Gestational intermittent hyperoxia rescues murine genetic congenital heart disease in part

Autor: Cassandra F. Doll, Natalia J. Pereira, Mustafa S. Hashimi, Tabor J. Grindrod, Fariz F. Alkassis, Lawrence X. Cai, Una Milovanovic, Adriana I. Sandino, Hideko Kasahara

Publikováno v: Scientific Reports, Vol 11, Iss 1, Pp 1-9 (2021)

Abstract Cardiac development is a dynamic process, temporally and spatially. When disturbed, it leads to congenital cardiac anomalies that affect approximately 1% of live births. Genetic variants in several loci lead to anomalies, with the transcript

Externí odkaz: https://doaj.org/article/497bb0ea0fb842698545a733bc10deff

Defective coronary vessel organization and reduction of VEGF‐A in mouse embryonic hearts with gestational mild hypoxia

Autor: Hideko Kasahara, Lawrence X. Cai, Fariz F. Alkassis

Publikováno v: Developmental Dynamics. 249:636-645

BACKGROUND Vasculature is formed by responding to homeostatic tissue demands including in developing hearts. Hypoxia generally stimulates vascular formation in which vascular endothelial growth factor A (VEGF-A) plays a critical role. Gestational hyp

Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::40ceb1320288e609b33bd86ac8679cec
https://doi.org/10.1002/dvdy.149

Gestational intermittent hyperoxia rescues murine genetic congenital heart disease in part

Autor: Una Milovanovic, Lawrence X. Cai, Cassandra F. Doll, Natalia J. Pereira, Mustafa S. Hashimi, Hideko Kasahara, Tabor Grindrod, Fariz F. Alkassis, Adriana I. Sandino

Publikováno v: Scientific Reports
Scientific Reports, Vol 11, Iss 1, Pp 1-9 (2021)

Cardiac development is a dynamic process, temporally and spatially. When disturbed, it leads to congenital cardiac anomalies that affect approximately 1% of live births. Genetic variants in several loci lead to anomalies, with the transcription facto

Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::dee448d9e6d9ceaaed7f4dcf123c04b5
https://pubmed.ncbi.nlm.nih.gov/33758249

Extracellular Matrix Disparities in an Nkx2-5 Mutant Mouse Model of Congenital Heart Disease.

Autor: Bousalis D; J. Crayton Pruitt Family Department of Biomedical Engineering, University of Florida, Gainesville, FL, United States., Lacko CS; J. Crayton Pruitt Family Department of Biomedical Engineering, University of Florida, Gainesville, FL, United States., Hlavac N; J. Crayton Pruitt Family Department of Biomedical Engineering, University of Florida, Gainesville, FL, United States., Alkassis F; Department of Physiology and Functional Genomics, University of Florida, Gainesville, FL, United States., Wachs RA; Department of Biological Systems Engineering, University of Nebraska-Lincoln, Lincoln, NE, United States., Mobini S; Instituto de Micro y Nanotecnología, IMN-CNM, CSIC (CEI UAM+CSIC), Madrid, Spain.; Centro de Biología Molecular Severo Ochoa (CBMSO, UAM-CSIC), Universidad Autónoma de Madrid, Madrid, Spain., Schmidt CE; J. Crayton Pruitt Family Department of Biomedical Engineering, University of Florida, Gainesville, FL, United States., Kasahara H; Department of Physiology and Functional Genomics, University of Florida, Gainesville, FL, United States.

Publikováno v: Frontiers in cardiovascular medicine [Front Cardiovasc Med] 2020 May 29; Vol. 7, pp. 93. Date of Electronic Publication: 2020 May 29 (Print Publication: 2020).