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. Author manuscript; available in PMC: 2015 Nov 18.
Published in final edited form as: Life Sci. 2014 Sep 28;118(1):1–6. doi: 10.1016/j.lfs.2014.09.014

Table.

Observations from OPN transgenic mice

Mouse model Transgenic mice Source of OPN Apoptosis Fibrosis LV function Ref
MI OPN−/− Interstitium/nonmyocytes (Trueblood et al., 2001)
Ang II infusion OPN−/− Interstitium (Matsui, et al., 2004)
Aldosteron e infusion OPN−/− ND (Sam, et al., 2004)
DOX treatment OPN−/− ND ND ND (Schunke et al., 2013)
Pressure Overload OPN−/− LV lysates ↓ hypertrophic response (Xie et al., 2004)
I/R (repetitive) OPN−/− Myocytes ND (↓ wall thickness) (Duerr, et al., 2014)
Diabetes OPN−/− Myocytes ↓ (myocytes) (Subramanian et al., 2007)
O/E Myocyte- specific expression Myocytes ↑ (myocytes) (Renault et al., 2010; Dalal, et al., 2014)

MI, myocardial infarction; Ang II, angiotensin II, Dox, doxorubicin; I/R, ischemia/reperfusion; O/E, mice overexpressing OPN in the heart; ND, not determined