Morphology regulation in vascular endothelial cells

Tsuji-Tamura, Kiyomi; Ogawa, Minetaro

doi:10.1186/s41232-018-0083-8

Inflammation and Regeneration

Table 1 Mouse phenotypes

From: Morphology regulation in vascular endothelial cells

Disrupted gene		Phenotype	References
Mef2 transcription factors
Mef2a		Perinatal death (cardiac sudden death), mitochondrial defects	[30]
Mef2b		Normal cardiac development	[32]
Mef2c		Embryonic death by day 9.5, cardiovascular defects, defects of smooth muscle cell differentiation	[28]
Mef2c (endothelial-specific deletion)		Promotion of vascular growth in oxygen-induced retinopathy	[31]
Mef2d		Resistance to cardiac hypertrophy induced by pressure overload	[33]
Ets and Foxc transcription factors
Etv2		Embryonic death by day 10.5, defects of blood and vessel development	[2, 37]
Etv2 (endothelial-specific deletion)		No obvious phenotype in steady state condition	[131]
Foxc1		Prenatal and perinatal death, cardiovascular abnormalities, skeletal defects	[40,41,42]
Foxc2		Prenatal and perinatal death, cardiovascular and lymphatic abnormalities, skeletal defects	[38, 39]
Foxc1 and Foxc2		Embryonic death by day 9.5, more severe defects of cardiovascular and lymphatic development than Foxc1 or Foxc2-null mice	[41, 43, 44]
Foxo transcription factors
Foxo1		Embryonic death by day 10.5–11, vasculature defects	[50, 51]
Foxo1 (endothelial-specific deletion)		Embryonic death by day 11, vasculature defects	[52]
Foxo3		Age-dependent infertility, abnormality of ovarian follicular development	[50, 51]
Foxo4		Normal	[50, 51]
Foxo6		Defects of memory consolidation	[58]
VEGF signaling
VEGF (heterozygous deletion)		Embryonic death by day 12, abnormality of vascular development	[65, 66]
VEGFR2	VEGF receptor	Embryonic death by day 9.5, defects of hematopoietic and endothelial cell development	[67]
PI3K-Akt signaling
p110α (general or endothelial-specific inactivation)	Class IA PI3K subunit	Embryonic death by day 12.5, vascular defects	[85]
p85α and p85β	Class IA PI3K subunit	Embryonic death by day 11.5, vascular defects, hemorrhage	[86]
PI3K-C2α (general or endothelial-specific deletion)	Class II PI3K subunit	Embryonic death by days 11.5–12.5, vascular defects, hemorrhage	[87]
Akt1		Growth retardation, reduction of vascularization in placenta	[88, 89]
Akt1 (endothelial-specific postnatal deletion)		Reduction of vascular development in retina	[90]
mTOR signaling
Raptor	mTORC1 subunit	Embryonic death at early stages of development	[97]
Raptor (endothelial cell-specific deletion)		Embryonic death	[98]
Rictor	mTORC2 subunit	Embryonic death by day 11.5, growth arrest, placental abnormalities	[97, 99]
Rictor (endothelial cell-specific deletion)		Embryonic death by days 11.5–12.5, growth retardation, reduction of peripheral vascularization	[98, 100]
Notch signaling
Notch1	Notch receptor	Embryonic death by day 11.5, delayed and disorganized somitogenesis	[120, 121]
Notch4	Notch receptor	Normal	[122]
Notch1 and Notch4		More severe phenotype than Notch1-null mice, defects of vascular remodeling	[122]
Dll4 (heterozygous deletion)	Notch ligand	Similar to phenotype of Notch1 and Notch4-null mice, defects of vascular remodeling	[123]
RBP-j	Notch transcriptional effector	Defects of vascular remodeling and somite formation	[123]
Hey1	Notch target gene	Normal	[124]
Hey2	Notch target gene	Cardiac hypertrophy after birth	[125]
Hey1 and Hey2		Embryonic death by days 9.5–11.5, defects of vascular remodeling, hemorrhage	[124, 126]
Hes1	Notch target gene	No obvious phenotype in vascular development	[127]
Hes5	Notch target gene	Normal	[127]
Hes1 and Hes5 (general or endothelial-specific deletion of Hes1 on Hes5-null background)		Defects of vascular remodeling in the brain	[127]

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ISSN: 1880-8190

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