ArticleThe Journal of biological chemistry2012
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.
Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 42 citations in OpenAlex.
- Age-dependent effects of chronic traumatic and social isolation stress on mice social behavior.Neurobiology of stress · 2026Article
- Decreased neurotensin induces ovulatory dysfunction via the NTSR1/ERK/EGR1 axis in polycystic ovary syndrome.Frontiers of medicine · 2025Article
- Loss of DJ-1 function contributes to Parkinson's disease pathogenesis in mice via RACK1-mediated PKC activation and MAO-B upregulation.Acta pharmacologica Sinica · 2023Article
- LDL-Dependent Regulation of TNFα/PGEInflammation · 2023Article
- Verproside, the Most Active Ingredient in YPL-001 Isolated fromInternational journal of molecular sciences · 2023Article
- Lysophosphatidic Acid Upregulates Recepteur D'origine Nantais Expression and Cell Invasion via Egr-1, AP-1, and NF-κB Signaling in Bladder Carcinoma Cells.International journal of molecular sciences · 2020Article
- The Emerging Role of Rab5 in Membrane Receptor Trafficking and Signaling Pathways.Biochemistry research international · 2020Review
- Lysophosphatidic acid increases mesangial cell proliferation in models of diabetic nephropathy via Rac1/MAPK/KLF5 signaling.Experimental & molecular medicine · 2019Article
- Early growth response factor-1 DNA enzyme 1 inhibits the formation of abdominal aortic aneurysm in rats.Experimental and therapeutic medicine · 2018Article
- GPER-independent inhibition of adrenocortical cancer growth by G-1 involves ROS/Egr-1/BAX pathway.Oncotarget · 2017Article
- Identification of cardioprotective agents from traditional Chinese medicine against oxidative damage.Molecular medicine reports · 2016Article
- PDGF induces SphK1 expression via Egr-1 to promote pulmonary artery smooth muscle cell proliferation.American journal of physiology. Cell physiology · 2016Article
- Epigenetic regulation of diacylglycerol kinase alpha promotes radiation-induced fibrosis.Nature communications · 2016Article
- Lysophospholipids and their G protein-coupled receptors in atherosclerosis.Frontiers in bioscience (Landmark edition) · 2016Review
- Inferring interaction type in gene regulatory networks using co-expression data.Algorithms for molecular biology : AMB · 2015Article
- Egr-1: new conductor for the tissue repair orchestra directs harmony (regeneration) or cacophony (fibrosis).The Journal of pathology · 2013Review
- Activation of Egr-1 in human lung epithelial cells exposed to silica through MAPKs signaling pathways.PloS one · 2013Article
- Transfected early growth response gene-1 DNA enzyme prevents stenosis and occlusion of autogenous vein graft in vivo.BioMed research international · 2013Article
- Disease progression mediated by egr-1 associated signaling in response to oxidative stress.International journal of molecular sciences · 2012Review
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Authors and funding
7 authors at 3 institutions in 3 countries.
Funding
Abstract
Lysophosphatidic acid (LPA) modulates vascular cell function in vitro and in vivo via regulating the expression of specific genes. Previously, we reported that a transcriptional mechanism controls LPA-induced expression of Egr-1 in vascular smooth muscle cells. Egr-1 is a master transcription factor mediating the expression of various genes that have been implied to modulate a broad spectrum of vascular pathologies. In this study, we determined the essential intracellular signaling pathway leading to LPA-induced Egr-1 expression. Our data demonstrate that activation of ERK1/2 and JNK, but not p38 MAPK, is required for LPA-induced Egr-1 expression in smooth muscle cells. We provide the first evidence that MEK-mediated JNK activation leads to LPA-induced gene expression. JNK2 is required for Egr-1 induction. Examining the upstream kinases that mediate ERK and JNK activation, leading to Egr-1 expression, we found that LPA-induced activation of MAPKs and expression of Egr-1 are dependent on PKC activation. We observed that LPA rapidly activates PKCδ and PKCθ. Overexpression of dominant-negative PKCδ, but not dominant-negative PKCθ, diminished activation of ERK and JNK and blocked LPA-induced expression of Egr-1 mRNA and protein. We also evaluated LPA receptor involvement. Our data reveal an intracellular regulatory mechanism: LPA induction of Egr-1 expression is via LPA cognate receptor (LPA receptor 1)-dependent and PKCδ-mediated ERK and JNK activation. This study provides the first evidence that PKCδ mediates ERK and JNK activation in the LPA signaling pathway and that this pathway is required for LPA-induced gene regulation as evidenced by Egr-1 expression.
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