ArticleMolecular and cellular biology2006
Platelet-derived growth factor BB induces nuclear export and proteasomal degradation of CREB via phosphatidylinositol 3-kinase/Akt signaling in pulmonary artery smooth muscle cells.
Article in Molecular and cellular biology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 53 citations in OpenAlex.
- Kisspeptins inhibit human airway smooth muscle proliferation.JCI insight · 2022Article
- What turns CREB on? And off? And why does it matter?Cellular and molecular life sciences : CMLS · 2020Review
- Anti-Remodeling Effects of Xanthohumol-Fortified Beer in Pulmonary Arterial Hypertension Mediated by ERK and AKT Inhibition.Nutrients · 2019Article
- PI3Kγ (Phosphoinositide 3-Kinase γ) Regulates Vascular Smooth Muscle Cell Phenotypic Modulation and Neointimal Formation Through CREB (Cyclic AMP-Response Element Binding Protein)/YAP (Yes-Associated Protein) Signaling.Arteriosclerosis, thrombosis, and vascular biology · 2019Article
- Estrogen receptor beta signaling inhibits PDGF induced human airway smooth muscle proliferation.Molecular and cellular endocrinology · 2018Article
- Article
- Prostaglandin E1 Attenuates Pulmonary Artery Remodeling by Activating Phosphorylation of CREB and the PTEN Signaling Pathway.Scientific reports · 2017Article
- Retardation of C2C12 myoblast cell proliferation by exposure to low-temperature atmospheric plasma.The journal of physiological sciences : JPS · 2014Article
- BMP4 protects rat pulmonary arterial smooth muscle cells from apoptosis by PI3K/AKT/Smad1/5/8 signaling.International journal of molecular sciences · 2014Article
- Baicalin inhibits hypoxia-induced pulmonary artery smooth muscle cell proliferation via the AKT/HIF-1α/p27-associated pathway.International journal of molecular sciences · 2014Article
- Targeting mitochondria to restore failed adaptation to exercise in diabetes.Biochemical Society transactions · 2014Review
- Nur77 suppresses pulmonary artery smooth muscle cell proliferation through inhibition of the STAT3/Pim-1/NFAT pathway.American journal of respiratory cell and molecular biology · 2014Article
- Inhibition of phosphatidylinositol 3-kinase/Akt signaling attenuates hypoxia-induced pulmonary artery remodeling and suppresses CREB depletion in arterial smooth muscle cells.Journal of cardiovascular pharmacology · 2013Article
- CaMKIIδ-dependent inhibition of cAMP-response element-binding protein activity in vascular smooth muscle.The Journal of biological chemistry · 2013Article
- Rapamycin reverses pulmonary artery smooth muscle cell proliferation in pulmonary hypertension.American journal of respiratory cell and molecular biology · 2013Article
- Impaired response to exercise intervention in the vasculature in metabolic syndrome.Diabetes & vascular disease research · 2013Article
- Crebinostat: a novel cognitive enhancer that inhibits histone deacetylase activity and modulates chromatin-mediated neuroplasticity.Neuropharmacology · 2013Article
- Hypoxia induces unique proliferative response in adventitial fibroblasts by activating PDGFβ receptor-JNK1 signalling.Cardiovascular research · 2012Article
- Vanin-1 pantetheinase drives smooth muscle cell activation in post-arterial injury neointimal hyperplasia.PloS one · 2012Article
- Beyond phosphorylation: nuclear export in vascular remodeling.Arteriosclerosis, thrombosis, and vascular biology · 2011Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
Cyclic AMP response element binding protein (CREB) content is diminished in smooth muscle cells (SMCs) in remodeled pulmonary arteries from animals with pulmonary hypertension and in the SMC layers of atherogenic systemic arteries and cardiomyocytes from hypertensive individuals. Loss of CREB can be induced in cultured SMCs by chronic exposure to hypoxia or platelet-derived growth factor BB (PDGF-BB). Here we investigated the signaling pathways and mechanisms by which PDGF elicits depletion of SMC CREB. Chronic PDGF treatment increased CREB ubiquitination in SMCs, while treatment of SMCs with the proteasome inhibitor lactacystin prevented decreases in CREB content. The nuclear export inhibitor leptomycin B also prevented depletion of SMC CREB alone or in combination with lactacystin. Subsequent studies showed that PDGF activated extracellular signal-regulated kinase, Jun N-terminal protein kinase, and phosphatidylinositol 3 (PI3)-kinase pathways in SMCs. Inhibition of these pathways blocked SMC proliferation in response to PDGF, but only inhibition of PI3-kinase or its effector, Akt, blocked PDGF-induced CREB loss. Finally, chimeric proteins containing enhanced cyan fluorescent protein linked to wild-type CREB or CREB molecules with mutations in several recognized phosphorylation sites were introduced into SMCs. PDGF treatment reduced the levels of each of these chimeric proteins except for one containing mutations in adjacent serine residues (serines 103 and 107), suggesting that CREB loss was dependent on CREB phosphorylation at these sites. We conclude that PDGF stimulates nuclear export and proteasomal degradation of CREB in SMCs via PI3-kinase/Akt signaling. These results indicate that in addition to direct phosphorylation, proteolysis and intracellular localization are key mechanisms regulating CREB content and activity in SMCs.
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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 OpenQuestion graph.