Data from: GATA2 controls lymphatic endothelial cell junctional integrity and lymphovenous valve morphogenesis through miR-126

Mahamud, Md. Riaj, Oklahoma Medical Research Foundation

Geng, Xin, Oklahoma Medical Research Foundation

Ho, YenChun, Oklahoma Medical Research Foundation

Cha, Boksik, Oklahoma Medical Research Foundation

Kim, Yuenhee, The University of Texas at Dallas

Ma, Jing, Tulane University

Chen, Lijuan, Oklahoma Medical Research Foundation

Myers, Greggory, University of Michigan Medical School

Camper, Sally, University of Michigan Medical School

Mustacich, Debbie, University of Arizona

Witte, Marlys, University of Arizona

Choi, Dongwon, University of Southern California

Hong, Young-Kwon, University of Southern California

Chen, Hong, Boston Children's Hospital

Varshney, Gaurav, Oklahoma Medical Research Foundation

Engel, James D, University of Michigan Medical School

Wang, Shusheng, Tulane University

Kim, Tae-Hoon, The University of Texas at Dallas

Lim, Kim-Chew, University of Michigan Medical School

Srinivasan, Sathish, Oklahoma Medical Research Foundation

sathish-srinivasan@omrf.org

Published Oct 25, 2019 on Dryad. https://doi.org/10.5061/dryad.3st9688

Cite this dataset

Mahamud, Md. Riaj et al. (2019). Data from: GATA2 controls lymphatic endothelial cell junctional integrity and lymphovenous valve morphogenesis through miR-126 [Dataset]. Dryad. https://doi.org/10.5061/dryad.3st9688

Abstract

Mutations in the transcription factor GATA2 cause lymphedema. GATA2 is necessary for the development of lymphatic valves (LVs) and lymphovenous valves (LVVs), and for the patterning of lymphatic vessels. Here, we report that GATA2 is not necessary for valvular endothelial cell (VEC) differentiation. Instead, GATA2 is required for VEC maintenance and morphogenesis. GATA2 is also necessary for the expression of cell junction molecules VE-Cadherin and Claudin5 in lymphatic vessels. We identified miR-126 as a target of GATA2, and miR-126-/- embryos recapitulate the phenotypes of mice lacking GATA2. Primary human lymphatic endothelial cells (HLECs) lacking GATA2 (GATA2ΔHLEC) have altered expression of Claudin5 and VE-Cadherin, and blocking miR-126 activity in HLECs phenocopies these changes in expression. Importantly, overexpression of miR-126 in GATA2ΔHLEC significantly rescues the cell junction defects. Thus, our work defines a new mechanism of GATA2 and uncovers miR-126 as a novel regulator of mammalian lymphatic vascular development.

Usage notes

GATA2KD1

RNA-seq data from primary human lymphatic endothelial cells treated with shGATA2 (Sample1).

GATA2KD2

RNA-seq data from primary human lymphatic endothelial cells treated with shGATA2 (Sample2).

GATA2KD3

RNA-seq data from primary human lymphatic endothelial cells treated with shGATA2 (Sample3).

CONTROL3

RNA-seq data from primary human lymphatic endothelial cells treated with pLV control viruses (Sample3).

CONTROL2

RNA-seq data from primary human lymphatic endothelial cells treated with pLV control viruses (Sample2).

CONTROL1

RNA-seq data from primary human lymphatic endothelial cells treated with pLV control viruses (Sample1).

mir126KD_1

RNA-seq data from primary human lymphatic endothelial cells treated with miR-126 sponge viruses (Sample1).

mir126KD_2

RNA-seq data from primary human lymphatic endothelial cells treated with miR-126 sponge viruses (Sample2).

mir126KD_3

RNA-seq data from primary human lymphatic endothelial cells treated with miR-126 sponge viruses (Sample3).

CTRL_3

RNA-seq data from primary human lymphatic endothelial cells treated with pSFFV control viruses (Sample3).

CTRL_2

RNA-seq data from primary human lymphatic endothelial cells treated with pSFFV control viruses (Sample2).

CTRL_1

RNA-seq data from primary human lymphatic endothelial cells treated with pSFFV control viruses (Sample1).