By Regulating Mitochondrial Ca²⁺-Uptake UCP2 Modulates Intracellular Ca²⁺ - Fig 3

Abstract

a-c) Ca2+ transients in wild-type (WT) and in UCP2-/- cardiomyocytes (UCP2). a-b) Statistical analysis of (Ca2+)c (left) and (Ca2+)m (right) and c) representative traces of (Ca2+)c (left) and (Ca2+)m (right): In UCP2-/- cardiomyocytes rate of rise of (Ca2+)c was significantly decreased while the amplitude of (Ca2+)c was unchanged vs. WT (*p2+)m of UCP2-/- cardiomyocytes were significantly decreased vs. WT (*p2+ transients in WT vs. UCP2-/- cardiomyocytes evoked in the presence of 0.2 μM ryanodine, 0.01 mM thapsigargin and 100 nM Ru360. d) Representative traces of transsarcolemmal (Ca2+)c in WT and UCP2-/-, and e-f) Statistical analysis of amplitude (e) and rate of rise (f): In UCP2-/- transsarcolemmal Ca2+ transient amplitude and rate of rise were significantly down-regulated (*pNCX WT vs. UCP2-/- cardiomyocytes: forward INCX was elicited by 1 s of exposure to 5 mM caffeine using a holding potential of -40 mV. No difference in caffeine induced INCX in WT compared to UCP2-/- was found. h) SR Ca2+ load in WT vs. UCP2-/- calculated via the integral of INCX recordings. No difference in SR Ca2+ load between WT and UCP2-/- was detected.</p