1992
DOI: 10.1016/0006-291x(92)92375-8
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Up-regulation of hepatocyte growth factor gene expression by interleukin-1 in human skin fibroblasts

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Cited by 157 publications
(80 citation statements)
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References 29 publications
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“…reactive protein is a non-specific, commonly used marker of the acute inflammatory response; inflammatory cells release cytokines that stimulate hepatocytes to release CRP and inflammatory cytokine reportedly stimulated HGF production in cultured cells. 13 In the present study, peak serum HGF levels in patients with AMI apparently correlated well with peak serum CRP levels, whereas there was only a weak relation between peak HGF levels and peak CK activity. It is possible that the serum CRP level reflects the process of infarct healing rather than the extent of myocardial necrosis.…”
Section: Discussionsupporting
confidence: 46%
“…reactive protein is a non-specific, commonly used marker of the acute inflammatory response; inflammatory cells release cytokines that stimulate hepatocytes to release CRP and inflammatory cytokine reportedly stimulated HGF production in cultured cells. 13 In the present study, peak serum HGF levels in patients with AMI apparently correlated well with peak serum CRP levels, whereas there was only a weak relation between peak HGF levels and peak CK activity. It is possible that the serum CRP level reflects the process of infarct healing rather than the extent of myocardial necrosis.…”
Section: Discussionsupporting
confidence: 46%
“…Given that ATL is a malignancy of activated mature T cells, the leukemic cells secrete a variety of cytokines, including tumor necrosis factor-a and interleukin-1b (Wano et al, 1987;Yamada et al, 1996). Both of these cytokines are potent inducers of HGF expression in fibroblasts (Matsumoto et al, 1992;Tamura et al, 1993), suggesting that ATL cells may indirectly increase the plasma HGF level through secretion of these cytokines and consequent activation of fibroblasts.…”
Section: Discussionmentioning
confidence: 99%
“…34 We found that HGF on day 7 was higher in the remodeling group than in the nonremodeling group, but did not differ between the 2 groups on admission and on days 14 and 21. The differences might reflect HGF interaction in the wound-healing process associated with inflammation after AMI, because production of HGF is stimulated by inflammatory cytokines, such as interleukin-1 and tumor necrosis factor-, 35,36 and it exerts a cytoprotective effect against ischemic injury. 37,38 Further, HGF correlates with C-reactive protein concentration in patients with AMI.…”
Section: Ventricular Remodeling and Hgf In Amimentioning
confidence: 99%