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  • 1.
    Dahlfors, Gunilla
    et al.
    Linköpings universitet, Institutionen för biomedicin och kirurgi, Cellbiologi. Linköpings universitet, Hälsouniversitetet.
    Chen, Yun
    Linköpings universitet, Institutionen för biomedicin och kirurgi, Cellbiologi. Linköpings universitet, Hälsouniversitetet.
    Gustafsson, Bertil
    Linköpings universitet, Institutionen för nervsystem och rörelseorgan, Patologi. Östergötlands Läns Landsting, Laboratoriemedicinskt centrum, Klinisk patologi och klinisk genetik. Linköpings universitet, Hälsouniversitetet.
    Arnqvist, Hans
    Linköpings universitet, Institutionen för medicin och vård, Internmedicin. Östergötlands Läns Landsting, MKC-2, GE: endomed. Linköpings universitet, Hälsouniversitetet.
    Inhibitory effect of diabetes on proliferation of vascular smooth muscle after balloon injury in rat aorta2000Inngår i: Experimental Diabetes Research, ISSN 1687-5214, E-ISSN 1687-5303, Vol. 1, nr 2, s. 101-109Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    The effect of streptozotocin-induced diabetes on cell proliferation in rat aortic intima-media, as well as on local gene expression of transforming growth factor-β1 (TGF-β1) was studied. TGF-β1 mRNA was measured by solution hybridization and TGF-β1 protein by ELISA. Proliferation was measured by bromodeoxyuridine incorporation into DNA two days after balloon injury. All BrdU-labelled cells observed were smooth muscle cells. After a diabetes duration of 2 and 4 weeks, labelled cells were significantly fewer compared with controls. Circulating levels of total TGF-β1 were lowered in rats with 2 weeks diabetes. Although the balloon injury procedure by itself stimulated the gene expression of TGF-β1, no significant difference in TGF-β1 mRNA content between diabetic and control rats after injury was found. In conclusion: vascular smooth muscle proliferation in vivo is inhibited by the diabetic state in this model of insulin deficient diabetes and this inhibition is not related to an impaired local expression of TGF-β1.

  • 2.
    Paulsson, Johan F
    et al.
    Department of Chemistry and The Skaggs Institute for Chemical Biology, The Scripps Research Institute, La Jolla, CA 92037, USA.
    Schultz, Sebastian
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Cellbiologi. Linköpings universitet, Hälsouniversitetet.
    Kohler, Martin
    The Rolf Luft Research Center for Diabetes and Endocrinology, Karolinska Institute, 17176 Stockholm, Sweden.
    Leibiger, Ingo
    The Rolf Luft Research Center for Diabetes and Endocrinology, Karolinska Institute, 17176 Stockholm, Sweden.
    Berggren, Per-Olof
    The Rolf Luft Research Center for Diabetes and Endocrinology, Karolinska Institute, 17176 Stockholm, Sweden.
    Westermark, Gunilla
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Cellbiologi. Linköpings universitet, Hälsouniversitetet.
    Real-Time Monitoring of Apoptosis by Caspase-3-Like Protease Induced FRET Reduction Triggered by Amyloid Aggregation2008Inngår i: Experimental Diabetes Research, ISSN 1687-5214, E-ISSN 1687-5303, Vol. 2008, nr 865850Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Amyloid formation is cytotoxic and can activate the caspase cascade. Here, we monitor caspase-3-like activity as reduction of fluorescence resonance energy transfer (FRET) using the contstruct pFRET2-DEVD containing enhanced cyan fluorescent protin (EYFP) linked by the caspase-3 specific cleavage site residues DEVD. Beta-TC-6 cells were transfected, and the fluoorescence was measured at 440 nm excitation and 535 nm (EYFP) and 480 nm (ECFP) emission wavelength. Cells were incubated with recombinant pro lset Amyloid Polypeptide (rec prolAPP) or the processing metabolites of prolAPP; the N-terminal flanking peptide withIAPP (recN+IAPP); IAPP with the C-terminal flanking peptied (recIAPP+C) and lslet Amyloid Polypeptide (recIAPP). Peptides were added in solubilized from (50 mu M) or as performed amyloid-like fibrils, or as a combination of these. FRET was measured and incubation with a mixture of solubilized peptide and performed fibrils resulted in loss of FRET and apoptosis was determined to occurein cells incubated with recproIAPP (49%), recN+IAPP (46%), recIAPP (72%) and recIAPP+C (59%). These results show that proIAPP and the processing intermediates reside the same cell toxic capacity as IAPP, and they can all have a central role in the reduction of beta-cell number in type 2 diabetes.

  • 3.
    Westermark, Gunilla
    et al.
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Cellbiologi. Linköpings universitet, Hälsouniversitetet.
    Westermark, Per
    Uppsala University.
    Importance of Aggregated Islet Amyloid Polypeptide for the Progressive Beta-Cell Failure in Type 2 Diabetes and in Transplanted Human Islets2008Inngår i: Experimental Diabetes Research, ISSN 1687-5214, E-ISSN 1687-5303, artikkel-id 528354Artikkel i tidsskrift (Annet vitenskapelig)
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