Stella Kourembanas, MD
Chief, Division of Newborn Medicine; Chair, Harvard Neonatal-Perinatal Medicine Program
Clement A. Smith Professor of Pediatrics, Harvard Medical School
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Stella Kourembanas, MD
Chief, Division of Newborn Medicine; Chair, Harvard Neonatal-Perinatal Medicine Program
Clement A. Smith Professor of Pediatrics, Harvard Medical School
Medical Services
Languages
English
Greek
Education
Undergraduate School
Barnard College
1978
New York
NY
Medical School
New York University School of Medicine
1982
New York
NY
Internship
Massachusetts General Hospital
1983
Boston
MA
Residency
Massachusetts General Hospital
1984
Boston
MA
Fellowship
Joint Program in Neonatology
Harvard Medical School
1987
Boston
MA
Certifications
American Board of Pediatrics (General)
American Board of Pediatrics (Neonatal-Perinatal Medicine)
Professional History
Dr. Stella Kourembanas is a practicing Neonatologist, the Chief of the Division of Newborn Medicine at Boston Children’s Hospital and the Academic Chair of the Harvard Neonatal-Perinatal Medicine Program. As a physician scientist, her research focuses on newborn lung biology exploring the pathophysiology of lung injury and repair and regenerative medicine, testing stem cell - based therapies for diseases affecting infants in the perinatal period. Her contributions to newborn health span the realm of basic science, translational research and clinical trials that have led to new treatments for critically ill neonates, including those with pulmonary hypertension and bronchopulmonary dysplasia.
Under her leadership, the Division of Newborn Medicine has pioneered unique programs aimed at providing science-based care to critically ill newborns in the level IV Boston Children’s Hospital Neonatal Intensive Care Unit. Such key initiatives include a Program in Neonatal Genomics headed by Dr. Pankaj Agrawal and a Center for Fetal Neonatal Neuroimaging & Developmental Science with Dr. Ellen Grant as founding director. Both programs aimed at the diagnosis, monitoring, and personalized treatment of sick newborns that is tailored to the individual patient’s condition. Another Program in Neonatal Epigenetics with Dr. Yang Shi as director, explores the epigenetic regulation of developmental diseases, innate immunity, and transgenerational heritability of disease. She has also established a Program in Newborn Regenerative Medicine headed by Dr. S. Alex Mitsialis, as well as a continually growing program in Neonatal Clinical Research directed by Dr. Martha Sola-Visner that includes over 100 clinical studies testing novel monitoring devices and therapies, including clinical trials in neonatal transfusion medicine and stem cell-based treatments for diseases of the newborn infant.
Dr. Kourembanas serves on many national scientific review committees including those in the National Institutes of Health. She has authored >100 original research papers as well as review articles on state-of-the-art next generation treatments for conditions affecting the newborn lung and brain in the perinatal period.
Approach to Care
In the Boston Children’s Hospital (BCH) Neonatal Intensive Care Unit (NICU) our philosophy is to ensure that every patient receives the best care for the best possible outcomes. We consider our “patient” to be the baby and the family; we are constantly striving to serve the needs of both. This requires a team based approach with all members being essential.
Publications
Immunoregulatory Macrophages Modify Local Pulmonary Immunity and Ameliorate Hypoxic Pulmonary Hypertension. View Abstract
Mesenchymal stromal cell extracellular vesicles improve lung development in mechanically ventilated preterm lambs. View Abstract
SOCS3 regulates pathological retinal angiogenesis through modulating SPP1 expression in microglia and macrophages. View Abstract
Photoreceptors inhibit pathological retinal angiogenesis through transcriptional regulation of Adam17 via c-Fos. View Abstract
No Place Like Home: Improving the Transition From NICU to Home Through the NICU to Nursery Program. View Abstract
Immunoregulatory macrophages modify local pulmonary immunity and ameliorate hypoxic-pulmonary hypertension. View Abstract
Pericytes Contribute to Flow-induced Pulmonary Hypertension. View Abstract
Harnessing the therapeutic potential of the stem cell secretome in neonatal diseases. View Abstract
Second International Pulmonary Hypertension/Heart Failure Symposium-Structural heart disease, right ventricular dysfunction, and stem cell therapy: The European Pediatric Pulmonary Vascular Disease Network. View Abstract
Mesenchymal Stromal/Stem Cell Extracellular Vesicles and Perinatal Injury: One Formula for Many Diseases. View Abstract
Diagnosis and management of pulmonary hypertension in infants with bronchopulmonary dysplasia. View Abstract
Urine Proteomics for Noninvasive Monitoring of Biomarkers in Bronchopulmonary Dysplasia. View Abstract
Antenatal Mesenchymal Stromal Cell Extracellular Vesicle Therapy Prevents Preeclamptic Lung Injury in Mice. View Abstract
Extracellular Vesicles Protect the Neonatal Lung from Hyperoxic Injury through the Epigenetic and Transcriptomic Reprogramming of Myeloid Cells. View Abstract
Antenatal mesenchymal stromal cell extracellular vesicle treatment preserves lung development in a model of bronchopulmonary dysplasia due to chorioamnionitis. View Abstract
Intratracheal transplantation of trophoblast stem cells attenuates acute lung injury in mice. View Abstract
Mesenchymal stromal cell-derived syndecan-2 regulates the immune response during sepsis to foster bacterial clearance and resolution of inflammation. View Abstract
Acetazolamide Improves Right Ventricular Function and Metabolic Gene Dysregulation in Experimental Pulmonary Arterial Hypertension. View Abstract
Mesenchymal Stromal Cell-Derived Extracellular Vesicles Restore Thymic Architecture and T Cell Function Disrupted by Neonatal Hyperoxia. View Abstract
Therapeutic Effects of Mesenchymal Stromal Cell-Derived Small Extracellular Vesicles in Oxygen-Induced Multi-Organ Disease: A Developmental Perspective. View Abstract
Mesenchymal stromal cell-derived extracellular vesicle therapy prevents preeclamptic physiology through intrauterine immunomodulation†. View Abstract
Perinatal Hypoxia-Inducible Factor Stabilization Preserves Lung Alveolar and Vascular Growth in Experimental Bronchopulmonary Dysplasia. View Abstract
Gene and Stem Cell Therapies for Fetal Care: A Review. View Abstract
Mesenchymal stromal cell-derived small extracellular vesicles restore lung architecture and improve exercise capacity in a model of neonatal hyperoxia-induced lung injury. View Abstract
Pulmonary hypertension in bronchopulmonary dysplasia. View Abstract
Echocardiographic markers of pulmonary hemodynamics and right ventricular hypertrophy in rat models of pulmonary hypertension. View Abstract
Mesenchymal stromal cell exosomes prevent and revert experimental pulmonary fibrosis through modulation of monocyte phenotypes. View Abstract
Heme oxygenase-1 dampens the macrophage sterile inflammasome response and regulates its components in the hypoxic lung. View Abstract
Carbonic Anhydrase Inhibition Ameliorates Inflammation and Experimental Pulmonary Hypertension. View Abstract
Macrophage Immunomodulation: The Gatekeeper for Mesenchymal Stem Cell Derived-Exosomes in Pulmonary Arterial Hypertension? View Abstract
PPAR? agonist pioglitazone reverses pulmonary hypertension and prevents right heart failure via fatty acid oxidation. View Abstract
Reply to Muraca et al.: Exosome Treatment of Bronchopulmonary Dysplasia: How Pure Should Your Exosome Preparation Be? View Abstract
Mesenchymal Stromal Cell Exosomes Ameliorate Experimental Bronchopulmonary Dysplasia and Restore Lung Function through Macrophage Immunomodulation. View Abstract
Impaired Pulmonary Arterial Vasoconstriction and Nitric Oxide-Mediated Relaxation Underlie Severe Pulmonary Hypertension in the Sugen-Hypoxia Rat Model. View Abstract
"Good things come in small packages": application of exosome-based therapeutics in neonatal lung injury. View Abstract
Toward Exosome-Based Therapeutics: Isolation, Heterogeneity, and Fit-for-Purpose Potency. View Abstract
Can We Cure Bronchopulmonary Dysplasia? View Abstract
Therapeutic Applications of Extracellular Vesicles: Perspectives from Newborn Medicine. View Abstract
Stem cell-based therapies for the newborn lung and brain: Possibilities and challenges. View Abstract
Systemic Administration of Human Bone Marrow-Derived Mesenchymal Stromal Cell Extracellular Vesicles Ameliorates Aspergillus Hyphal Extract-Induced Allergic Airway Inflammation in Immunocompetent Mice. View Abstract
The Sugen 5416/hypoxia mouse model of pulmonary hypertension revisited: long-term follow-up. View Abstract
Exosomes: vehicles of intercellular signaling, biomarkers, and vectors of cell therapy. View Abstract
An Argonaute 2 switch regulates circulating miR-210 to coordinate hypoxic adaptation across cells. View Abstract
Expanding the pool of stem cell therapy for lung growth and repair. View Abstract
Stem cell-based therapy for newborn lung and brain injury: feasible, safe, and the next therapeutic breakthrough? View Abstract
MSC microvesicles for the treatment of lung disease: a new paradigm for cell-free therapy. View Abstract
Endothelial indoleamine 2,3-dioxygenase protects against development of pulmonary hypertension. View Abstract
Cell therapy for lung diseases. Report from an NIH-NHLBI workshop, November 13-14, 2012. View Abstract
Diffuse lung disease in children: summary of a scientific conference. View Abstract
Exosomes mediate the cytoprotective action of mesenchymal stromal cells on hypoxia-induced pulmonary hypertension. View Abstract
Perinatal stress, brain inflammation and risk of autism-review and proposal. View Abstract
Mesenchymal stem cell-mediated reversal of bronchopulmonary dysplasia and associated pulmonary hypertension. View Abstract
Regenerative pulmonary medicine: potential and promise, pitfalls and challenges. View Abstract
Bronchioalveolar stem cells increase after mesenchymal stromal cell treatment in a mouse model of bronchopulmonary dysplasia. View Abstract
Vasculoprotective effects of heme oxygenase-1 in a murine model of hyperoxia-induced bronchopulmonary dysplasia. View Abstract
Improved pulmonary vascular reactivity and decreased hypertrophic remodeling during nonhypercapnic acidosis in experimental pulmonary hypertension. View Abstract
Early macrophage recruitment and alternative activation are critical for the later development of hypoxia-induced pulmonary hypertension. View Abstract
Mesenchymal stromal cells expressing heme oxygenase-1 reverse pulmonary hypertension. View Abstract
In-house neonatology: what are we waiting for? View Abstract
Bone marrow stromal cells attenuate lung injury in a murine model of neonatal chronic lung disease. View Abstract
Divergent cardiopulmonary actions of heme oxygenase enzymatic products in chronic hypoxia. View Abstract
Mutation of murine adenylate kinase 7 underlies a primary ciliary dyskinesia phenotype. View Abstract
Absence of cyclooxygenase-2 exacerbates hypoxia-induced pulmonary hypertension and enhances contractility of vascular smooth muscle cells. View Abstract
Absence of COX-2 exacerbates hypoxia-induced pulmonary hypertension and enhances contractility of vascular smooth muscle cells View Abstract
Hypoxia regulates bone morphogenetic protein signaling in vascular smooth muscle cells through CtBP-1 View Abstract
Hypoxia regulates bone morphogenetic protein signaling through C-terminal-binding protein 1. View Abstract
Bone marrow derived mesenchymal stem cells expressing human heme oxygenase-1 (HO-1) reverse hypoxic pulmonary hypertension in HO-1 null mice View Abstract
Heme oxygenase-1 (HO-1) overexpression prevents fibrosis and iron deposition in developmental lung injury View Abstract
Exacerbation of hypoxia-induced pulmonary hypertension and vascular remodeling in COX-2 deficient mice View Abstract
Mechanisms of heme oxygenase-1-mediated cardiac and pulmonary vascular protection in chronic hypoxia: roles of carbon monoxide and bilirubin. View Abstract
Pulmonary hypertension and right ventricular dysfunction in growth-restricted, extremely low birth weight neonates. View Abstract
Extracellular acidosis induces heme oxygenase-1 expression in vascular smooth muscle cells. View Abstract
HO-1 mediated cardiac protection in chronic hypoxia: Role of carbon monoxide and bilirubin View Abstract
Bone-marrow derived mesenchymal stem cells expressing human HO-1 reverse hypoxic pulmonary hypertension in HO-1 null mice View Abstract
Heme Oxygenase-1 overexpression decreases alveolar remodeling and iron deposition in developmental lung injury View Abstract
Hypoxia induces macrophage inflammatory protein-2 (MIP-2) gene expression in murine macrophages via NF-kappaB: the prominent role of p42/ p44 and PI3 kinase pathways. View Abstract
Hypoxia suppresses bone morphogenetic protein mediated Id1 gene activation n human pulmonary artery smooth muscle cells View Abstract
Mechanisms of HO-1 cytoprotection in hypoxic pulmonary hypertension View Abstract
Shock View Abstract
Effect of heme oxygenase-1 overexpression in two models of lung inflammation. View Abstract
Regulation of heme oxygenase-1 (HO-1) gene expression in vascular smooth muscle cells by extracellular acidosis View Abstract
Hypoxia and carbon monoxide in the vasculature. View Abstract
Response of the developing lung to injury (Haddad GG, Abman S, Chernik V, eds.) View Abstract
Regulation of macrophage inflammatory protein-2 (MIP-2) gene expression by hypoxia View Abstract
Targeted expression of heme oxygenase-1 and pulmonary responses to hypoxia View Abstract
Mechanisms of telomerase induction during vascular smooth muscle cell proliferation. View Abstract
Targeted expression of heme oxygenase-1 prevents the pulmonary inflammatory and vascular responses to hypoxia. View Abstract
Child health status, neurodevelopmental outcome, and parental satisfaction in a randomized, controlled trial of nitric oxide for persistent pulmonary hypertension of the newborn. View Abstract
Hypoxia extends the life span of vascular smooth muscle cells through telomerase activation. View Abstract
Inhaled nitric oxide reduces the need for extracorporeal membrane oxygenation in infants with persistent pulmonary hypertension of the newborn. View Abstract
Prevention of hypoxia-induced pulmonary hypertension by enhancement of endogenous heme oxygenase-1 in the rat. View Abstract
Transgenic mice overexpressing heme oxygenase-1 (HO-1) in the lung are protected from development of hypoxia-induced pulmonary hypertension: Evidence of antiinflammatory effects of HO-1 View Abstract
Heme oxygenase and pulmonary responses to hypoxia View Abstract
Herbimycin A and geldanamycin inhibit the hypoxic induction of the vascular endothelial growth factor (VEGF) gene in pulmonary artery endothelial cells View Abstract
Extracellular acidosis induces heme oxygenase-1 (HO-1) gene expression in vascular smooth muscle cells View Abstract
The role of heme oxygenase-1 in the regulation of cardiomyocyte death during ischemia/reperfusion View Abstract
Generation of a dominant-negative mutant of endothelial PAS domain protein 1 by deletion of a potent C-terminal transactivation domain. View Abstract
Hypoxia induces severe right ventricular dilatation and infarction in heme oxygenase-1 null mice. View Abstract
Functional analysis of endothelial PAS domain Protein 1: Generation of a dominant negative mutant by deleting C-terminal potent transactivation domain View Abstract
Inhaled nitric oxide does not affect adenosine 5'-diphosphate-dependent platelet activation in infants with persistent pulmonary hypertension of the newborn. View Abstract
Hypoxic responses of vascular cells. View Abstract
Carbon monoxide and nitric oxide suppress the hypoxic induction of vascular endothelial growth factor gene via the 5' enhancer. View Abstract
Increased vascular endothelial growth factor production in the lungs of rats with hypoxia-induced pulmonary hypertension. View Abstract
Characterization of functional domains of endothelial PAS domain protein-1 and generation of a dominant negative mutant View Abstract
Combination of inhaled nitric oxide with high frequency ventilation reduces the need for extracorporeal membrane oxygenation in infants with persistant pulmonary hypertension of the newborn: Results from a single center trial View Abstract
Activation of KDR/flk-1 promoter by endothelial PAS domain protein-1: Potential role of endothelial PAS domain protein-1 in endothelial cell differentiation View Abstract
Shock View Abstract
Carbon monoxide controls the proliferation of hypoxic vascular smooth muscle cells. View Abstract
Improved oxygenation in a randomized trial of inhaled nitric oxide for persistent pulmonary hypertension of the newborn. View Abstract
Endothelin-1 production during the acute chest syndrome in sickle cell disease. View Abstract
Effect of inhaled nitric oxide on endothelin-1 and cyclic guanosine 5'-monophosphate plasma concentrations in newborn infants with persistent pulmonary hypertension. View Abstract
Mechanisms by which oxygen regulates gene expression and cell-cell interaction in the vasculature. View Abstract
Prevention of hypoxia-induced pulmonary hypertension by enhancement of endogenous heme oxygenase-1 in the rat View Abstract
Endogenous carbon monoxide regulates tube formation by human microvascular endothelial cells under high glucose View Abstract
Inhaled nitric oxide does not inhibit platelet activation in infants with persistent pulmonary hypertension of the newborn (PPHN) View Abstract
Regulation of Carbon Monoxide Producation and Vascular Responses View Abstract
Improved oxygenation in a randomized trial of inhaled nitric oxide for PPHN View Abstract
Endothelial cell expression of vasoconstrictors and growth factors is regulated by smooth muscle cell-derived carbon monoxide. View Abstract
Basic fibroblast growth factor increases nitric oxide synthase production in bovine endothelial cells. View Abstract
Hypoxia regulates vascular endothelial growth factor gene expression in endothelial cells. Identification of a 5' enhancer. View Abstract
Smooth muscle cell-derived carbon monoxide is a regulator of vascular cGMP. View Abstract
Structural characterization and specificity of expression of E2F-5: a new member of the E2F family of transcription factors. View Abstract
Inhaled NO for PPHN: Basic Biology to Clinical Application (Fanaroff AA and Klaus MH, eds.) View Abstract
Increased epithelial cell expression of vascular endothelial growth factor (VEGF) in the lungs of animals with hypoxia-induced pulmonary hypertension View Abstract
Smooth muscle cell-derived carbon monoxide is a regulator of endothelial cell gene expression and cGMP content View Abstract
Persistent pulmonary hypertension of the newborn: Role of nitric oxide View Abstract
Hypoxia upregulates the transcription of human vascular endothelial growth factor gene via a 28-bp enhancer View Abstract
Hypoxia increases cGMP levels in rat vascular smooth muscle cells via inducation of heme oxygenase-1 View Abstract
Hypoxia inhibits expression of eNOS via transcriptional and posttranscriptional mechanisms. View Abstract
Hypoxia and endothelial-smooth muscle cell interactions in the lung. View Abstract
Transforming growth factor-beta 1, but not dexamethasone, down-regulates nitric-oxide synthase mRNA after its induction by interleukin-1 beta in rat smooth muscle cells. View Abstract
Inhaled nitric oxide (NO) alters endogenous endothelin-1 (ET-1) and cGMP levels in newborns with persistent pulmonary hypertension (PPHN) View Abstract
Nitric oxide regulates the expression of vasoconstrictors and growth factors by vascular endothelium under both normoxia and hypoxia. View Abstract
Hypoxia inhibits nitric oxide synthase (NOS) gene expression and nitric oxide (NO) production in endothelial cells View Abstract
Tumor necrosis factor increases transcription of the heparin-binding epidermal growth factor-like growth factor gene in vascular endothelial cells. View Abstract
Hypoxic responses of the neonatal endothelium. View Abstract
Feedback loops regulated the production of vasoactive agents by human endothelial cells View Abstract
Hypoxia induces endothelin gene expression and secretion in cultured human endothelium. View Abstract
Shock View Abstract
Molecular mechanisms contrbuting to hypoxic vasoconstriction View Abstract
Oxygen tension regulates the expression of the platelet-derived growth factor-B chain gene in human endothelial cells. View Abstract
Fetal rat lung fibroblasts produce a TGF beta homolog that blocks alveolar type II cell maturation. View Abstract
Molecular mechanisms contributing to vaso-occlusion in sickle cell disease View Abstract
Platelet-derived growth factor production by human umbilical vein endothelial cells is regulated by basic fibroblast growth factor. View Abstract
Hypoxia stimulates platelet-derived growth factor (PDGF) production by human umbilical vein endothelial cells (HUVEC) View Abstract
Regulation of platelet-derived growth factor (PDGF) gene expression by basic fibroblast growth factor (bFGF) in human umbilical vein endothelial cells View Abstract
Endothelial cells synthesize basic fibroblast growth factor and transforming growth factor beta. View Abstract
Immortalization of human endothelial cells by murine sarcoma viruses, without morphologic transformation. View Abstract
Increases in the 35kDa surfactant-associated protein and its mRNA following in vivo dexamethasone treatment of fetal and neonatal rats View Abstract
Primary translation products, biosynthesis, and tissue specificity of the major surfactant protein in rat. View Abstract
Developmental profile of surgactant associated protein (Apoprotein A) in the rat lung View Abstract
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