ArticleAmerican journal of respiratory cell and molecular biology2013
BMP4 increases canonical transient receptor potential protein expression by activating p38 MAPK and ERK1/2 signaling pathways in pulmonary arterial smooth muscle cells.
Article in American journal of respiratory cell and molecular biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 39 citations in OpenAlex.
- NCAM1 modulates the proliferation and migration of pulmonary arterial smooth muscle cells in pulmonary hypertension.Respiratory research · 2024Article
- Role of autocrine bone morphogenetic protein signaling in trophoblast stem cells†.Biology of reproduction · 2022Article
- The Role of Bone Morphogenetic Protein 4 in Ovarian Function and Diseases.Reproductive sciences (Thousand Oaks, Calif.) · 2021Review
- Mechanosensitivity in Pulmonary Circulation: Pathophysiological Relevance of Stretch-Activated Channels in Pulmonary Hypertension.Biomolecules · 2021Review
- Expression of canonical transient receptor potential channels in U-2 OS and MNNG-HOS osteosarcoma cell lines.Oncology letters · 2021Article
- Regulation of bone morphogenetic protein 4 on epithelial tissue.Journal of cell communication and signaling · 2020Review
- Heart‑lung crosstalk in pulmonary arterial hypertension following myocardial infarction (Review).International journal of molecular medicine · 2020Review
- TRPC and TRPV Channels' Role in Vascular Remodeling and Disease.International journal of molecular sciences · 2020Review
- BMP-2 upregulates the AKT/mTOR pathway in breast cancer with microcalcification and indicates a poor prognosis.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2020Article
- Tetramethylpyrazine: A promising drug for the treatment of pulmonary hypertension.British journal of pharmacology · 2020Article
- 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
- Isolation, culture and identification of pulmonary arterial smooth muscle cells from rat distal pulmonary arteries.Cytotechnology · 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
- Smooth Muscle Ion Channels and Regulation of Vascular Tone in Resistance Arteries and Arterioles.Comprehensive Physiology · 2017Review
- Notoginsenoside Rb1 inhibits activation of ERK and p38 MAPK pathways induced by hypoxia and hypercapnia.Experimental and therapeutic medicine · 2016Article
- A Molecular View of Pathological Microcalcification in Breast Cancer.Journal of mammary gland biology and neoplasia · 2016Review
- NADPH oxidases-do they play a role in TRPC regulation under hypoxia?Pflugers Archiv : European journal of physiology · 2016Review
- Hypoxia inducible factor-1-dependent up-regulation of BMP4 mediates hypoxia-induced increase of TRPC expression in PASMCs.Cardiovascular research · 2015Article
- Noggin inhibits hypoxia-induced proliferation by targeting store-operated calcium entry and transient receptor potential cation channels.American journal of physiology. Cell physiology · 2015Article
- Bone morphogenetic protein-4: a novel therapeutic target for pathological cardiac hypertrophy/heart failure.Heart failure reviews · 2014Review
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
Abnormal bone morphogenetic protein (BMP) signaling has been implicated in the pathogenesis of pulmonary hypertension. We previously found that BMP4 elevated basal intracellular Ca(2+) ([Ca(2+)]i) concentrations in distal pulmonary arterial smooth muscle cells (PASMCs), attributable in large part to enhanced store-operated Ca(2+) entry through store-operated Ca(2+) channels (SOCCs). Moreover, BMP4 up-regulated the expression of canonical transient receptor potential (TRPC) proteins thought to compose SOCCs. The present study investigated the signaling pathways through which BMP4 regulates TRPC expression and basal [Ca(2+)]i in distal PASMCs. Real-time quantitative PCR was used for the measurement of mRNA, Western blotting was used for the measurement of protein, and fluorescent microscopic for [Ca(2+)]i was used to determine the involvement of p38 and extracellular regulated kinase (ERK)-1/2 mitogen-activated protein kinase (MAPK) signaling in BMP4-induced TRPC expression and the elevation of [Ca(2+)]i in PASMCs. We found that the treatment of BMP4 led to the activation of both p38 MAPK and ERK1/2 in rat distal PASMCs. The induction of TRPC1, TRPC4, and TRPC6 expression, and the increases of [Ca(2+)]i caused by BMP4 in distal PASMCs, were inhibited by treatment with either SB203580 (10 μM), the selective inhibitor for p38 activation, or the specific p38 small interfering RNA (siRNA). Similarly, those responses induced by BMP4 were also abolished by treatment with PD98059 (5 μM), the selective inhibitor of ERK1/2, or by the knockdown of ERK1/2 using its specific siRNA. These results indicate that BMP4 participates in the regulation of Ca(2+) signaling in PASMCs by modulating TRPC channel expression via activating p38 and ERK1/2 MAPK pathways.
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