ArticleAmerican journal of physiology. Cell physiology2015
Noggin inhibits hypoxia-induced proliferation by targeting store-operated calcium entry and transient receptor potential cation channels.
Article in American journal of physiology. Cell physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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13 citing papers in PubMed, 28 citations in OpenAlex.
- The mutual interaction of TRPC5 channel with polycystin proteins.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2025Article
- Noggin contributes to brain metastatic colonization of lung cancer cells.Cancer cell international · 2023Article
- Disturbing cytoskeleton by engineered nanomaterials for enhanced cancer therapeutics.Bioactive materials · 2023Review
- Bone Morphogenic Proteins and Their Antagonists in the Lower Airways of Stable COPD Patients.Biology · 2023Article
- Thrombotic Alterations under Perinatal Hypoxic Conditions: HIF and Other Hypoxic Markers.International journal of molecular sciences · 2023Review
- Biological heterogeneity in idiopathic pulmonary arterial hypertension identified through unsupervised transcriptomic profiling of whole blood.Nature communications · 2021Article
- 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
- Altered expression of PPAR‑γ and TRPC in neonatal rats with persistent pulmonary hypertension.Molecular medicine reports · 2017Article
- BMP4 inhibits PDGF-induced proliferation and collagen synthesis via PKA-mediated inhibition of calpain-2 in pulmonary artery smooth muscle cells.American journal of physiology. Lung cellular and molecular physiology · 2017Article
- The Role of Transient Receptor Potential Channel 6 Channels in the Pulmonary Vasculature.Frontiers in immunology · 2017Review
- Article
- "TRP inflammation" relationship in cardiovascular system.Seminars in immunopathology · 2016Review
- NOGGIN: a new therapeutic target for PH? Focus on "Noggin inhibits hypoxia-induced proliferation by targeting store-operated calcium entry and transient receptor potential cation channels".American journal of physiology. Cell physiology · 2015Article
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9 authors at 5 institutions in 2 countries.
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Abstract
Abnormally elevated bone morphogenetic protein 4 (BMP4) expression and mediated signaling play a critical role in the pathogenesis of chronic hypoxia-induced pulmonary hypertension (CHPH). In this study, we investigated the expression level and functional significance of four reported naturally occurring BMP4 antagonists, noggin, follistatin, gremlin1, and matrix gla protein (MGP), in the lung and distal pulmonary arterial smooth muscle cell (PASMC). A 21-day chronic hypoxic (10% O2) exposure rat model was utilized, which has been previously shown to successfully establish experimental CHPH. Among the four antagonists, noggin, but not the other three, was selectively downregulated by hypoxic exposure in both the lung tissue and PASMC, in correlation with markedly elevated BMP4 expression, suggesting that the loss of noggin might account for the hypoxia-triggered BMP4 signaling transduction. Then, by using treatment of extrogenous recombinant noggin protein, we further found that noggin significantly normalized 1) BMP4-induced phosphorylation of cellular p38 and ERK1/2; 2) BMP4-induced phosphorylation of cellular JAK2 and STAT3; 3) hypoxia-induced PASMC proliferation; 4) hypoxia-induced store-operated calcium entry (SOCE), and 5) hypoxia-increased expression of transient receptor potential cation channels (TRPC1 and TRPC6) in PASMC. In combination, these data strongly indicated that the hypoxia-suppressed noggin accounts, at least partially, for hypoxia-induced excessive PASMC proliferation, while restoration of noggin may be an effective way to inhibit cell proliferation by suppressing SOCE and TRPC expression.
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