Secretion of plasminogen activator by cerebral astrocytes and its modulation

Toshniwal, Pradip K.; Tiku, M. L.; Tiku, Katherine; Skosey, John L.

doi:10.1016/0022-510x(87)90165-1

Cited by 16 publications

(8 citation statements)

References 28 publications

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“…Astrocytes synthesize and secrete plasminogen activator. 17,46 The secretion of plasminogen activator is stimulated by basic fibroblastic growth factor (bFGF). 38 Meningeal cells contain bFGF 12 and possibly stimulate the secretion of plasminogen activator by astrocytes thus enhancing the formation of the astro-meningeal gap observed in the cocultures.…”

Section: Discussionmentioning

confidence: 99%

Cocultures of meningeal and astrocytic cells—A model for the formation of the glial‐limiting membrane

Struckhoff

1995

Intl J of Devlp Neuroscience

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The glial-limiting membrane at the border of the central nervous system (CNS) consists of glial endfeet covered by a basal lamina. The formation of the glia limitans seems to be controlled by adjacent meninges but only little is known about this interaction. In the present study astrocytes and meningeal cells were investigated in vitro to see if cocultures of these cells can serve as a suitable model for the differentiation of the glial-limiting membrane and can be used to define the conditions under which the glial-limiting membrane develops. The following observations were made in cocultures of meningeal and astrocytic cells of two-day-old rats: (i) epithelioid astrocytes were transformed into stellate cells; (ii) single colonies of proliferating epithelioid astrocytes were generated; (iii) the area around these colonies becomes devoid of meningeal cells, which seem to form a circular border around the astroglial islands; (iv) from the glial colonies long thin glial processes grow towards the surrounding meningeal cells, terminating at the site of contact; (v) in the contact zone between meningeal cells and astrocytes irregular shaped deposits of electron dense material resembling a basal lamina were seen. These observations indicate that indeed a structure resembling a glial-limiting membrane develops in cocultures of meningeal and astrocytic cells. Its formation depends on the balance of growth promoting effects of meningeal cells on astrocytes and growth inhibiting effects of astrocytes on meningeal cells. Both activities can be enriched from conditioned media of pure astrocytic or meningeal cell culture. The proposed model of meningo-astrocytic cocultures may be a helpful instrument for further investigations on the formation of the glia limitans.

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Section: Discussionmentioning

confidence: 99%

Cocultures of meningeal and astrocytic cells—A model for the formation of the glial‐limiting membrane

Struckhoff

1995

Intl J of Devlp Neuroscience

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“…The most abundant CNS glial cell, the astrocyte, plays a major role in CNS development (Small et al, 1987;Watanabe and Raff, 1988) as well as in the remodelling of mature brain (Garcia-Segura et al, 1986;Hatton et al, 1984;Montagnese et al, 1988). Three components of the PA system have been identified in astrocytes in culture: t-PA, u-PA, and PAI-1 (Kalderon et al, 1990;Toshniwal et al, 1987). Preliminary evidence suggests that PAS regulate astrocytic proliferation (Moonen et al, 1985).…”

Section: Introductionmentioning

confidence: 99%

Regulation of plasminogen activators and type‐1 plasminogen activator inhibitor by cyclic AMP and phorbol ester in rat astrocytes

Tranque

Robbins

Naftolin³

et al. 1992

Glia

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Two plasminogen activators (PAs): tissue-type plasminogen activator (t-PA) and urokinase-type plasminogen activator (u-PA), as well as the type-1 plasminogen activator inhibitor (PAI-1) are synthesized and secreted by rat astrocytes. Preliminary studies suggest that PA activity plays a role in astrocyte development and differentiation. We have examined the regulation of the PA system by the cAMP-dependent protein kinase (PKA) and protein kinase C (PKC) in purified rat astrocyte cultures. PKA activity was increased by exposing cultured astrocytes to forskolin or dibutyryl cyclic AMP, whereas PKC activity was stimulated with phorbol-12-myristate 13-acetate (PMA). Activation of both second-messenger pathways produced a time- and dose-dependent increase in the total PA activity. However, based on SDS-PAGE/zymography we found that forskolin increased t-PA activity and reduced u-PA activity, whereas PMA treatment caused a significant increase in u-PA activity without altering t-PA activity. Reverse zymography analysis revealed that astrocyte PAI-1 activity is decreased by forskolin and increased by PMA. Together, these results demonstrate that the components of the PA system in rat astrocytes are independently and reciprocally regulated by PKA and PKC. Our findings raise the possibility that the plasminogen activator system could be involved in some of the actions of growth factors and/or neuromodulators that modulate PKC or PKA in astrocytes.

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“…to be associated with migrating neural crest cells and cerebellar granule cells (Krystosek and Seeds, 1981a ;Soreq and Miskin, 1981 ;Moonen et al, 1982;Valinsky and Le Douarin, 1985) and with growth cones of cultured neurons and neuroblastoma cells (Krystosek and Seeds, 1981b ;Soreq et al, 1983 ;Pittman et al, 1989;Leprince et al, 1991) . PAs have also been detected in glial cells in the CNS and PNS, where they have been suggested to play a role during development and regeneration Alvarez-Buylla and Valinsky, 1985;Baron-Van Evercooren et al, 1987;Toshniwal et al, 1987;Kalderon et al, 1990;Sallés et al, 1990;Rogister et al, 1990;Tranque et al, 1992Tranque et al, , 1994 .…”

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confidence: 99%

Components of the Plasminogen Activator System in Astrocytes Are Modulated by Tumor Necrosis Factor‐α and Interleukin‐1β Through Similar Signal Transduction Pathways

Faber-Elman¹,

Miskin

Schwartz³

1995

Journal of Neurochemistry

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Migration of astrocytes is thought to play a role in nerve regeneration and to be mediated, at least in part, by inflammation‐associated cytokines. Plasminogen activators are secreted proteases that function in fibrinolysis and participate in cellular migration and invasion and, in some cases, are modulated by cytokines. Here, we show that two cytokines, tumor necrosis factor‐α and interleukin‐1β, can modulate plasminogen activation in astrocytes, each causing 90% reduction of total plasminogen activator activity. Direct and reverse zymography indicated that this reduction resulted from two simultaneous events, a pronounced decrease in tissue‐type plasminogen activator activity and an induction of plasminogen activator inhibitor‐1. Northern hybridization analysis indicated a 30‐fold increase of the steady‐state level of plasminogen activator inhibitor‐1 mRNA following treatment with each of the two cytokines. Both of the cytokine‐induced effects could be blocked by cycloheximide or actinomycin D. When signal transduction pathways were blocked, the results indicated the involvement of reduction in cyclic AMP levels, protein kinase activity, and arachidonic metabolites of the lipoxygenase pathway. The results thus show that the two cytokines reduce the ability of astrocytes to conduct fibrinolysis and extracellular proteolysis, and suggest that the effect of these cytokines on members of the plasminogen activation system is through a common signal transduction pathway.

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Secretion of plasminogen activator by cerebral astrocytes and its modulation

Cited by 16 publications

References 28 publications

Cocultures of meningeal and astrocytic cells—A model for the formation of the glial‐limiting membrane

Cocultures of meningeal and astrocytic cells—A model for the formation of the glial‐limiting membrane

Regulation of plasminogen activators and type‐1 plasminogen activator inhibitor by cyclic AMP and phorbol ester in rat astrocytes

Components of the Plasminogen Activator System in Astrocytes Are Modulated by Tumor Necrosis Factor‐α and Interleukin‐1β Through Similar Signal Transduction Pathways

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