AMP-Kinase Dysfunction Alters Notch Ligands to Impair Angiogenesis in Neonatal Pulmonary Hypertension
Decreased angiogenesis contributes to persistent pulmonary hypertension of the newborn (PPHN); mechanisms remain unclear. AMPK (5'AMP activated protein kinase) is a key regulator of cell metabolism. We investigated the hypothesis that a decrease in AMPK function leads to mitochondrial dysfuncti...
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| creator | Rana, Ujala Callan, Emily Entringer, Brianna Michalkiewicz, Teresa Joshi, Amit Parchur, Abdul K Teng, Ru-Jeng Konduri, Girija G |
| description | Decreased angiogenesis contributes to persistent pulmonary hypertension of the newborn (PPHN); mechanisms remain unclear. AMPK (5'AMP activated protein kinase) is a key regulator of cell metabolism. We investigated the hypothesis that a decrease in AMPK function leads to mitochondrial dysfunction and altered balance of notch ligands delta-like 4 (DLL4) and Jagged 1 (Jag1) to impair angiogenesis in PPHN. Studies were done in fetal lambs with PPHN induced by prenatal ductus arteriosus constriction and gestation-matched control lambs. PPHN lambs were treated with saline or AMPK agonist metformin. Angiogenesis was assessed in lungs with micro-computed tomography angiography and histology. AMPK function; expression of mitochondrial electron transport chain (ETC) complex proteins I-V, Dll4, and Jag1; mitochondrial number; and
angiogenesis function were assessed in pulmonary artery endothelial cells (PAEC) from control and PPHN lambs. AMPK function was decreased in PPHN PAEC and lung sections. Expression of mitochondrial transcription factor, PGC-1α, ETC complex proteins I-V, and mitochondrial number were decreased in PPHN.
angiogenesis of PAEC and capillary number and vessel volume fraction in the lung were decreased in PPHN. Expression of DLL4 was increased and Jag1 was decreased in PAEC from PPHN lambs. AMPK agonists A769662 and metformin increased the mitochondrial complex proteins and number,
angiogenesis, and Jag1 levels and decreased DLL4 levels in PPHN PAEC. Infusion of metformin
increased the vessel density in PPHN lungs. Decreased AMPK function contributes to impaired angiogenesis in PPHN by altered balance of notch ligands in PPHN. |
| doi_str_mv | 10.1165/rcmb.2019-0275OC |
| format | Article |
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angiogenesis function were assessed in pulmonary artery endothelial cells (PAEC) from control and PPHN lambs. AMPK function was decreased in PPHN PAEC and lung sections. Expression of mitochondrial transcription factor, PGC-1α, ETC complex proteins I-V, and mitochondrial number were decreased in PPHN.
angiogenesis of PAEC and capillary number and vessel volume fraction in the lung were decreased in PPHN. Expression of DLL4 was increased and Jag1 was decreased in PAEC from PPHN lambs. AMPK agonists A769662 and metformin increased the mitochondrial complex proteins and number,
angiogenesis, and Jag1 levels and decreased DLL4 levels in PPHN PAEC. Infusion of metformin
increased the vessel density in PPHN lungs. Decreased AMPK function contributes to impaired angiogenesis in PPHN by altered balance of notch ligands in PPHN.</description><identifier>ISSN: 1044-1549</identifier><identifier>EISSN: 1535-4989</identifier><identifier>DOI: 10.1165/rcmb.2019-0275OC</identifier><identifier>PMID: 32048878</identifier><language>eng</language><publisher>United States: American Thoracic Society</publisher><subject>AMP ; Angiogenesis ; Angiography ; Animals ; Animals, Newborn ; Computed tomography ; Ductus Arteriosus - embryology ; Ductus Arteriosus - surgery ; Electron Transport ; Electron transport chain ; Endothelial cells ; Endothelial Cells - enzymology ; Enzyme Activation ; Female ; Fetuses ; Gestation ; Hypertension ; Hypertension, Pulmonary - enzymology ; Hypertension, Pulmonary - physiopathology ; Intracellular Signaling Peptides and Proteins - metabolism ; Jagged-1 Protein - metabolism ; Ligands ; Lung - pathology ; Membrane Proteins - metabolism ; Metformin ; Metformin - pharmacology ; Metformin - therapeutic use ; Mitochondria ; Mitochondria - metabolism ; Neonates ; Neovascularization, Pathologic - drug therapy ; Neovascularization, Pathologic - enzymology ; Original Research ; Persistent Fetal Circulation Syndrome - drug therapy ; Persistent Fetal Circulation Syndrome - enzymology ; Persistent Fetal Circulation Syndrome - pathology ; Persistent Fetal Circulation Syndrome - physiopathology ; Phosphorylation ; Pregnancy ; Protein kinase ; Protein Kinases - metabolism ; Protein Kinases - physiology ; Protein transport ; Pulmonary artery ; Pulmonary hypertension ; Pyrones - pharmacology ; Receptors, Notch - metabolism ; Sheep ; Thiophenes - pharmacology ; Threonine - metabolism ; Transfection</subject><ispartof>American journal of respiratory cell and molecular biology, 2020-06, Vol.62 (6), p.719-731</ispartof><rights>Copyright American Thoracic Society Jun 2020</rights><rights>Copyright © 2020 by the American Thoracic Society 2020</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c471t-9830029fb18b1e0aeb6ddce17286f894c1366839e3853afdb9577f2109b0f26a3</citedby><cites>FETCH-LOGICAL-c471t-9830029fb18b1e0aeb6ddce17286f894c1366839e3853afdb9577f2109b0f26a3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,776,780,881,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/32048878$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Rana, Ujala</creatorcontrib><creatorcontrib>Callan, Emily</creatorcontrib><creatorcontrib>Entringer, Brianna</creatorcontrib><creatorcontrib>Michalkiewicz, Teresa</creatorcontrib><creatorcontrib>Joshi, Amit</creatorcontrib><creatorcontrib>Parchur, Abdul K</creatorcontrib><creatorcontrib>Teng, Ru-Jeng</creatorcontrib><creatorcontrib>Konduri, Girija G</creatorcontrib><title>AMP-Kinase Dysfunction Alters Notch Ligands to Impair Angiogenesis in Neonatal Pulmonary Hypertension</title><title>American journal of respiratory cell and molecular biology</title><addtitle>Am J Respir Cell Mol Biol</addtitle><description>Decreased angiogenesis contributes to persistent pulmonary hypertension of the newborn (PPHN); mechanisms remain unclear. AMPK (5'AMP activated protein kinase) is a key regulator of cell metabolism. We investigated the hypothesis that a decrease in AMPK function leads to mitochondrial dysfunction and altered balance of notch ligands delta-like 4 (DLL4) and Jagged 1 (Jag1) to impair angiogenesis in PPHN. Studies were done in fetal lambs with PPHN induced by prenatal ductus arteriosus constriction and gestation-matched control lambs. PPHN lambs were treated with saline or AMPK agonist metformin. Angiogenesis was assessed in lungs with micro-computed tomography angiography and histology. AMPK function; expression of mitochondrial electron transport chain (ETC) complex proteins I-V, Dll4, and Jag1; mitochondrial number; and
angiogenesis function were assessed in pulmonary artery endothelial cells (PAEC) from control and PPHN lambs. AMPK function was decreased in PPHN PAEC and lung sections. Expression of mitochondrial transcription factor, PGC-1α, ETC complex proteins I-V, and mitochondrial number were decreased in PPHN.
angiogenesis of PAEC and capillary number and vessel volume fraction in the lung were decreased in PPHN. Expression of DLL4 was increased and Jag1 was decreased in PAEC from PPHN lambs. AMPK agonists A769662 and metformin increased the mitochondrial complex proteins and number,
angiogenesis, and Jag1 levels and decreased DLL4 levels in PPHN PAEC. Infusion of metformin
increased the vessel density in PPHN lungs. Decreased AMPK function contributes to impaired angiogenesis in PPHN by altered balance of notch ligands in PPHN.</description><subject>AMP</subject><subject>Angiogenesis</subject><subject>Angiography</subject><subject>Animals</subject><subject>Animals, Newborn</subject><subject>Computed tomography</subject><subject>Ductus Arteriosus - embryology</subject><subject>Ductus Arteriosus - surgery</subject><subject>Electron Transport</subject><subject>Electron transport chain</subject><subject>Endothelial cells</subject><subject>Endothelial Cells - enzymology</subject><subject>Enzyme Activation</subject><subject>Female</subject><subject>Fetuses</subject><subject>Gestation</subject><subject>Hypertension</subject><subject>Hypertension, Pulmonary - enzymology</subject><subject>Hypertension, Pulmonary - physiopathology</subject><subject>Intracellular Signaling Peptides and Proteins - metabolism</subject><subject>Jagged-1 Protein - metabolism</subject><subject>Ligands</subject><subject>Lung - pathology</subject><subject>Membrane Proteins - metabolism</subject><subject>Metformin</subject><subject>Metformin - pharmacology</subject><subject>Metformin - therapeutic use</subject><subject>Mitochondria</subject><subject>Mitochondria - metabolism</subject><subject>Neonates</subject><subject>Neovascularization, Pathologic - drug therapy</subject><subject>Neovascularization, Pathologic - enzymology</subject><subject>Original Research</subject><subject>Persistent Fetal Circulation Syndrome - drug therapy</subject><subject>Persistent Fetal Circulation Syndrome - enzymology</subject><subject>Persistent Fetal Circulation Syndrome - pathology</subject><subject>Persistent Fetal Circulation Syndrome - physiopathology</subject><subject>Phosphorylation</subject><subject>Pregnancy</subject><subject>Protein kinase</subject><subject>Protein Kinases - metabolism</subject><subject>Protein Kinases - physiology</subject><subject>Protein transport</subject><subject>Pulmonary artery</subject><subject>Pulmonary hypertension</subject><subject>Pyrones - pharmacology</subject><subject>Receptors, Notch - metabolism</subject><subject>Sheep</subject><subject>Thiophenes - pharmacology</subject><subject>Threonine - metabolism</subject><subject>Transfection</subject><issn>1044-1549</issn><issn>1535-4989</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkc1vEzEQxS1ERUvhzglZ4sJlW48_1vYFKQqUVg1tD3C2vBtv6mrXDrYXKf99HaVU0MNoRpr3nmb0Q-gDkDOAVpynfurOKAHdECrF7fIVOgHBRMO10q_rTDhvQHB9jN7m_EAIUAXwBh0zSrhSUp0gt_hx11z7YLPDX3d5mENffAx4MRaXMr6Jpb_HK7-xYZ1xifhq2lqf8CJsfNy44LLP2Ad842KwxY74bh6nOqYdvtxtXSou5Br3Dh0Ndszu_VM_Rb8uvv1cXjar2-9Xy8Wq6bmE0mjFCKF66EB14Ih1Xbte9w4kVe2gNO-Bta1i2jElmB3WnRZSDhSI7shAW8tO0ZdD7nbuJletoSQ7mm3yUz3JROvN_5vg780m_jGSCqUoqQGfnwJS_D27XMzkc-_G0QYX52woExxky-Ve-umF9CHOKdT3DOUgVFuLVRU5qPoUc05ueD4GiNkzNHuGZs_QHBhWy8d_n3g2_IXGHgHrz5mI</recordid><startdate>202006</startdate><enddate>202006</enddate><creator>Rana, Ujala</creator><creator>Callan, Emily</creator><creator>Entringer, Brianna</creator><creator>Michalkiewicz, Teresa</creator><creator>Joshi, Amit</creator><creator>Parchur, Abdul K</creator><creator>Teng, Ru-Jeng</creator><creator>Konduri, Girija G</creator><general>American Thoracic Society</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7T5</scope><scope>7TM</scope><scope>7TO</scope><scope>H94</scope><scope>K9.</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>202006</creationdate><title>AMP-Kinase Dysfunction Alters Notch Ligands to Impair Angiogenesis in Neonatal Pulmonary Hypertension</title><author>Rana, Ujala ; Callan, Emily ; Entringer, Brianna ; Michalkiewicz, Teresa ; Joshi, Amit ; Parchur, Abdul K ; Teng, Ru-Jeng ; Konduri, Girija G</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c471t-9830029fb18b1e0aeb6ddce17286f894c1366839e3853afdb9577f2109b0f26a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>AMP</topic><topic>Angiogenesis</topic><topic>Angiography</topic><topic>Animals</topic><topic>Animals, Newborn</topic><topic>Computed tomography</topic><topic>Ductus Arteriosus - embryology</topic><topic>Ductus Arteriosus - surgery</topic><topic>Electron Transport</topic><topic>Electron transport chain</topic><topic>Endothelial cells</topic><topic>Endothelial Cells - enzymology</topic><topic>Enzyme Activation</topic><topic>Female</topic><topic>Fetuses</topic><topic>Gestation</topic><topic>Hypertension</topic><topic>Hypertension, Pulmonary - enzymology</topic><topic>Hypertension, Pulmonary - physiopathology</topic><topic>Intracellular Signaling Peptides and Proteins - metabolism</topic><topic>Jagged-1 Protein - metabolism</topic><topic>Ligands</topic><topic>Lung - pathology</topic><topic>Membrane Proteins - metabolism</topic><topic>Metformin</topic><topic>Metformin - pharmacology</topic><topic>Metformin - therapeutic use</topic><topic>Mitochondria</topic><topic>Mitochondria - metabolism</topic><topic>Neonates</topic><topic>Neovascularization, Pathologic - drug therapy</topic><topic>Neovascularization, Pathologic - enzymology</topic><topic>Original Research</topic><topic>Persistent Fetal Circulation Syndrome - drug therapy</topic><topic>Persistent Fetal Circulation Syndrome - enzymology</topic><topic>Persistent Fetal Circulation Syndrome - pathology</topic><topic>Persistent Fetal Circulation Syndrome - physiopathology</topic><topic>Phosphorylation</topic><topic>Pregnancy</topic><topic>Protein kinase</topic><topic>Protein Kinases - metabolism</topic><topic>Protein Kinases - physiology</topic><topic>Protein transport</topic><topic>Pulmonary artery</topic><topic>Pulmonary hypertension</topic><topic>Pyrones - pharmacology</topic><topic>Receptors, Notch - metabolism</topic><topic>Sheep</topic><topic>Thiophenes - pharmacology</topic><topic>Threonine - metabolism</topic><topic>Transfection</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Rana, Ujala</creatorcontrib><creatorcontrib>Callan, Emily</creatorcontrib><creatorcontrib>Entringer, Brianna</creatorcontrib><creatorcontrib>Michalkiewicz, Teresa</creatorcontrib><creatorcontrib>Joshi, Amit</creatorcontrib><creatorcontrib>Parchur, Abdul K</creatorcontrib><creatorcontrib>Teng, Ru-Jeng</creatorcontrib><creatorcontrib>Konduri, Girija G</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Immunology Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>American journal of respiratory cell and molecular biology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Rana, Ujala</au><au>Callan, Emily</au><au>Entringer, Brianna</au><au>Michalkiewicz, Teresa</au><au>Joshi, Amit</au><au>Parchur, Abdul K</au><au>Teng, Ru-Jeng</au><au>Konduri, Girija G</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>AMP-Kinase Dysfunction Alters Notch Ligands to Impair Angiogenesis in Neonatal Pulmonary Hypertension</atitle><jtitle>American journal of respiratory cell and molecular biology</jtitle><addtitle>Am J Respir Cell Mol Biol</addtitle><date>2020-06</date><risdate>2020</risdate><volume>62</volume><issue>6</issue><spage>719</spage><epage>731</epage><pages>719-731</pages><issn>1044-1549</issn><eissn>1535-4989</eissn><abstract>Decreased angiogenesis contributes to persistent pulmonary hypertension of the newborn (PPHN); mechanisms remain unclear. AMPK (5'AMP activated protein kinase) is a key regulator of cell metabolism. We investigated the hypothesis that a decrease in AMPK function leads to mitochondrial dysfunction and altered balance of notch ligands delta-like 4 (DLL4) and Jagged 1 (Jag1) to impair angiogenesis in PPHN. Studies were done in fetal lambs with PPHN induced by prenatal ductus arteriosus constriction and gestation-matched control lambs. PPHN lambs were treated with saline or AMPK agonist metformin. Angiogenesis was assessed in lungs with micro-computed tomography angiography and histology. AMPK function; expression of mitochondrial electron transport chain (ETC) complex proteins I-V, Dll4, and Jag1; mitochondrial number; and
angiogenesis function were assessed in pulmonary artery endothelial cells (PAEC) from control and PPHN lambs. AMPK function was decreased in PPHN PAEC and lung sections. Expression of mitochondrial transcription factor, PGC-1α, ETC complex proteins I-V, and mitochondrial number were decreased in PPHN.
angiogenesis of PAEC and capillary number and vessel volume fraction in the lung were decreased in PPHN. Expression of DLL4 was increased and Jag1 was decreased in PAEC from PPHN lambs. AMPK agonists A769662 and metformin increased the mitochondrial complex proteins and number,
angiogenesis, and Jag1 levels and decreased DLL4 levels in PPHN PAEC. Infusion of metformin
increased the vessel density in PPHN lungs. Decreased AMPK function contributes to impaired angiogenesis in PPHN by altered balance of notch ligands in PPHN.</abstract><cop>United States</cop><pub>American Thoracic Society</pub><pmid>32048878</pmid><doi>10.1165/rcmb.2019-0275OC</doi><tpages>13</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | AMP Angiogenesis Angiography Animals Animals, Newborn Computed tomography Ductus Arteriosus - embryology Ductus Arteriosus - surgery Electron Transport Electron transport chain Endothelial cells Endothelial Cells - enzymology Enzyme Activation Female Fetuses Gestation Hypertension Hypertension, Pulmonary - enzymology Hypertension, Pulmonary - physiopathology Intracellular Signaling Peptides and Proteins - metabolism Jagged-1 Protein - metabolism Ligands Lung - pathology Membrane Proteins - metabolism Metformin Metformin - pharmacology Metformin - therapeutic use Mitochondria Mitochondria - metabolism Neonates Neovascularization, Pathologic - drug therapy Neovascularization, Pathologic - enzymology Original Research Persistent Fetal Circulation Syndrome - drug therapy Persistent Fetal Circulation Syndrome - enzymology Persistent Fetal Circulation Syndrome - pathology Persistent Fetal Circulation Syndrome - physiopathology Phosphorylation Pregnancy Protein kinase Protein Kinases - metabolism Protein Kinases - physiology Protein transport Pulmonary artery Pulmonary hypertension Pyrones - pharmacology Receptors, Notch - metabolism Sheep Thiophenes - pharmacology Threonine - metabolism Transfection |
| title | AMP-Kinase Dysfunction Alters Notch Ligands to Impair Angiogenesis in Neonatal Pulmonary Hypertension |
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