ArticleProceedings of the National Academy of Sciences of the United States of America2005
Chlamydia pneumoniae infection promotes a proliferative phenotype in the vasculature through Egr-1 activation in vitro and in vivo.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 44 citations in OpenAlex.
- The association of common infectious exposures with cognitive performance in community-dwelling older adults.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- Hijacking and Use of Host Kinases by Chlamydiae.Pathogens (Basel, Switzerland) · 2020Review
- Bioresponsive Nanoparticles Targeted to Infectious Microenvironments for Sepsis Management.Advanced materials (Deerfield Beach, Fla.) · 2018Article
- The Host Cell Transcription Factor EGR1 Is Induced by Bacteria through the EGFR-ERK1/2 Pathway.Frontiers in cellular and infection microbiology · 2017Article
- Construction of a highly flexible and comprehensive gene collection representing the ORFeome of the human pathogen Chlamydia pneumoniae.BMC genomics · 2012Article
- Lysophosphatidic acid induces early growth response-1 (Egr-1) protein expression via protein kinase Cδ-regulated extracellular signal-regulated kinase (ERK) and c-Jun N-terminal kinase (JNK) activation in vascular smooth muscle cells.The Journal of biological chemistry · 2012Article
- Impact of a low-oxygen environment on the efficacy of antimicrobials against intracellular Chlamydia trachomatis.Antimicrobial agents and chemotherapy · 2011Article
- Hypoxia abrogates antichlamydial properties of IFN-γ in human fallopian tube cells in vitro and ex vivo.Proceedings of the National Academy of Sciences of the United States of America · 2010Article
- Monocyte 15-lipoxygenase gene expression requires ERK1/2 MAPK activity.Journal of immunology (Baltimore, Md. : 1950) · 2010Article
- Chlamydia pneumoniae hides inside apoptotic neutrophils to silently infect and propagate in macrophages.PloS one · 2009Article
- Pitavastatin suppresses mitogen activated protein kinase-mediated Erg-1 induction in human vascular smooth muscle cells.European journal of pharmacology · 2009Article
- Chlamydia pneumoniae aggravates vein graft intimal hyperplasia in a rat model.BMC microbiology · 2007Article
- Host cell responses to Chlamydia pneumoniae in gamma interferon-induced persistence overlap those of productive infection and are linked to genes involved in apoptosis, cell cycle, and metabolism.Infection and immunity · 2007Article
- Mycoplasma fermentans and TNF-beta interact to amplify immune-modulating cytokines in human lung fibroblasts.American journal of physiology. Lung cellular and molecular physiology · 2006Article
- Chlamydia trachomatis infection induces cleavage of the mitotic cyclin B1.Infection and immunity · 2006Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Atherosclerosis is characterized by inflammation and proliferation of vascular cells. The intracellular bacterium Chlamydia (Chlamydophila) pneumoniae uses blood monocytes [peripheral blood mononuclear cells (PBMCs)] for dissemination, has been found to persist in atherosclerotic lesions, and has been implicated in atherogenesis by small GTPase activation and T lymphocyte recruitment. Infection of human coronary artery smooth muscle cells with C. pneumoniae significantly induced mRNA and protein for the angiogenic transcription factor Egr-1, resulting in enhanced coronary artery smooth muscle cell proliferation, which was reduced by transfection with small interfering RNA duplexes targeted at Egr-1 mRNA. These effects required viable chlamydiae and depended on p44/42 mitogen-activated protein kinase activity but not on the p38 mitogen-activated protein kinase pathway. Postinfectious Egr-1 mRNA up-regulation in arterial vessels was confirmed ex vivo in a rat aortic ring model of focal vascular chlamydial infection. An in vivo model based on the injection of C. pneumoniae-infected PBMCs into mice confirmed Egr-1 mRNA up-regulation within 24 h of endovascular infection. Arterial injury from repeated direct chlamydial infections and cell-to-cell contact with C. pneumoniae-infected PBMCs might represent a chronic focus of proliferative activity linked to the media proliferation seen in advanced atherosclerosis. Overall, chlamydial infection induces a proliferative phenotype in vascular cells via transcription factor Egr-1 activation in vitro, ex vivo, and in vivo.
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