ArticleMolecular biology of the cell2018
Egr-1 mediates leptin-induced PPARγ reduction and proliferation of pulmonary artery smooth muscle cells.
Article in Molecular biology of the cell, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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Who cites it
8 citing papers in PubMed, 18 citations in OpenAlex.
- Egr‑1 promotes the proliferation and migration of vascular smooth muscle cells by transcriptionally activating Egr‑2 in arteriovenous fistulas.International journal of molecular medicine · 2025Article
- Adipokines in pulmonary hypertension: angels or demons?Heliyon · 2023Review
- Comparative transcription profiling of mRNA and lncRNA in pulmonary arterial hypertension after C75 treatment.BMC pulmonary medicine · 2023Article
- Early Growth Response-1, an Integrative Sensor in Cardiovascular and Inflammatory Disease.Journal of the American Heart Association · 2021Review
- Tissue-Specific Effects of Leptin on Glucose and Lipid Metabolism.Endocrine reviews · 2021Review
- Transcriptome Analysis Reveals the Anti-cancerous Mechanism of Licochalcone A on Human Hepatoma Cell HepG2.Frontiers in nutrition · 2021Article
- The Crucial Role of PPARγ-Egr-1-Pro-Inflammatory Mediators Axis in IgG Immune Complex-Induced Acute Lung Injury.Frontiers in immunology · 2021Article
- The Role and Regulation of Pulmonary Artery Smooth Muscle Cells in Pulmonary Hypertension.International journal of hypertension · 2020Review
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Loss of peroxisome proliferator-activated receptor γ (PPARγ) has been found to contribute to pulmonary artery smooth muscle cell (PASMC) proliferation and pulmonary arterial remodeling therefore the development of pulmonary hypertension (PH). Yet, the molecular mechanisms underlying PPARγ reduction in PASMC remain poorly understood. Here, we demonstrated that leptin dose- and time-dependently inducued PPARγ down-regulation and proliferation of primary cultured rat PASMC, this was accompanied with the activation of extracellular regulated kinase1/2 (ERK1/2) signaling pathway and subsequent induction of early growth response-1 (Egr-1) expression. The presence of MEK inhibitors U0126 or PD98059, or prior silencing Egr-1 with small interfering RNA suppressed leptin-induced PPARγ reduction. In addition, activation of PPARγ by pioglitazone or targeting ERK1/2/Egr-1 suppressed leptin-induced PASMC proliferation. Taken together, our study indicates that ERK1/2 signaling pathway-mediated leptin-induced PPARγ reduction and PASMC proliferation through up-regulation of Egr-1 and suggests that targeting leptin/ERK1/2/Egr-1 pathway might have potential value in ameliorating vascular remodeling and benefit PH.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.