S
S. Alex Mitsialis
Researcher at Boston Children's Hospital
Publications - 52
Citations - 5219
S. Alex Mitsialis is an academic researcher from Boston Children's Hospital. The author has contributed to research in topics: Pulmonary hypertension & Mesenchymal stem cell. The author has an hindex of 27, co-authored 50 publications receiving 4229 citations. Previous affiliations of S. Alex Mitsialis include Columbia University & Harvard University.
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Journal ArticleDOI
Exosomes Mediate the Cytoprotective Action of Mesenchymal Stromal Cells on Hypoxia-Induced Pulmonary Hypertension
Changjin Lee,S. Alex Mitsialis,Muhammad Aslam,Sally H. Vitali,Eleni Vergadi,Georgios Konstantinou,Konstantinos Sdrimas,Angeles Fernandez-Gonzalez,Stella Kourembanas +8 more
TL;DR: This study indicates that MEX exert a pleiotropic protective effect on the lung and inhibit pulmonary hypertension through suppression of hyperproliferative pathways, including STAT3-mediated signaling induced by hypoxia.
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Bone Marrow Stromal Cells Attenuate Lung Injury in a Murine Model of Neonatal Chronic Lung Disease
Muhammad Aslam,Rajiv Baveja,Olin D. Liang,Angeles Fernandez-Gonzalez,Changjin Lee,S. Alex Mitsialis,Stella Kourembanas +6 more
TL;DR: BMSCs act in a paracrine manner via the release of immunomodulatory factors to ameliorate the parenchymal and vascular injury of BPD in vivo.
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Mesenchymal Stromal Cell Exosomes Ameliorate Experimental Bronchopulmonary Dysplasia and Restore Lung Function through Macrophage Immunomodulation
Gareth R. Willis,Angeles Fernandez-Gonzalez,Jamie N. Anastas,Sally H. Vitali,Xianlan Liu,Maria Ericsson,April Kwong,S. Alex Mitsialis,Stella Kourembanas +8 more
TL;DR: MSC‐exo treatment blunts HyrX‐associated inflammation and alters the hyperoxic lung transcriptome, which results in alleviation of HYRX‐induced BPD, improvement of lung function, decrease in fibrosis and pulmonary vascular remodeling, and amelioration of pulmonary hypertension.
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Targeted expression of heme oxygenase-1 prevents the pulmonary inflammatory and vascular responses to hypoxia
Tohru Minamino,Helen Christou,Chung-Ming Hsieh,Yuxiang Liu,Vijender Dhawan,Nader G. Abraham,Mark A. Perrella,S. Alex Mitsialis,Stella Kourembanas +8 more
TL;DR: Heme oxygenase-1 transgenic mice were protected from the development of both pulmonary inflammation as well as hypertension and vessel wall hypertrophy induced by hypoxia, suggesting an important protective function of enzymatic products of HO-1 activity as inhibitors of Hypoxia-induced vasoconstrictive and proinflammatory pathways.
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Carbon Monoxide Controls the Proliferation of Hypoxic Vascular Smooth Muscle Cells
TL;DR: It is reported here that under hypoxia, VSMC-derived CO is an important regulator of VSMC proliferation, andLimiting VSMC growth by increasing the release of CO may represent a key event in the body’s compensatory responses to Hypoxia.