The platelet‐derived growth factor isomers, PDGF‐AA, PDGF‐AB and PDGF‐BB, induce contraction of vascular smooth muscle cells by different intracellular mechanisms

Sachinidis, Agapios; Locher, Rudolf; Hoppe, Jürgen; Vetter, W

doi:10.1016/0014-5793(90)81447-v

Cited by 66 publications

(43 citation statements)

References 15 publications

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“…Recombinant PDGF has caused potent concentration-dependent contraction on rat aortic strips within 2 minutes after the application; however, it did not constrict rat intracerebral arterioles (perforating arteries) in vitro. [42][43][44] In the present study it was first demonstrated that exogenous PDGF-BB caused delayed and prolonged but not rapid vasoconstriction on cerebral arteries in rabbits. The peak of the vasoconstriction (24 hours) was earlier than that of vasospasm in rabbits (48 hours) caused by blood injection 17 ; however, it can be speculated that a time delay of approximately 1 day is due to a phase for the active production of PDGF-BB after thrombin activation in the subarachnoid space or within the vascular wall.…”

Section: Discussionsupporting

confidence: 48%

Broad-Spectrum and Selective Serine Protease Inhibitors Prevent Expression of Platelet-Derived Growth Factor–BB and Cerebral Vasospasm After Subarachnoid Hemorrhage

Zhang

Nagata

Kikuchi

et al. 2001

Stroke

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Background and Purpose-Plasma serine protease cascade, including the complement system and thrombin, is activated in the subarachnoid space during the acute phase after subarachnoid hemorrhage (SAH). To examine the effect of protease cascade-based inflammation and subsequent vascular repair in the development of cerebral vasospasm, we examined the effect of 2 synthetic serine protease inhibitors-FUT-175, an inhibitor of thrombin and the complement system, and argatroban, a selective inhibitor of thrombin-on the development of cerebral vasospasm in a rabbit SAH model. Methods-One hundred Japanese White male rabbits were used in the study. The SAH was simulated by a single injection of autologous arterial blood into the cisterna magna. To evaluate the development of cerebral vasospasm, the caliber of the basilar artery was measured on x-ray film before and at 2 days after SAH. Nine groups of rabbits (nϭ6 each) were treated with continuous intravenous injection of FUT-175 (2.5, 5, 10, or 20 mg/d), argatroban (1.25, 2.5, or 5 mg/d), or the same amount of saline (vehicle) for 48 hours, starting 40 minutes after SAH. Two days after SAH, the expression of homodimer of platelet-derived growth factor-BB (PDGF-BB) in the basilar artery was examined with immunohistochemical techniques. In 20 normal rabbits, 5 g of recombinant PDGF-BB or vehicle was injected into the cisterna magna, and the basilar arteries were examined on angiograms for 48 hours. Results-Significant differences were observed in the caliber of the basilar arteries between the vehicle group and the groups with the 3 larger doses of FUT-175 (vehicle, 52Ϯ5.0%; 5 mg, 79Ϯ5.7%; 10 mg, 80Ϯ2.5%; 20 mg, 80Ϯ3.7%) and between the vehicle group and the groups with the 2 larger doses of argatroban (vehicle, 52Ϯ6.4%; 2.5 mg, 81Ϯ9.0%; 5 mg, 85Ϯ4.1%) (PϽ0.05). In the histological examination, administration of effective doses of FUT-175 or argatroban suppressed the expression of PDGF-BB in the endothelial and medial smooth muscle cell layers. Exogenous PDGF-BB caused delayed and prolonged vasoconstriction on normal basilar arteries. Conclusions-Activation

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Section: Discussionsupporting

confidence: 48%

Broad-Spectrum and Selective Serine Protease Inhibitors Prevent Expression of Platelet-Derived Growth Factor–BB and Cerebral Vasospasm After Subarachnoid Hemorrhage

Zhang

Nagata

Kikuchi

et al. 2001

Stroke

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“…[17][18][19] To determine whether BST406, a newly synthesized benzylideneacetophenone derivative (Fig. 1A), inhibits PDGF-BB-stimulated VSMC proliferation, we assessed the effect of BST406 on DNA synthesis, cell proliferation, and cell viability.…”

Section: Resultsmentioning

confidence: 99%

“…17,25) The receptor tyrosine kinases for PDGF-BB activate PLCg1, phosphatidyl inositol 3 (PI3)-kinase, and mitogen activated protein (MAP) kinase, and their signaling pathways are important in early intracellular mitogenic signal transduction for cell growth and survival.…”

Section: Discussionmentioning

confidence: 99%

Inhibitory Effects of BST406, a Newly Synthesized Benzylideneacetophenone Derivative, on Abnormal Vascular Smooth Muscle Cell Proliferation

Kim

Han

Kim

et al. 2010

Biological & Pharmaceutical Bulletin

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“…Fluorescence was corrected for cellular autofluorescence and was calibrated. 38,57,58 Gel electrophoresis and immunostaining SDS-polyacrylamide gel electrophoresis was performed essentially as described 59 using 8% acrylamide gels for RSK, PKC-isoforms and p70 S6 -kinase, 12% for MAP-kinase (30/0.3 (w/w) acrylamide/ bisacrylamide). Mini gels of 0.75 mm thickness were used (BioRad Mini Protean).…”

Section: Measurement Of [Ca 2+ ] Imentioning

confidence: 99%

ATP and adenosine prevent via different pathways the activation of caspases in apoptotic AKR-2B fibroblasts

Hoppe

Sachinidis

1999

Cell Death Differ

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Confluent AKR-2B fibroblasts rapidly disintegrate after serum deprivation. 27 ATP or adenosine added immediately after serum removal afforded substantial protection against cell death even for a long period of 24 h. ED 50 values were 14 and 110 mM for ATP and adenosine, respectively. In the presence of 5 mg/ml cycloheximide the protective effect of both substances was suppressed, indicating that protein synthesis is required. The protective effect of ATP was highly specific since among numerous tested derivatives only ATP-[g-S] exhibited a substantial protective effect.The ability of ATP and adenosine to modulate cell division was analyzed. Both substances did not exhibit any mitogenic effect. Adenosine completely blocked PDGF-BB induced cell division, whereas ATP had no effect. Unlike adenosine, ATP strongly stimulated Ca 2+ -release from intracellular stores. On the other hand, adenosine stimulated an increase in the intracellular concentration of cAMP from 0.4 ± 1.5 mM, whereas ATP decreased the content below 0.1 mM. ATP stimulated the phosphorylation of MAP-kinase, RSK and p70 S6 -kinase; adenosine was inactive. After complexation of [Ca 2+ ] i the protective effect of ATP was greatly lost while adenosine was still active. Surprisingly neither ATP nor adenosine caused an activation of PKC-isoforms. After incubation with pertussis toxin, the protection by ATP was reduced indicating an involvement of G i -proteins in the signal transduction induced by ATP. Our results indicate that ATP as well as adenosine are potent inhibitors of cell death caused by serum deprivation and that this protective effect apparently occurs via distinct pathways. However, both pathways must converge at the point of caspase activation, since the stimulation of DEVDaseand VEIDase-activities, respectively, are suppressed by either ATP or adenosine.

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The platelet‐derived growth factor isomers, PDGF‐AA, PDGF‐AB and PDGF‐BB, induce contraction of vascular smooth muscle cells by different intracellular mechanisms

Cited by 66 publications

References 15 publications

Broad-Spectrum and Selective Serine Protease Inhibitors Prevent Expression of Platelet-Derived Growth Factor–BB and Cerebral Vasospasm After Subarachnoid Hemorrhage

Broad-Spectrum and Selective Serine Protease Inhibitors Prevent Expression of Platelet-Derived Growth Factor–BB and Cerebral Vasospasm After Subarachnoid Hemorrhage

Inhibitory Effects of BST406, a Newly Synthesized Benzylideneacetophenone Derivative, on Abnormal Vascular Smooth Muscle Cell Proliferation

ATP and adenosine prevent via different pathways the activation of caspases in apoptotic AKR-2B fibroblasts

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