TABLE 2.

Summary of the phenotype of mice with genetic overexpression of endothelin-1

Animal Model	Site (Cre)	Phenotype	References
Overexpressing
ET-1+	Whole body	Lung: chronic inflammation; normal pulmonary pressure	Hocher et al., 1997, 2000;
		Kidney: increased renal cyst formation; renal interstitial fibrosis; glomerulosclerosis; age-dependent salt-sensitive hypertension	Shindo et al., 2002; Kalk et al., 2009
ET-1+/+/NOS2−/−	Whole body	increased blood pressure	Quaschning et al., 2008
ET-1+/NOS3−/−	Whole body	elevated blood pressure, reduced heart rate	Quaschning et al., 2007, Vignon-Zellweger et al., 2011, 2014
eET-1	Endothelium (Tie2-CRE)	Vascular endothelial dysfunction; vascular remodeling; increased lipid metabolism gene expression; normal blood pressure	Amiri et al., 2004; Simeone et al., 2011
TET-1	Endothelium(Tie1-CRE)	Elevated blood pressure; endothelial dysfunction	Leung et al., 2004
Apoe−/−eET-1	Whole body ApoE knockout, endothelial ET-1 overexpression	High-fat diet-induced atherosclerosis, abdominal aortic aneurysms, increase oxidative stress; increase immune cell infiltration	Simeone et al., 2011; Li et al., 2013
Inducible cardiomyocyte ET1+/+	Cardiomyocytes (alpha-myosin heavy chain -Cre)	Pulmonary and hepatic congestion; heart inflammation and hypertrophy	Yang et al., 2004
GET-1	Astrocyte (glial fibrillary acidic protein-Cre)	Normal development; normotensive; larger infarct size in response to ischemia/reperfusion injury; alleviates inflammatory pain	Lo et al., 2005; Hung et al., 2012
ETA ET-1/+	Where ETA is expressed, ET-1 will be expressed	Constitutive ETA activation; mandibular arch instead of maxillary arch; perinatal death	Sato et al., 2008
ET-1 H/+	Whole body	350% increased expression of ET-1; decreased plasma volume, heavy stiff hearts	Hathaway et al., 2015

ApoE, apolipoprotein E.