Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:1.14.11.2 (prolyl hydroxylase)
 1,814 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To clarify the link between cytotoxic damage to the hepatocyte and the development of fibrosis, we immunoenzymatically measured serum prolyl hydroxylase (hPH), type IV collagen (CL-IV) and circulating intercellular adhesion molecule-1 (clCAM-1). The population studied was comprised of 122 patients with liver disease (acute hepatitis; mild chronic liver disease; cirrhosis; hepatocellular carcinoma) and 33 patients with extrahepatic diseases. Similar patterns were observed for hPH, CL-IV, and clCAM-1, that were higher in patients with acute hepatitis and hepatocellular carcinoma than in those with mild chronic liver disease (Bonferroni's test for pairwise comparisons, p < 0.01). Liver function tests and markers of fibrosis showed a strict correlation, which disappeared when the linear effect of clCAM-1 was removed. The ability to predict serum hPH and CL-IV from clCAM-1 might suggest the existence of a causal relationship between fibrosis and targeting of cytotoxic damage.
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PMID:Prediction of serum markers of fibrosis by levels of circulating intercellular adhesion molecule-1 in acute and chronic liver disease. 786 19

Lung fibroblast plays a pivotal role in lung repair and remodeling, and also contributes to lung inflammation. The present study investigated differential protein profiling of normal human lung fibroblasts stimulated with tumor necrosis factor (TNF)-alpha. Total proteins from lung fibroblasts were separated by 2-DE, and differentially expressed proteins were identified by MALDI-TOF MS. TNF-alpha was found for the first time to alter the expression levels of myxovirus resistance protein A, interferon-stimulated gene 15, plasminogen activator inhibitor-2, lysyl hydroxylase 2 (isoform a), and prolyl 4-hydroxylase (alpha subunit) in human lung fibroblasts. In particular, dendritic cell-derived interferon-gamma-induced protein (DCIP) was upregulated by TNF-alpha in lung fibroblasts and its biological function is at present unknown. We found that TNF-alpha-induced DCIP expression was dependent on the transcription factor interferon regulatory factor-1. DCIP-selective antisense oligodeoxynucleotide inhibited the expression of TNF-alpha-responsive gene targets including vascular cell adhesion molecule-1, intercellular adhesion molecule-1, IL-6, IL-8, IP-10, and thymic stromal lymphopoietin. In a lipopolysaccharide-induced acute lung injury mouse model, DCIP mRNA level was elevated together with that of TNF-alpha. We have demonstrated for the first time that DCIP is upregulated by TNF-alpha and also mediates TNF-alpha stimulation of human lung fibroblasts. Further studies on the role of DCIP in airway inflammation and remodeling are warranted.
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PMID:Dendritic cell-derived interferon-gamma-induced protein mediates tumor necrosis factor-alpha stimulation of human lung fibroblasts. 1854 54