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.