ArticleAmerican journal of respiratory cell and molecular biology2015
Role of microRNA-150 and glycoprotein nonmetastatic melanoma protein B in angiogenesis during hyperoxia-induced neonatal lung injury.
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 22 papers.
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Who cites it
22 citing papers in PubMed, 40 citations in OpenAlex.
- Decoding STAT3: a new frontier in understanding and treating hyperoxic lung injury.Frontiers in immunology · 2025Review
- Research progress of microvascular development in bronchopulmonary dysplasia.Pediatric investigation · 2024Review
- GPNMB Ameliorates Neuroinflammation Via the Modulation of AMPK/NFκB Signaling Pathway After SAH in Mice.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2023Article
- Downregulation of glycoprotein non-metastatic melanoma protein B prevents high glucose-induced angiogenesis in diabetic retinopathy.Molecular and cellular biochemistry · 2023Article
- Oxygen toxicity: cellular mechanisms in normobaric hyperoxia.Cell biology and toxicology · 2023Review
- MicroRNA-150 (miR-150) and Diabetic Retinopathy: Is miR-150 Only a Biomarker or Does It Contribute to Disease Progression?International journal of molecular sciences · 2022Review
- Insight Into the Roles of Non-coding RNA in Bronchopulmonary Dysplasia.Frontiers in medicine · 2021Review
- Glycoprotein nonmetastatic melanoma protein B: A key mediator and an emerging therapeutic target in autoimmune diseases.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Review
- Transgenic Overexpression of GPNMB Protects Against MPTP-Induced Neurodegeneration.Molecular neurobiology · 2020Article
- MicroRNAs in Vascular Eye Diseases.International journal of molecular sciences · 2020Review
- Hyperoxia causes miR199a-5p-mediated injury in the developing lung.Pediatric research · 2019Article
- Targeting miR-34a/EMBO molecular medicine · 2019Article
- MicroRNA-124 alleviates hyperoxia-induced inflammatory response in pulmonary epithelial cell by inhibiting TLR4/NF-κB/CCL2.International journal of clinical and experimental pathology · 2018Article
- Hyperoxia causes miR-34a-mediated injury via angiopoietin-1 in neonatal lungs.Nature communications · 2017Article
- MicroRNA in late lung development and bronchopulmonary dysplasia: the need to demonstrate causality.Molecular and cellular pediatrics · 2016Review
- Retinal expression of small non-coding RNAs in a murine model of proliferative retinopathy.Scientific reports · 2016Article
- XBP1 splicing triggers miR-150 transfer from smooth muscle cells to endothelial cells via extracellular vesicles.Scientific reports · 2016Article
- Deletion of miR-150 Exacerbates Retinal Vascular Overgrowth in High-Fat-Diet Induced Diabetic Mice.PloS one · 2016Article
- MicroRNA expression profiles and target prediction in neonatal Wistar rat lungs during the development of bronchopulmonary dysplasia.International journal of molecular medicine · 2015Article
- Endothelial microRNA-150 is an intrinsic suppressor of pathologic ocular neovascularization.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
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7 authors at 1 institution in 1 country.
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Abstract
Glycoprotein nonmetastatic melanoma protein B (GPNMB), a transmembrane protein, has been reported to have an important role in tissue repair and angiogenesis. Recently, we have demonstrated that hyperoxia exposure down-regulates microRNA (miR)-150 expression and concurrent induction of its target gene, GPNMB, in neonatal rat lungs. This study aimed to test the hypothesis that soluble GPNMB (sGPNMB) promotes angiogenesis in the hyperoxic neonatal lungs. Wild-type (WT) or miR-150 knockout (KO) neonates, exposed to 95% O2 for 3, 6, and 10 days, were evaluated for lung phenotypes, GPNMB protein expression in the lungs, and sGPNMB levels in the bronchoalveolar lavage. Angiogenic effects of sGPNMB were examined both in vitro and in vivo. After a 6-day exposure, similar analyses were performed in WT and miR-150 KO neonates during recovery at 7, 14, and 21 days. miR-150 KO neonates displayed an increased capillary network, decreased inflammation, and less alveolar damage compared with WT neonates after hyperoxia exposure. The early induction of GPNMB and sGPNMB were found in miR-150 KO neonates. The recombinant GPNMB, which contained a soluble portion of GPNMB, promoted endothelial tube formation in vitro and enhanced angiogenesis in vivo. The increased capillaries in the hyperoxic lungs of miR-150 KO neonates appeared dysmorphic. They were abnormally enlarged in size and occasionally laid at subepithelial regions in the alveoli. However, the lung architecture returned to normal during recovery, suggesting that abnormal vascularity during hyperoxia does not affect postnatal lung development. GPNMB plays an important role in angiogenesis during hyperoxia injury. Treatment with GPNMB may offer a novel therapeutic approach in reducing pathologic complications in bronchopulmonary dysplasia.
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