ArticleJournal of cellular physiology2008
Pleiotrophin induces nitric oxide dependent migration of endothelial progenitor cells.
Article in Journal of cellular physiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
18 citing papers in PubMed, 42 citations in OpenAlex.
- Midkine and pleiotrophin in glioma: From mechanistic insights to therapeutic potential.Neoplasia (New York, N.Y.) · 2026Review
- Identification of a key smooth muscle cell subset driving ischemic cardiomyopathy progression through single-cell RNA sequencing.Scientific reports · 2025Article
- Single-cell RNA sequencing reveals the potential role of Postn(+) fibroblasts in promoting the progression of myocardial fibrosis after myocardial infarction.Scientific reports · 2025Article
- Cyclin-dependent kinase 5 mediates pleiotrophin-induced endothelial cell migration.Scientific reports · 2018Article
- Pathogenic role and therapeutic potential of pleiotrophin in mouse models of ocular vascular disease.Angiogenesis · 2017Article
- Bone Niches, Hematopoietic Stem Cells, and Vessel Formation.International journal of molecular sciences · 2017Review
- Article
- Overexpression of Nitric Oxide Synthase Restores Circulating Angiogenic Cell Function in Patients With Coronary Artery Disease: Implications for Autologous Cell Therapy for Myocardial Infarction.Journal of the American Heart Association · 2016Article
- Central role of eNOS in the maintenance of endothelial homeostasis.Antioxidants & redox signaling · 2015Review
- Brain derived neurotrophic factor contributes to the cardiogenic potential of adult resident progenitor cells in failing murine heart.PloS one · 2015Article
- Protein engineering to develop a redox insensitive endothelial nitric oxide synthase.Redox biology · 2014Article
- Pleiotrophin gene therapy for peripheral ischemia: evaluation of full-length and truncated gene variants.PloS one · 2013Article
- Higher fasting glucose levels are associated with reduced circulating angiogenic cell migratory capacity among healthy individuals.American journal of cardiovascular disease · 2012Article
- Hypomethylation of functional retrotransposon-derived genes in the human placenta.Mammalian genome : official journal of the International Mammalian Genome Society · 2011Article
- Nitric oxide counters the inhibitory effects of uremic toxin indoxyl sulfate on endothelial cells by governing ERK MAP kinase and myosin light chain activation.Biochemical and biophysical research communications · 2011Article
- Nitric oxide synthase expression and functional response to nitric oxide are both important modulators of circulating angiogenic cell response to angiogenic stimuli.Arteriosclerosis, thrombosis, and vascular biology · 2010Article
- Article
- Targeted in vivo extracellular matrix formation promotes neovascularization in a rodent model of myocardial infarction.PloS one · 2010Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Pleiotrophin (PTN) is produced under ischemic conditions and has been shown to induce angiogenesis in vivo. We studied whether or not PTN exerts chemotaxis of pro-angiogenic early endothelial progenitor cells (EPCs), a population of circulating cells that have been reported to participate in and stimulate angiogenesis. Chemotaxis of EPCs, isolated from blood of healthy humans (n = 5), was measured in transwell assays. PTN at 10-500 ng/ml elicited dose-dependent chemotaxis of both EPCs and human umbilical vein endothelial cells (HUVECs), but not of human coronary artery smooth muscle cells (CASMCs) and T98G glioblastoma cells that lack PTN receptors. The degree of chemotaxis was comparable to that induced by the angiogenic factors VEGF and SDF-1alpha. Chemotaxis to PTN was blocked by the NOS inhibitors L-NNA and L-NMMA, the NO scavenger PTIO, the phosphoinositide-3 kinase inhibitor wortmannin, and the guanylyl cyclase inhibitor ODQ, suggesting dependence of EPC chemotaxis on these pathways. PTN induced NOS-dependent production of NO to a similar degree as did VEGF, as indicated by the NO indicator DAF-2. PTN increased proliferation in EPCs and HUVECs to a similar extent as VEGF, but did not induce proliferation of CASMCs. While L-NNA abolished PTN-induced migration in EPCs and HUVECs, it did not inhibit PTN- and VEGF-enhanced proliferation and also caused proliferation by itself. These data suggest that PTN may mediate its pro-angiogenic effects by increasing the local number of not only endothelial cells but also early EPCs at angiogenic sites.
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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.