ArticleAmerican journal of respiratory cell and molecular biology2015
Peroxisome Proliferator-Activated Receptor γ-Mediated Inhibition on Hypoxia-Triggered Store-Operated Calcium Entry. A Caveolin-1-Dependent Mechanism.
Article in American journal of respiratory cell and molecular biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 31 citations in OpenAlex.
- Integrating GPCR Regulation and Calcium Dynamics in Airway Smooth Muscle Function: A Comprehensive Review.Cells · 2026Review
- The Potential Role of Calcium Channels in Pulmonary Hypertension.BioMed research international · 2026Review
- The Role of Ion Channels in Pulmonary Hypertension: A Review.Pulmonary circulation · 2025Review
- Caveolin-1 accelerates hypoxia-induced endothelial dysfunction in high-altitude cerebral edema.Cell communication and signaling : CCS · 2022Article
- Sildenafil protects against pulmonary hypertension induced by hypoxia in neonatal rats via activation of PPARγ‑mediated downregulation of TRPC.International journal of molecular medicine · 2022Article
- Bortezomib Inhibits Hypoxia-Induced Proliferation by Suppressing Caveolin-1/SOCE/[CaBioMed research international · 2021Article
- Caveolae as Potential Hijackable Gates in Cell Communication.Frontiers in cell and developmental biology · 2020Review
- Identification of key regulators in parathyroid adenoma using an integrative gene network analysis.Bioinformation · 2020Article
- Redox Biology of Peroxisome Proliferator-Activated Receptor-γ in Pulmonary Hypertension.Antioxidants & redox signaling · 2019Review
- Article
- Pharmacological activation of PPARγ inhibits hypoxia-induced proliferation through a caveolin-1-targeted and -dependent mechanism in PASMCs.American journal of physiology. Cell physiology · 2018Article
- Revisiting the Role of TRP, Orai, and ASIC Channels in the Pulmonary Arterial Response to Hypoxia.Frontiers in physiology · 2018Review
- 5-HT induces PPAR γ reduction and proliferation of pulmonary artery smooth muscle cells via modulating GSK-3β/β-catenin pathway.Oncotarget · 2017Article
- Altered expression of PPAR‑γ and TRPC in neonatal rats with persistent pulmonary hypertension.Molecular medicine reports · 2017Article
- Orai1, 2, 3 and STIM1 promote store-operated calcium entry in pulmonary arterial smooth muscle cells.Cell death discovery · 2017Article
- A possible regulatory link between Twist 1 and PPARγ gene regulation in 3T3-L1 adipocytes.Lipids in health and disease · 2016Article
- Bortezomib alleviates experimental pulmonary hypertension by regulating intracellular calcium homeostasis in PASMCs.American journal of physiology. Cell physiology · 2016Article
- Sodium tanshinone IIA sulfonate inhibits hypoxia-induced enhancement of SOCE in pulmonary arterial smooth muscle cells via the PKG-PPAR-γ signaling axis.American journal of physiology. Cell physiology · 2016Article
- Orai channel-mediated Ca2+ signals in vascular and airway smooth muscle.American journal of physiology. Cell physiology · 2016Review
- Reduction of blood pressure by store-operated calcium channel blockers.Journal of cellular and molecular medicine · 2015Article
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
Our previous publication demonstrated that peroxisome proliferator-activated receptor γ (PPARγ) inhibits the pathogenesis of chronic hypoxia (CH)-induced pulmonary hypertension by targeting store-operated calcium entry (SOCE) in rat distal pulmonary arterial smooth muscle cells (PASMCs). In this study, we aim to determine the role of a membrane scaffolding protein, caveolin-1, during the suppressive process of PPARγ on SOCE. Adult (6-8 weeks) male Wistar rats (200-250 g) were exposed to CH (10% O2) for 21 days to establish CH-induced pulmonary hypertension. Primary cultured rat distal PASMCs were applied for the molecular biological experiments. First, hypoxic exposure led to 2.5-fold and 1-fold increases of caveolin-1 protein expression in the distal pulmonary arteries and PASMCs, respectively. Second, effective knockdown of caveolin-1 significantly reduced hypoxia-induced SOCE for 58.2% and 41.5%, measured by Mn(2+) quenching and extracellular Ca(2+) restoration experiments, respectively. These results suggested that caveolin-1 acts as a crucial regulator of SOCE, and hypoxia-up-regulated caveolin-1 largely accounts for hypoxia-elevated SOCE in PASMCs. Then, by using a high-potency PPARγ agonist, GW1929, we detected that PPARγ activation inhibited SOCE and caveolin-1 protein for 62.5% and 59.8% under hypoxia, respectively, suggesting that caveolin-1 also acts as a key target during the suppressive process of PPARγ on SOCE in PASMCs. Moreover, by using effective small interfering RNAs against PPARγ and caveolin-1, and PPARγ antagonist, T0070907, we observed that PPARγ plays an inhibitory role on caveolin-1 protein by promoting its lysosomal degradation, without affecting the messenger RNA level. PPARγ inhibits SOCE, at least partially, by suppressing cellular caveolin-1 protein in PASMCs.
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