L
Laura S. Haneline
Researcher at Indiana University
Publications - 67
Citations - 3206
Laura S. Haneline is an academic researcher from Indiana University. The author has contributed to research in topics: Progenitor cell & Haematopoiesis. The author has an hindex of 29, co-authored 64 publications receiving 2991 citations. Previous affiliations of Laura S. Haneline include VU University Medical Center & University of Missouri–St. Louis.
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Journal ArticleDOI
Human CD34+AC133+VEGFR-2+ cells are not endothelial progenitor cells but distinct, primitive hematopoietic progenitors
Jamie Case,Laura E. Mead,Waylan K. Bessler,Daniel N. Prater,Hilary White,M. Reza Saadatzadeh,Janak R. Bhavsar,Mervin C. Yoder,Laura S. Haneline,David A. Ingram +9 more
TL;DR: It is found that CD34+AC133+VEGFR-2+ cells are HPCs that do not yield EC progeny, and the biological mechanism for their correlation with cardiovascular disease needs to be reexamined.
Journal ArticleDOI
BMP10 is essential for maintaining cardiac growth during murine cardiogenesis.
Hanying Chen,Shu Shi,Lourdes Acosta,Weiming Li,Jonathan T. Lu,Shideng Bao,Zhuang Chen,Zuocheng Yang,Michael D. Schneider,Kenneth R. Chien,Simon J. Conway,Mervin C. Yoder,Laura S. Haneline,Diego Franco,Weinian Shou +14 more
TL;DR: An important pathway that involves a genetic interaction between BMP10, cell cycle regulatory proteins and several major cardiac transcription factors in orchestrating this transition in cardiogenesis at mid-gestation may provide an underlying mechanism for understanding the pathogenesis of both structural and functional congenital heart defects.
Journal ArticleDOI
Multiple Inhibitory Cytokines Induce Deregulated Progenitor Growth and Apoptosis in Hematopoietic Cells From Fac−/− Mice
Laura S. Haneline,Hal E. Broxmeyer,Scott Cooper,Giao Hangoc,Madeleine Carreau,Manuel Buchwald,D. Wade Clapp +6 more
TL;DR: A role of Fac in affecting the signaling of multiple cytokine pathways is suggested and cytokine-mediated apoptosis as a major mechanism responsible for BM failure observed in FA patients is suggested.
Journal ArticleDOI
Loss of FancC Function Results in Decreased Hematopoietic Stem Cell Repopulating Ability
Laura S. Haneline,Laura S. Haneline,Troy A. Gobbett,Troy A. Gobbett,Rema Ramani,Rema Ramani,Madeleine Carreau,Madeleine Carreau,Manuel Buchwald,Manuel Buchwald,Mervin C. Yoder,Mervin C. Yoder,D. Wade Clapp,D. Wade Clapp +13 more
TL;DR: It is indicated that loss of FancC function results in reduced in vivo repopulating ability of pluripotential hematopoietic stem cells, which may play a role in the development of the BM failure in FA patients.
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In vitro hyperglycemia or a diabetic intrauterine environment reduces neonatal endothelial colony forming cell numbers and function
David A. Ingram,Izlin Z. Lien,Laura E. Mead,Myka L. Estes,Daniel N. Prater,Ethel Derr-Yellin,Linda A. DiMeglio,Laura S. Haneline +7 more
TL;DR: It is demonstrated that hyperglycemia or exposure to a diabetic intrauterine environment diminishes neonatal ECFC function both in vitro and in vivo, providing potential mechanistic insights into the long-term cardiovascular complications observed in newborns of diabetic pregnancies.