J.F.M. Van Straaten

University of Groningen, Groningen, Groningen, Netherlands

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Publications (5)21.88 Total impact

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    ABSTRACT: To characterize the possible role of a dysregulated proliferative capacity of pulmonary fibroblasts in insufficient tissue repair in lungs from patients with pulmonary emphysema, the authors undertook in vitro proliferative studies with pulmonary fibroblasts obtained from lung tissue of patients with emphysema. A comparison was made with fibroblasts from control subjects. The authors determined the in vitro proliferative capacity of fibroblasts at basal culture conditions and after modulation with interleukin-1beta, interferon-gamma, transforming growth factor-beta(1), and basic fibroblast growth factor. Proliferative capacity was determined by measurement of 5-bromo-2-deoxyuridine (BrdU) incorporation. BrdU incorporation by fibroblast cultures from both groups was very similar. Fibroblast cultures from control subjects, however, incorporated more BrdU after incubation with interleukin-1beta than cultures from patients with emphysema (P<.05). On the other hand, transforming growth factor-beta(1) decreased incorporation of BrdU stronger in fibroblast cultures from control subjects than from patients with emphysema (P<.05). Thus, the proliferative capacity of fibroblast cultures isolated from lung tissue of patients with pulmonary emphysema is different from that of control subjects. Although the difference is small, it may be an essential contribution to the development of pulmonary emphysema that only occurs after repeated smoke-induced injury over many years of an individual's life.
    No preview · Article · Jul 2003 · Experimental Lung Research
  • J.F.M. Van Straaten · W Coers · JA Noordhoek · S Huitema · J.T.M. Flipsen · H F Kauffman · W Timens · D S Postma
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    ABSTRACT: To characterize the changes in the extracellular matrix in smoking-related pulmonary emphysema, we undertook immunohistochemical studies in lung tissues from controls (n = 7), from patients with mild (n = 11) and severe (n = 8) emphysema, and from patients with lung fibrosis (n = 6). We studied collagens, laminin, fibronectin, proteoglycans (PGs), and beta1-integrins. The majority of the patients with severe emphysema showed diminished staining for the interstitial PGs, decorin and biglycan, in the peribronchiolar area, compared with patients in the control and fibrosis groups. Only a minority of patients with mild emphysema showed this diminished staining. In contrast, decorin and biglycan were well preserved in the perivascular area of all of the specimens from the emphysema group. Heparan sulfate PG staining was diminished in the respiratory airspace walls of patients with emphysema and fibrosis. Staining for Types I, III, and IV collagen, as well as for laminin, fibronectin, and the integrins, showed no differences between the four groups. The specific loss of interstitial PGs may be crucial for elastic recoil loss and subsequent bronchiolar obstruction, as seen in patients with smoking-related emphysema.
    No preview · Article · Aug 1999 · Modern Pathology
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    ABSTRACT: The survival of microencapsulated islet grafts is limited, even if capsular overgrowth is restricted to a small percentage of the capsules. In search of processes other than overgrowth contributing to graft failure, we have studied the islets in non-overgrown capsules at several time points after allotransplantation in the rat. All recipients of islet allografts became normoglycemic. Grafts were retrieved at 4 and 8 weeks after implantation and at 15.3 +/- 2.3 weeks postimplant, 2 weeks after the mean time period at which graft failure occurred. Overgrowth of capsules was complete within 4 weeks postimplant, and it was usually restricted to <10% of the capsules. During the first 4 weeks of implantation, 40% of the initial number of islets was lost. Thereafter, we observed a decrease in function rather than in numbers of islets, as illustrated by a decline in the ex vivo glucose-induced insulin response. At 4 and 8 weeks postimplant, beta-cell replication was 10-fold higher in encapsulated islets than in islets in the normal pancreas, but these high replication rates were insufficient to prevent a progressive increase in the percentage of nonviable tissue in the islets. Necrosis and not apoptosis proved to be the major cause of cell death in the islets. The necrosis mainly occurred in the center of the islets, which indicates insufficient nutrition as a major causative factor. Our study demonstrates that not only capsular overgrowth but also an imbalance between beta-cell birth and beta-cell death contributes to the failure of encapsulated islet grafts. Our observations indicate that we should focus on finding or creating a transplantation site that, more than the unmodified peritoneal cavity, permits for close contact between the blood and the encapsulated islet tissue.
    Full-text · Article · Jul 1999 · Diabetes
  • J.F.M. Van Straaten · D S Postma · W Coers · JA Noordhoek · H F Kauffman · W Timens
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    ABSTRACT: To provide information concerning a possible biologic role of nitric oxide (NO) in smoking-related emphysema, we performed immunohistochemical studies in lung tissue from control subjects and patients with mild and severe emphysema. We studied the presence of inducible and endothelial NO synthases (iNOS and eNOS, respectively) and determined nicotinamide diphosphate (NADPH) diaphorase activity. Patients with severe emphysema showed lower percentages of iNOS- and eNOS-positive alveolar macrophages in situ than did patients with mild emphysema. In patients with both iNOS and eNOS immunoreactivity in macrophages, the majority of the macrophages expressed either iNOS or eNOS, whereas only a minority of the macrophages showed iNOS and eNOS immunoreactivity simultaneously. Immunoreactivity for eNOS in endothelial and/or bronchiolar epithelial cells and NADPH diaphorase activity in macrophages and in endothelial, epithelial, and smooth muscle cells were similar in the three studied groups. The expression of eNOS in macrophages suggests that eNOS plays an additional role, besides iNOS, in the NO housekeeping in inflammatory processes in pulmonary tissue. We suggest that NO might have a protective role in maintenance of structural integrity of pulmonary tissue after smoke-induced damage.
    No preview · Article · Aug 1998 · Modern Pathology
  • W. Timens · W. Coers · J.F.M. Van Straaten · D.S. Postma
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    ABSTRACT: Emphysema is a progressive lung disease in which the alveoli are destroyed, ultimately resulting in a high morbidity and mortality. One of the main causes of emphysema is smoking, though emphysema occurs in only 10-20% of the smoking population. The destruction is thought to take place via an imbalance in proteolytic enzymes (released from neutrophils and macrophages) and the antiproteases in the lung, together with an imbalance in oxidants (from cells and inhaled smoke) and anti-oxidants. As neither of these hypotheses explain why not all smokers develop emphysema, this review will discuss whether other, additional mechanisms can be important for the development of emphysema. Emphysema also occurs by mechanisms other than increased destruction of lung tissue; improper repair mechanisms may be important as well. One of the most important cells in tissue repair is the fibroblast, which synthesizes most constituents of the extracellular matrix (ECM). Apart from the main structural matrix proteins, such as collagens, fibronectin, elastin and laminin, there are other minor constituents, the proteoglycans, which have important structural and functional properties. Proteoglycans can function as cell-surface receptors, transmitting signals from the outside to the inside, and have a regulatory role in inflammation and tissue repair, exerted by the capacity to bind various cytokines. The cytokine binding capacities play a role in the immediate response to tissue destruction, as well as binding surplus cytokines as a method of downregulation of inflammatory reactions. It can be hypothesized that in pulmonary emphysema the production of matrix proteins is qualitatively, or quantitatively, hampered by an intrinsic dysfunction of pulmonary fibroblasts. This can affect the binding, release or regulation of matrix-bound cytokines, becoming obvious after chronic exogenous damage (smoking). Further research into the pathogenesis of pulmonary emphysema should aim not only at destructive events, but also at the role and regulation of tissue repair.
    No preview · Article · Jan 1997 · European Respiratory Review

Publication Stats

267 Citations
21.88 Total Impact Points


  • 1999-2003
    • University of Groningen
      • • Department of Pathology and Laboratory Medicine
      • • Department of Allergology
      Groningen, Groningen, Netherlands