Evidence that interleukin‐1 induction of synovial cell plasminogen activator is mediated via prostaglandin E<sub>2</sub> and cAMP

Mochan, Eugene; Uhl, Joanne; Newton, Robert

doi:10.1002/art.1780290904

Cited by 66 publications

(38 citation statements)

References 24 publications

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“…Specifically, IL-1p stimulates lymphocytes to release other cytokines (Lowenthal et al, 1986) and causes fibroblasts and synovial cells to produce prostaglandin E2 (Antoni et al, 1986;Mochan et al, 1986;O'Byrne et al, 1990b). In the present study twofold evidence was obtained that IL-1P enhanced capsaicin-induced hyperaemia in the rat hindpaw via secondary mediators released from immunocompetent or other cells.…”

Section: Discussionmentioning

confidence: 99%

Interleukin‐1β enhances capsaicin‐induced neurogenic vasodilatation in the rat skin

Herbert

Holzer

1994

British J Pharmacology

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This study examined the effect of interleukin‐1β (IL‐1β) on the capsaicin‐induced increase in cutaneous blood flow of anaesthetized rats as measured by laser Doppler flowmetry. The substances were administered by intraplantar subcutaneous injection of 10 μl‐volumes, saline being injected into one hindpaw and IL‐1β into the other. IL‐1β (0.5–500 pg) was without effect on blood flow on its own but dose‐dependently enhanced the hyperaemic response to intraplantar capsaicin (0.3 μg) up to 180% (P < 0.05) of the response seen in saline‐treated paws. Il‐1β‐(163–171), a fragment devoid of proinflammatory activity, failed to enhance capsaicin‐induced hyperaemia when given at a dose of 50 pg. Indomethacin (10 mg kg−1, i.p.) did not alter the capsaicin‐induced vasodilatation but prevented IL‐1β (50 pg) from augmenting the hyperaemic response to capsaicin. The hyperaemia evoked by intraplantar calcitonin gene‐related peptide (0.038–3.8 ng) was not altered by IL‐1β (50 pg). These data indicate that IL‐1β enhances the cutaneous hyperaemic response to afferent nerve stimulation with capsaicin in a prostaglandin‐dependent manner. This proinflammatory action of the cytokine appears to arise from sensitization of afferent nerve endings.

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Section: Discussionmentioning

confidence: 99%

Interleukin‐1β enhances capsaicin‐induced neurogenic vasodilatation in the rat skin

Herbert

Holzer

1994

British J Pharmacology

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“…This has also been observed with chondrocytes (Hulkower et al, 1991 a). However, a recent study by Munoz et al (1990) describes both the translocation of PKC and phosphorylation of its 80-kDa protein substrate in response to IL-1 treatment in the T helper cell line DIO.A. A possible resolution of these contradictions would be the involvement, in some cclls, of PKC activity which eludes detection by the translocation assay.…”

Section: Discussionmentioning

confidence: 99%

“…As this occurred in the presence of indomethacin, a secondary response to the generation of PGEz presumably does not explain their data. However, indomethacin does block IL-I-induced production of plasminogen activator by synovial fibroblasts (Mochan et al, 1986). This effect is overcome by the dibutyryl derivative of CAMP or PGE2, suggesting that if IL-1 does directly elevate the intracellular concentration of CAMP, the amount produced is insufficient for plasminogen activator induction.…”

mentioning

confidence: 99%

Synovial protein kinase C and its apparent insensitivity to interleukin‐1

Hulkower

Sagi‐Eisenberg

Traub

et al. 1992

European Journal of Biochemistry

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Lapine synovial fibroblasts produce prostaglandin E2 (PGE2) and neutral metalloproteinases in response to phorbol 12‐myristate 13‐acetate (PMA), human recombinant interleukin‐1 (hrIL‐1) and, in an autocrine fashion, in response to partially purified preparations of their own cytokines known as cell‐activating factors (CAF). Here we have examined the possible role of protein kinase C (PKC) in these responses. Whereas the 80‐kDa substrate for PKC could not be detected in synovial fibroblasts, these cells contained a 35‐kDa protein which fulfilled the criteria for qualifying as a specific substrate of PKC. Translocation assays based upon phosphorylation of the 35‐kDa protein and Western blotting techniques allowed the movement of PKC from the cytosolic to the particulate fraction in response to PMA and CAF to be detected but not in response to 4α‐PMA or hrIL‐1. Inhibitors of PKC suppressed synovial activation by PMA, partially blocked activation by CAF but had no effect on activation by hrIL‐1. There thus appear to be PKC‐dependent and PKC‐independent routes to synovial cell activation. Our data suggest that IL‐1 uses the latter, while CAF contains cytokines which utilize both routes.

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“…In addition to lymphocyte proliferation activity, IL-I has been reported to promote the production of collagenase [2-41, other matrix metalloproteinases [5] and plasminogen activator [6,7] from synovial fibroblasts or chondrocytes.…”

Section: Introductionmentioning

confidence: 99%

Human recombinant interleukin‐1α‐mediated stimulation of procollagenase production and suppression of biosynthesis of tissue inhibitor of metalloproteinases in rabbit uterine cervical fibroblasts

Ito¹,

Goshowaki²,

Sato³

et al. 1988

FEBS Letters

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Influence of human recombinant interleukin‐1 (hrIL‐1) on collagen metabolism was investigated with rabbit uterine cervical fibroblasts. Enzyme‐linked immunosorbent assays for collagenase and tissue inhibitor of metalloproteinases (TIMP) indicated that hrIL‐1 participates in both stimulation of procollagenase production and suppression of TIMP synthesis by uterine cervical cells. IL‐1 did not modulate collagen synthesis. In addition, the sensitivity to IL‐1 of uterine cervix from ovariectomized rabbits was augmented by estradiol‐17β treatment. Thus it is proposed that IL‐1 accelerates collagenolysis in the cervical tissue and its effect on uterine cervix is hormonally regulated.

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Evidence that interleukin‐1 induction of synovial cell plasminogen activator is mediated via prostaglandin E₂ and cAMP

Cited by 66 publications

References 24 publications

Interleukin‐1β enhances capsaicin‐induced neurogenic vasodilatation in the rat skin

Interleukin‐1β enhances capsaicin‐induced neurogenic vasodilatation in the rat skin

Synovial protein kinase C and its apparent insensitivity to interleukin‐1

Human recombinant interleukin‐1α‐mediated stimulation of procollagenase production and suppression of biosynthesis of tissue inhibitor of metalloproteinases in rabbit uterine cervical fibroblasts

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Evidence that interleukin‐1 induction of synovial cell plasminogen activator is mediated via prostaglandin E2 and cAMP

Cited by 66 publications

References 24 publications

Interleukin‐1β enhances capsaicin‐induced neurogenic vasodilatation in the rat skin

Interleukin‐1β enhances capsaicin‐induced neurogenic vasodilatation in the rat skin

Synovial protein kinase C and its apparent insensitivity to interleukin‐1

Human recombinant interleukin‐1α‐mediated stimulation of procollagenase production and suppression of biosynthesis of tissue inhibitor of metalloproteinases in rabbit uterine cervical fibroblasts

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Evidence that interleukin‐1 induction of synovial cell plasminogen activator is mediated via prostaglandin E₂ and cAMP