping, Sweden Karolinska Hosp, Karolinska Inst, Ctr Mol Med, Stockholm, Sweden.
    Decreased levels of precursor transforming growth factor beta(1) in human colorectal cancer2001In: International Journal of Molecular Medicine, ISSN 1107-3756, E-ISSN 1791-244X, Vol. 7, no 6, p. 597-601Article in journal (Refereed)
    Abstract [en]

    Transforming growth factor (TGF) beta (1) is a growth factor with wide-ranging effects on proliferation, differentiation, immunosuppression, apoptosis and matrix remodelling. TGF beta (1) seems to have an antitumorigenic role in the gastrointestinal tract but may also be associated with the development of colorectal cancer. Initially, TGF beta (1) is produced in a latent (precursor) form in epithelial cells and then is activated by a not clearly understood multistep process. In this study, we analysed precursor TGF beta (1) protein expression (n=40) and TGF beta (1) gene expression (n=49) in human colorectal adenocarcinomas and 49 normal adjacent tissue. Out of these 49 normal tissues 40 were matched. Western blot analysis revealed that the precursor TGF beta (1) protein levels were generally lower in colorectal cancerous tissue compared to adjacent noncancerous tissue (P <0.001). Furthermore, with real-time PCR our results cannot reflect a statistically significant difference in TGF beta (1) gene expression between the tumour tissue and normal tissue. These finds indicate that it is likely that there are mechanisms which control precursor TGF beta (1) protein expression by factor(s) at the level of pre-translation of the TGF beta (1) transcript and/or at the level of post-translation of the TGF beta (1) protein in the tumours. This process may be related to carcinogenesis and poses the question whether the suppression of the precursor TGF beta (1) is an early event, in vivo, in the human colorectal adenoma-carcinoma sequence.

  • 2.
    Dimberg, Jan
    et al.
    University College of Health Sciences, Jönköping, Sweden.
    Hugander, Anders
    Ryhov County Hospital, Jönköping, Sweden.
    Löfgren, Sture
    Ryhov County Hospital, Jönköping, Sweden; .
    Wågsäter, Dick
    Karolinska Institute, Stockholm, Sweden.
    Polymorphism and circulating levels of the chemokine CXCL12 in colorectal cancer patients2007In: International Journal of Molecular Medicine, ISSN 1107-3756, E-ISSN 1791-244X, Vol. 19, no 1, p. 11-15Article in journal (Refereed)
    Abstract [en]

    The chemokine CXCL12, also known as stromal cell-derived factor-1 (SDF-1), is a small protein that regulates leukocyte trafficking and is variably expressed in a number of normal and cancer tissues. CXCL12 as ligand and its receptor CXCR4 have been implicated in colorectal cancer (CRC) progression including angiogenesis and metastasis. A CXCL12 gene variant CXCL12-A (CXCL12-G801A, a single nucleotide polymorphism in the 3 untranslated region) is associated with increased susceptibility to breast cancer. Based on the suggested role of CXCL12 in the pathogenesis of cancer we examined the association of the gene variant CXCL12-A with CRC. The polymorphism was analysed with PCR and RFLP methods. Furthermore, the plasma CXCL12 levels from patients with CRC were also examined. There was no significant difference in genotype distribution and allelic frequencies between CRC patients (n=151) and controls (n=141). On the other hand, we found that the carrying rate of allele CXCL12-A was higher in colon cancer patients compared with rectal cancer patients (P=0.017). Analyses by ELISA showed that CRC patients (n=63) had a lower CXCL12 plasma level compared with controls (P less than 0.0001). Moreover, patients with tumours classified as Dukes stage B and C revealed lower levels than patients with tumours in Dukes stage A. Further studies with larger samples of patients are necessary to determine whether the CXCL 12 polymorphism and plasma level reflect the clinical outcome of CRC and have an impact on CRC progression.

  • 3.
    Evertsson, Sofia
    et al.
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Biomedicine and Surgery, Oncology.
    Sun, Xiao-Feng
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Biomedicine and Surgery, Oncology.
    Protein expression of NF-KB in human colorectal adenocarcinoma2002In: International Journal of Molecular Medicine, ISSN 1107-3756, E-ISSN 1791-244X, Vol. 10, p. 547-550Article in journal (Refereed)
  • 4.
    Farnebo, Lovisa
    et al.
    Linköping University, Department of Clinical and Experimental Medicine, Oto-Rhiono-Laryngology and Head & Neck Surgery . Linköping University, Faculty of Health Sciences. Östergötlands Läns Landsting, Reconstruction Centre, Department of ENT - Head and Neck Surgery UHL.
    Jedlinski, Adam
    Linköping University, Department of Clinical and Experimental Medicine. Linköping University, Faculty of Health Sciences.
    Ansell, Anna
    Linköping University, Department of Clinical and Experimental Medicine, Oto-Rhiono-Laryngology and Head & Neck Surgery . Linköping University, Faculty of Health Sciences.
    Vainikka, Linda
    Linköping University, Department of Clinical and Experimental Medicine, Cell Biology. Linköping University, Faculty of Health Sciences.
    Thunell, Lena
    Linköping University, Department of Clinical and Experimental Medicine, Cell Biology. Linköping University, Faculty of Health Sciences.
    Grenman, Reidar
    University of Turku.
    Johansson, Ann-Charlotte
    Linköping University, Department of Clinical and Experimental Medicine, Experimental Pathology . Linköping University, Faculty of Health Sciences.
    Roberg, Karin
    Linköping University, Department of Clinical and Experimental Medicine, Oto-Rhiono-Laryngology and Head & Neck Surgery . Linköping University, Faculty of Health Sciences. Östergötlands Läns Landsting, Reconstruction Centre, Department of ENT - Head and Neck Surgery UHL.
    Proteins and single nucleotide polymorphisms involved in apoptosis, growth control, and DNA repair predict cisplatin sensitivity in head and neck cancer cell lines2009In: International Journal of Molecular Medicine, ISSN 1107-3756, E-ISSN 1791-244X, Vol. 24, no 4, p. 549-556Article in journal (Refereed)
    Abstract [en]

    The present study was undertaken to evaluate the possibility of using a panel of proteins and single nucleotide polymorphisms (SNPs) involved in apoptosis, growth control, and DNA repair as predictive markers for cisplatin sensitivity. For this purpose the intrinsic cisplatin sensitivity (ICS) was determined in 39 cell lines derived from squamous cell carcinomas of the head and neck using a colony-forming assay. In these cell lines and in normal oral keratinocytes (NOK), the expression of epidermal growth factor receptor (EGFR), Hsp70, Bax, Bcl-2, Bcl-XL, survivin, and COX-2 was determined. Moreover, the p53, MDM2, FGFR4, XPC, XPD, XRCC1, and XRCC3 genes were analyzed for the presence of specific single nucleotide polymorphisms (SNPs). Pearsons correlation test showed that EGFR was the only protein that was significantly correlated to the ICS (r=0.388, p=0.015). The combination of EGFR, Hsp70, Bax, and Bcl-2 gave the strongest correlation (r=0.566, p andlt;= 0.001), whereas Bax alone had the second highest influence on the ICS. Furthermore, all four SNPs within genes involved in DNA repair, i.e. XPC, XPD, XRCC1, and XRCC3, tended to influence the ICS. In order to find the combination of factors, on both protein and gene levels, with the highest correlation to ICS, a multivariate statistical calculation was performed. Our results indicate that SNPs in DNA repair genes (XRCC3(241) and XPD751) influence the ICS and together with the expression of EGFR, Hsp70, Bax, and Bcl-2, they could predict the cisplatin sensitivity of head and neck cancer cell lines (r=0.614, p andlt;= 0.001).

  • 5. Li, C
    et al.
    Grönberg, H
    Matsuyama, H
    Weber, G
    Nordenskjöld, M
    Naito, K
    Bergh, A
    Bergerheim, Ulf
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Biomedicine and Surgery, Urology. Östergötlands Läns Landsting, Centre of Surgery and Oncology, Department of Urology in Östergötland.
    Damber, JE
    Larsson, C
    Ekman, P
    Difference between Swedish and Japanese men in the association between AR CAG repeats and prostate cancer suggesting a susceptibility-modifying locus overlapping the androgen receptor gene2003In: International Journal of Molecular Medicine, ISSN 1107-3756, E-ISSN 1791-244X, Vol. 11, p. 529-533Article in journal (Refereed)
  • 6.
    Rossignoli, Aranzazu
    et al.
    Karolinska Inst, Sweden.
    Vorkapic, Emina
    Linköping University, Department of Medical and Health Sciences, Division of Drug Research. Linköping University, Faculty of Medicine and Health Sciences.
    Wanhainen, Anders
    Uppsala Univ, Sweden.
    Länne, Toste
    Linköping University, Department of Medical and Health Sciences, Division of Cardiovascular Medicine. Linköping University, Faculty of Medicine and Health Sciences. Region Östergötland, Heart and Medicine Center, Department of Thoracic and Vascular Surgery.
    Skogberg, Josefin
    Karolinska Inst, Sweden.
    Folestad, Erika
    Karolinska Inst, Sweden.
    Wågsäter, Dick
    Linköping University, Department of Medical and Health Sciences, Division of Drug Research. Linköping University, Faculty of Medicine and Health Sciences.
    Plasma cholesterol lowering in an AngII-infused atherosclerotic mouse model with moderate hypercholesterolemia2018In: International Journal of Molecular Medicine, ISSN 1107-3756, E-ISSN 1791-244X, Vol. 42, no 1, p. 471-478Article in journal (Refereed)
    Abstract [en]

    Atherosclerosis is the main underlying causes of cardiovascular disease. There is a well-established association between high blood cholesterol levels and the extent of atherosclerosis. Furthermore, atherosclerosis has been proposed to augment abdominal aortic aneurysm (AAA) formation. As patients with AAA often have parallel atherosclerotic disease and are therefore often on cholesterol-lowering therapy, it is not possible to fully address the independent effects of plasma cholesterol lowering (PCL) treatment on AAA. The present study investigated the effect of angiotensin II (AngII)-infusion in modestly hypercholesterolemic Ldlr(-/-)Apob(100/100)Mttp(flox/flox)Mx1-Cre mice with or without PCL treatment on a morphological and molecular level, in terms of atherosclerosis and AAA development. AngII infusion in the study mice resulted in an increased atherosclerotic lesion area and increased infiltration of inflammatory leukocytes, which was not observed in mice with PCL induced prior to AngII infusion. This suggested that AngII infusion in this mouse model induced atherosclerosis development, and that plasma cholesterol levels represent a controlling factor. Furthermore, AngII infusion in Ldlr(-/-)Apob(100/100)Mttp(flox/flox)Mx1-Cre mice caused a modest aneurysmal phenotype, and no differences in AAA development were observed between the different study groups. However, the fact that modest hypercholesterolemic mice did not develop AAA in a classical aneurysmal model indicated that plasma cholesterol levels are important for disease development.

  • 7. Salahshor, S
    et al.
    Hou, H
    Diep, CB
    Loukala, A
    Zhang, Hong
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Biomedicine and Surgery, Dermatology.
    Liu, T
    Chen, J
    Iselius, L
    Rubio, C
    Lothe, RA
    Aaltonen, L
    Sun, Xiao-Feng
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Biomedicine and Surgery, Oncology.
    Lindmark, G
    Lindblom, A
    A germline E-cadherin mutation in a family with gastric and colon cancer.2001In: International Journal of Molecular Medicine, ISSN 1107-3756, E-ISSN 1791-244X, Vol. 8, p. 439-443Article in journal (Refereed)
  • 8.
    Wågsäter, Dick
    et al.
    University of Örebro, Sweden.
    Dimberg, Jan
    University of Örebro, Sweden.
    Sirsjö, Allan
    University of Örebro, Sweden.
    Induction of ATP-binding cassette A1 by all-trans retinoic acid: possible role of liver X receptor-alpha2003In: International Journal of Molecular Medicine, ISSN 1107-3756, E-ISSN 1791-244X, Vol. 11, no 4, p. 419-423Article in journal (Refereed)
    Abstract [en]

    ATP binding cassette A1 (ABCA1) is involved in the lipid metabolism of macrophages and has been suggested to play an important role in the development of foam cells and in the pathogenesis of atherosclerosis. We have investigated the effects of all-trans retinoic acid (atRA) on the mRNA and protein levels of ABCA1 in THP-1 cells. Our results show that both mRNA and protein levels of ABCA1 were significantly increased upon treatment with atRA. Since ABCA1 is highly regulated by liver X receptor (LXR) we also analysed the mRNA and protein expressions of LXR-alpha and LXR-6 in the THP-1 cells after treatment with atRA. Also the levels of LXR-alpha were increased by atRA. In conclusion, our results show that LXR-alpha and ABCA1 are simultaneously induced by atRA. The results also imply that the induction of ABCA1 by atRA may in part depend on the induction of LXR.

  • 9.
    Wågsäter, Dick
    et al.
    University of Örebro, Sweden.
    Hugander, Anders
    University of Örebro, Sweden .
    Dimberg, Jan
    University of Örebro, Sweden .
    Expression of CXCL16 in human rectal cancer2004In: International Journal of Molecular Medicine, ISSN 1107-3756, E-ISSN 1791-244X, Vol. 14, no 1, p. 65-69Article in journal (Refereed)
    Abstract [en]

    Local immunoregulation mediated by infiltration of inflammatory cells into colorectal adenocarcinomas is important for tumour progression. Tumour-associated macrophages and T cells are predominant components of chemokine-guided infiltrate of most colorectal tumours. CXCL16 is a newly discovered CXC chemokine expressed by antigen presenting cells attracting Th1, Tc and NK T cells. In this study, which is the first report on expression of the chemokine CXCL16 in human rectal cancer, CXCL16 gene and protein expression were analysed in cancer and normal adjacent tissue. Immunohistochemistry revealed CXCL16 expression in macrophages in normal tissue. The CXCL16 was found to a very limited extent in tumour-associated macrophages. Western blot analysis showed a suppression of CXCL16 protein in rectal cancer compared to non-cancer tissue in 83% of the patients (n=23, P=0.003). However, with real-time PCR mRNA was not down-regulated in the cancer compared to normal tissue, which may depend on regulated factor(s) at the level of translation and/or post-translation. The results may reflect one of the immunological mechanisms underlying carcinogenesis.

  • 10.
    Wågsäter, Dick
    et al.
    University of Örebro, Sweden.
    Sheikine, Y
    University of Örebro, Sweden.
    Sirsjö, A
    University of Örebro, Sweden.
    All-trans retinoic acid regulates CXCL16/SR-PSOX expression2005In: International Journal of Molecular Medicine, ISSN 1107-3756, E-ISSN 1791-244X, Vol. 16, no 4, p. 661-665Article in journal (Refereed)
    Abstract [en]

    Several studies have shown the ability of retinoids to modulate inflammatory response. CXCL16/SR-PSOX is a novel protein functioning as a chemokine and a scavenger receptor. We investigated effects of all-trans retinoic acid (atRA) on CXCL16/SR-PSOX expression in several cell types. Real-time PCR showed that atRA increased CXCL16/SRPSOX mRNA expression in THP-1 and endothelial cells, which corresponded to increased release of CXCL16 protein from the cells, measured by ELISA. In THP-1 cells this effect was reduced by retinoic acid receptor (RAR) antagonist, which indicates receptor-mediated inhibition. RAR-alpha and RAR-gamma agonists increased CXCL16 release, which suggests RAR-mediated effect of atRA, which is not selective for a particular RAR subtype. In smooth muscle cells, up-regulation of CXCL16 mRNA was observed only after 96 h of treatment, while protein expression did not change. These findings suggest that retinoid signaling might be a pathway modulating inflammatory response by regulating CXCL16 expression in a cell-specific manner.

  • 11.
    Wågsäter, Dick
    et al.
    Karolinska Institute, Solna, Stockholm, Sweden.
    Zhu, Chaoyong
    Karolinska Institute, Solna, Stockholm, Sweden.
    Björkegren, Johan
    Karolinska Institute, Solna, Stockholm, Sweden.
    Skogsberg, Josefin
    Karolinska Institute, Solna, Stockholm, Sweden.
    Eriksson, Per
    Karolinska Institute, Solna, Stockholm, Sweden.
    MMP-2 and MMP-9 are prominent matrix metalloproteinases during atherosclerosis development in the LdlrApob100/100 mouse2011In: International Journal of Molecular Medicine, ISSN 1107-3756, E-ISSN 1791-244X, Vol. 28, no 2, p. 247-253Article in journal (Refereed)
    Abstract [en]

    Matrix-degrading proteases capable of degrading components of the extracellular matrix may play an important role in development and progression of atherosclerotic lesions. In the present study, we used the Ldlr(-/-)Apob(100/100) mouse model, which has a plasma lipoprotein profile similar to that of humans with atherosclerosis, to study the expression of matrix metalloproteinases (MMPs) during early stages of atherosclerosis development. We analyzed the expression of 11 proteases and three protease inhibitors in 5- to 40-week-old Ldlr(-/-)Apob(100/100) mice. Expression and activity of MMP-2 and MMP-9 was increased in advanced atherosclerotic lesions followed by macrophage infiltration as shown by real-time PCR, gel-based and in situ zymography and immunohistochemistry. Expression of other investigated MMPs did not increase during disease progression. However, the mRNA expression of MMP-8 and MMP-13 was down-regulated, which could explain the relatively high amount of collagen observed in the vessels in this model. In conclusion, low proteolytic expression at early stages of atherogenesis and a limited repertoire of proteolytic enzymes were associated with the progression of atherosclerosis in Ldlr(-/-)Apob(100/100) mice. The study suggests that MMP-2 and MMP-9 are the main proteases involved in atherogenesis in this mouse model.

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