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10.1165/rcmb.2013-0229OC http://scihub22266oqcxt.onion/10.1165/rcmb.2013-0229OC C4370256!4370256 !25054647     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=25054647 &cmd=llinks): Failed to open stream: HTTP request failed! 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Pigment epithelium-derived factor mediates impaired lung vascular development in neonatal hyperoxia |pdf=|usr=}}{{25054647 }} gab.com Text Pigment epithelium-derived factor mediates impaired lung vascular development in neonatal hyperoxia JO: Am J Respir Cell Mol Biol http://www.kidney.de/pget.php?&tw=1&pmid=25054647 #FOAvip Bronchopulmonary dysplasia is a chronic lung disease of preterm infants characterized by arrested microvascularization and alveolarization. Studies show the importance of proangiogenic factors for alveolarization, but the importance of antiangiogenic factors is unknown. We proposed that hyperoxia increases the potent angiostatin, pigment epithelium-derived factor (PEDF), in neonatal lungs, inhibiting alveolarization and microvascularization. Wild-type (WT) and PEDF(-/-) mice were exposed to room air (RA) or 0.9 fraction of inspired oxygen from Postnatal Day 5 to 13. PEDF protein was increased in hyperoxic lungs compared with RA-exposed lungs (P < 0.05). In situ hybridization and immunofluorescence identified PEDF production primarily in alveolar epithelium. Hyperoxia reduced alveolarization in WT mice (P < 0.05) but not in PEDF(-/-) mice. WT hyperoxic mice had fewer platelet endothelial cell adhesion molecule (PECAM)-positive cells per alveolus (1.4 ± 0.4) than RA-exposed mice (4.3 ± 0.3; P < 0.05); this reduction was absent in hyperoxic PEDF(-/-) mice. The interactive regulation of lung microvascularization by vascular endothelial growth factor and PEDF was studied in vitro using MFLM-91U cells, a fetal mouse lung endothelial cell line. Vascular endothelial growth factor stimulation of proliferation, migration, and capillary tube formation was inhibited by PEDF. MFLM-91U cells exposed to conditioned medium (CM) from E17 fetal mouse lung type II (T2) cells cultured in 0.9 fraction of inspired oxygen formed fewer capillary tubes than CM from T2 cells cultured in RA (hyperoxia CM, 51 ± 10% of RA CM, P < 0.05), an effect abolished by PEDF antibody. We conclude that PEDF mediates reduced vasculogenesis and alveolarization in neonatal hyperoxia. Bronchopulmonary dysplasia likely results from an altered balance between pro- and antiangiogenic factors. Twit Text FOAVip Pigment epithelium-derived factor mediates impaired lung vascular development in neonatal hyperoxia ????Am J Respir Cell Mol Biol http://www.kidney.de/pget.php?&tw=1&pmid=25054647 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25054647 #FOAvip English Wikipedia <ref>{{Cite pmid|25054647 }}</ref> Pigment epithelium-derived factor mediates impaired lung vascular development in neonatal hyperoxia #MMPMID25054647 Chetty A ; Bennett M ; Dang L ; Nakamura D ; Cao GJ ; Mujahid S ; Volpe M ; Herman I ; Becerra SP ; Nielsen HC Am J Respir Cell Mol Biol 2015[Mar]; 52 (3 ): 295-303 PMID25054647 show ga Bronchopulmonary dysplasia is a chronic lung disease of preterm infants characterized by arrested microvascularization and alveolarization. Studies show the importance of proangiogenic factors for alveolarization, but the importance of antiangiogenic factors is unknown. We proposed that hyperoxia increases the potent angiostatin, pigment epithelium-derived factor (PEDF), in neonatal lungs, inhibiting alveolarization and microvascularization. Wild-type (WT) and PEDF(-/-) mice were exposed to room air (RA) or 0.9 fraction of inspired oxygen from Postnatal Day 5 to 13. PEDF protein was increased in hyperoxic lungs compared with RA-exposed lungs (P < 0.05). In situ hybridization and immunofluorescence identified PEDF production primarily in alveolar epithelium. Hyperoxia reduced alveolarization in WT mice (P < 0.05) but not in PEDF(-/-) mice. WT hyperoxic mice had fewer platelet endothelial cell adhesion molecule (PECAM)-positive cells per alveolus (1.4 ± 0.4) than RA-exposed mice (4.3 ± 0.3; P < 0.05); this reduction was absent in hyperoxic PEDF(-/-) mice. The interactive regulation of lung microvascularization by vascular endothelial growth factor and PEDF was studied in vitro using MFLM-91U cells, a fetal mouse lung endothelial cell line. Vascular endothelial growth factor stimulation of proliferation, migration, and capillary tube formation was inhibited by PEDF. MFLM-91U cells exposed to conditioned medium (CM) from E17 fetal mouse lung type II (T2) cells cultured in 0.9 fraction of inspired oxygen formed fewer capillary tubes than CM from T2 cells cultured in RA (hyperoxia CM, 51 ± 10% of RA CM, P < 0.05), an effect abolished by PEDF antibody. We conclude that PEDF mediates reduced vasculogenesis and alveolarization in neonatal hyperoxia. Bronchopulmonary dysplasia likely results from an altered balance between pro- and antiangiogenic factors. |Angiostatins/metabolism [MESH] |Animals [MESH] |Animals, Newborn/*metabolism [MESH] |Bronchopulmonary Dysplasia/metabolism [MESH] |Cell Line [MESH] |Cell Movement/physiology [MESH] |Cell Proliferation/physiology [MESH] |Endothelium, Vascular/*metabolism [MESH] |Eye Proteins/*metabolism [MESH] |Hyperoxia/*metabolism [MESH] |Lung/*metabolism [MESH] |Mice [MESH] |Mice, Inbred C57BL [MESH] |Nerve Growth Factors/*metabolism [MESH] |Oxygen/metabolism [MESH] |Platelet Endothelial Cell Adhesion Molecule-1/metabolism [MESH] |Serpins/*metabolism [MESH]Pigment epithelium-derived factor mediates impaired lung vascular deve(epmc).pdf DeepDyve Pubget Overpricing