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Involvement of MMPs in delayed neuronal death after global ischemia

100%
Zalewska T., Ziemka-Nalecz M., Sarnowska A., Domanska-Janik K.
Acta Neurobiologiae Experimentalis
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2002
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vol. 62
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issue 2
53-61
EN
Spatial and temporal relations between metalloproteinase (MMP-2 and MMP-9) activation and laminin degradation in gerbil hippocampus after transient cerebral ischemia has been studied. Activity of MMPs was determined by gelatin zymography in homogenates from dorsal (DP, an equivalent of CA1 sector) and abdominal (AbP, containing CA2-4 and gyrus dentatus) parts of hippocampus. A significant activation of both investigated metalloproteinases was found at 72 h of recovery. Whereas MMP-2 up-regulation did not show any spatial preferences, the increase of MMP-9 activity was observed exclusively in DP. Activation of MMP-9 at this time point correlated spatially with degradation of laminin - protein of extracellular matrix. These results show that MMP pathway may function as a component of delayed neuronal death cascade in the apoptogenic CA1 sector after transient global ischemia.t
2

The biological activity of synthetic analogs of the laminin active sequences: YIGSR, RGD, SIKVAV

100%
Hill-Bator A., Opolski A.
Postępy Higieny i Medycyny Doświadczalnej
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2002
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vol. 56
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issue 5
579-588
EN
The invasion of malignant cells through the basement membrane is a critical step in local infiltration and metastasis. Adhesion and invasion of malignant cells may be modulated by their receptor mediated binding to the basement membrane glycoprotein laminin. Laminin consists of the sequences with anticancer and antimetastatic activity. Its peptide fragment YIGSR is known to inhibit experimental metastases of several tumors. This sequence and a tripeptide RGD of laminin inhibits both angiogenesis and tumor growth. In contrary, the sequence SIKVAV initiates angiogenesis and tumor progression. Moreover, laminin plays also other functions in human organism. One of them is influence on platelet aggregation and trombegenesis.
3
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Laminin promotes oligogliogenesis and increases MMPs activity in human neural stem cells of HUCB-NSC line

88%
Sypecka J., Dragun-Szymczak P., Zalewska T., Domanska-Janik K.
Acta Neurobiologiae Experimentalis
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2009
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vol. 69
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issue 1
37-45
EN
Oligodendrocytes, the cells responsible for myelin formation and maintenance in CNS, are depleted in many acute and chronic conditions. The stem/progenitor cells stimulation or transplantation might be seriously considered as a long hoped for therapeutic perspective. Better understanding of the mechanism(s) regulating the activation of the cell lineage from the endogenous progenitor reservoir might be helpful. Therefore an efficient source of donor cells for transplantation in humans is being craved for. In this study we show that the application of extracellular matrix component-laminin promotes oligogliogenesis from neural stem-like cells of human cord blood cells (HUCB-NSC). Although oligodendrocytes constitute a minor subpopulation of spontaneously differentiated HUCB-NSC, the manipulation of active compounds regulating the process of cell commitment results in a several fold increase in their number. Thus cells of the HUCB-NSC line could be considered as a potential source of glial cells, fulfilling the suitable candidate criteria for oligodendrocyte replacement therapy.
4

Deconstructing B cell tolerance to basement membranes

88%
Foster M. H., Zhang Y., Clark A. G.
Archivum Immunologiae et Therapiae Experimentalis
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2006
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vol. 54
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issue 4
227-237
EN
Basement membrane antigens are frequent targets of autoantibody attack in systemic and organ-restricted autoimmunity. These specialized and highly organized matrices are composed of multiple components with restricted tissue distributions and limited epitope exposure. To the dissect mechanisms controlling humoral autoimmunity to nephritogenic basement membrane antigens, we developed autoantibody transgenic models. In mice bearing the LamH Ig transgene encoding B cell receptors specific for laminin, autoreactive B cells are readily generated but actively regulated in vivo. In this model, anti-laminin B cells are immunologically censored by mechanisms that include central deletion, k light-chain editing, and anergy. Tolerance is maintained when the transgene is established in MRL and BXSB genetic backgrounds with inherited autoimmune susceptibility, and despite provocation with potent environmental stimulants. Collectively, these studies indicate that the pathogenic anti-laminin reactivity characteristic of systemic lupus is tightly regulated. A novel anti-collagen transgenic model is used to assess the tolerogenesis of a structurally distinct pathogenic basement membrane epitope and to determine if the reactivity to putative cryptic epitopes targeted in organ-restricted disease is regulated. These studies should provide insight into the molecular mechanisms controlling basement membrane autoreactivity and ultimately facilitate the development of novel strategies to inactivate autoreactive cells and treat autoimmune disease.
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