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http://purl.uniprot.org/citations/21849907http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/21849907http://www.w3.org/2000/01/rdf-schema#comment"

Background

Angiotensin-converting enzyme inhibitors (ACEIs) are used to control hypertension and are superior to other antihypertensive agents in protecting the progressive deterioration of autoimmune-related nephritis. An imbalance of T helper 1 (Th1)/Th2 is thought to contribute to the pathogenesis of autoimmune diseases and their related glomerulonephritis. I-309 is a Th2-related chemokine involved in the recruitment of Th2 cells toward Th2-related inflammation. Tumor necrosis factor α (TNF-α) and Th1-related chemokines, interferon-inducible protein 10 (IP-10)/CXCL10 are also involved in autoimmune glomerulonephritis. However, the modulatory effects and the mechanisms of ACEIs on TNF-α and Th1- and Th2-related chemokines in monocytes remain poorly defined.

Objective

We investigated the effects of imidapril and perindopril, 2 ACEIs, on the expression of IP-10, I-309, and TNF-α in human monocytes and also the associated intracellular mechanism.

Results

Imidapril and perindopril significantly downregulated lipopolysaccharide (LPS)-induced TNF-α, I-309, and IP-10 in THP-1 cells and human primary monocytes. All 3 mitogen-activated protein kinase inhibitors suppressed LPS-induced TNF-α and I-309 expression in human primary monocytes. Only extracellular signal-regulated kinases and c-Jun N-terminal kinases (JNK) mitogen-activated protein kinase inhibitors suppressed LPS-induced IP-10 expression. Lipopolysaccharide-induced mitogen-activated protein kinase kinase 4 (MKK4), p-JNK, and c-Jun expression in human primary monocytes was suppressed by imidapril.

Conclusions

These data demonstrate that ACEI is effective in downregulating LPS-induced TNF-α, I-309, and IP-10, which play important roles in the pathogenesis of inflammation. Its suppressive effect on TNF-α, I-309, and IP-10 may, at least in part, involve the down-regulation of LPS-induced MKK4-JNK-c-Jun expression."xsd:string
http://purl.uniprot.org/citations/21849907http://purl.org/dc/terms/identifier"doi:10.2310/jim.0b013e31822ba7fb"xsd:string
http://purl.uniprot.org/citations/21849907http://purl.uniprot.org/core/author"Lin C.H."xsd:string
http://purl.uniprot.org/citations/21849907http://purl.uniprot.org/core/author"Hung C.H."xsd:string
http://purl.uniprot.org/citations/21849907http://purl.uniprot.org/core/author"Huang M.Y."xsd:string
http://purl.uniprot.org/citations/21849907http://purl.uniprot.org/core/author"Kuo C.H."xsd:string
http://purl.uniprot.org/citations/21849907http://purl.uniprot.org/core/author"Yang S.N."xsd:string
http://purl.uniprot.org/citations/21849907http://purl.uniprot.org/core/author"Tsai M.K."xsd:string
http://purl.uniprot.org/citations/21849907http://purl.uniprot.org/core/author"Chen H.N."xsd:string
http://purl.uniprot.org/citations/21849907http://purl.uniprot.org/core/author"Jan R.L."xsd:string
http://purl.uniprot.org/citations/21849907http://purl.uniprot.org/core/date"2011"xsd:gYear
http://purl.uniprot.org/citations/21849907http://purl.uniprot.org/core/name"J Investig Med"xsd:string
http://purl.uniprot.org/citations/21849907http://purl.uniprot.org/core/pages"1141-1146"xsd:string
http://purl.uniprot.org/citations/21849907http://purl.uniprot.org/core/title"Suppressive effects of imidapril on Th1- and Th2-related chemokines in monocytes."xsd:string
http://purl.uniprot.org/citations/21849907http://purl.uniprot.org/core/volume"59"xsd:string
http://purl.uniprot.org/citations/21849907http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/21849907
http://purl.uniprot.org/citations/21849907http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/21849907
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http://purl.uniprot.org/uniprot/#_A0A411D318-mappedCitation-21849907http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/21849907
http://purl.uniprot.org/uniprot/#_A0A1U9X8M9-mappedCitation-21849907http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/21849907
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http://purl.uniprot.org/uniprot/#_C1K3N5-mappedCitation-21849907http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/21849907
http://purl.uniprot.org/uniprot/#_B5BUQ6-mappedCitation-21849907http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/21849907
http://purl.uniprot.org/uniprot/#_A0A977WMN2-mappedCitation-21849907http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/21849907
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