1999
DOI: 10.1016/s8756-3282(99)00008-3
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Involvement of p42/p44 MAP kinase in endothelin-1-induced interleukin-6 synthesis in osteoblast-like cells

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Cited by 20 publications
(22 citation statements)
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“…Three major MAP kinases, p44/p42 MAP kinase, p38 MAP kinase, and SAPK/JNK, are recognized to transduce signals in mammalian cells (27). We earlier reported that ET-1 activates p44/p42 MAP kinase and p38 MAP kinase in osteoblast-like MC3T3-E1 cells and that p38 MAP kinase, but not p44/p42 MAP kinase, plays a role in ET-1-stimulated HSP27 induction (13,14). We have recently demonstrated that ET-1 activates SAPK/JNK in addition to p44/p42 MAP kinase and p38 MAP kinase in MC3T3-E1 cells (15).…”
Section: Discussionmentioning
confidence: 99%
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“…Three major MAP kinases, p44/p42 MAP kinase, p38 MAP kinase, and SAPK/JNK, are recognized to transduce signals in mammalian cells (27). We earlier reported that ET-1 activates p44/p42 MAP kinase and p38 MAP kinase in osteoblast-like MC3T3-E1 cells and that p38 MAP kinase, but not p44/p42 MAP kinase, plays a role in ET-1-stimulated HSP27 induction (13,14). We have recently demonstrated that ET-1 activates SAPK/JNK in addition to p44/p42 MAP kinase and p38 MAP kinase in MC3T3-E1 cells (15).…”
Section: Discussionmentioning
confidence: 99%
“…We have shown that ET-1 stimulates phosphatidylcholine hydrolysis by PLD in osteoblast-like MC3T3-E1 cells (12). In addition, we have reported that ET-1 activates both p44/p42 mitogen-activated protein (MAP) kinase and p38 MAP kinase in these cells, and that p38 MAP kinase, but not p44/p42 MAP kinase, plays a role in ET-1-stimulated HSP27 induction (13,14). Recently, we demonstrated that ET-1 activates stress-activated protein kinase/c-Jun N-terminal kinase (SAPK/JNK), another member of the MAP kinase family (15).…”
Section: Introductionmentioning
confidence: 99%
“…In various cell types, the signaling pathways including p42/44 extracellular signal-regulated kinase (ERK), p38 mitogen-activated protein kinase (MAPK), cyclic AMP/protein kinase A (PKA) and protein kinase C (PKC) are demonstrated to be involved for IL-6 production [17][18][19][20][21]. In addition, up-regulation of IL-6 is controlled by the activity of several transcription factors with known consensus sequences in the IL-6 promoter region, including AP-1, C/EBP-b and NF-kB [22,23].…”
Section: Introductionmentioning
confidence: 99%
“…Stimulation of tyrosine phosphorylation also was shown, (23) indicating that MAPK pathway(s) might be activated on stimulation with ET‐1. Indeed, ET‐1‐induced production of interleukin (IL)‐6 (24) was shown to be dependent on activation of p42/44 MAPK, (25) whereas p38 MAPK is involved in ET‐1‐induced expression of hsp27 mRNA (26) . In addition, ET‐1 is able to stimulate phosphatidylcholine breakdown by PLC‐independent activation of phospholipase D (PLD), (27) which is involved in ET‐1‐stimulated release of arachidonic acid (28) .…”
Section: Introductionmentioning
confidence: 99%