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1.
Figure 6

Figure 6. From: Single histidine-substituted cardiac troponin I confers protection from age-related systolic and diastolic dysfunction.

Changes in protein expression and phosphorylation in non-transgenic and transgenic mice. (A) Western blots of calcium-handling proteins including the sarco-endoplasmic reticulum ATPase (SERCA2a), phospholamban (PLN), the sodium calcium exchanger (NCX), serine 16 phosphorylation of phospholamban (pPLN), and tandem serine 23/24 phosphorylation of troponin I (pTnI) for young and aged non-transgenic and transgenic mice. Coomassie was used to normalize for protein loading (W, Western; C, Coomassie). (B) Mean summary data for differences in the expression of calcium-handling proteins including CSQ, NCX, PLN, SERCA2a, the SERCA2a/PLN ratio, pPLN, and pTnI. Two-way ANOVA main effects (P < 0.05): age (double dagger), SERCA2a, and pPLN; and genotype (single dagger), PLN, SERCA2a. Ntg, nontransgenic; Tg, transgenic.

Nathan J. Palpant, et al. Cardiovasc Res. 2008 November 1;80(2):209-218.
2.
Figure 5

Figure 5. From: Single histidine-substituted cardiac troponin I confers protection from age-related systolic and diastolic dysfunction.

Analysis of calcium homoeostasis in young mice. (A) Raw traces of calcium transients from FURA 2AM loaded isolated myocytes during pacing with 1 Hz (left and middle) as well as raw calcium transient traces normalized to the peak amplitude (right). (B) Raw calcium transients after acute addition of 20 mM caffeine to release sarcoplasmic reticulum calcium (horizontal black bars). (C) Summarized data from calcium-handling experiments (n = 20–24 myocytes per group). Values are expressed as mean ± SEM. *P < 0.05 for non-transgenic vs. transgenic. Ntg, nontransgenic; Tg, transgenic.

Nathan J. Palpant, et al. Cardiovasc Res. 2008 November 1;80(2):209-218.
3.
Figure 4

Figure 4. From: Single histidine-substituted cardiac troponin I confers protection from age-related systolic and diastolic dysfunction.

In vivo haemodynamic function and survival of aged mice during an acute hypoxic challenge. (A) Averaged left ventricular haemodynamic function including end systolic pressure (ESp), stroke volume (SV), cardiac output (CO), stroke work (SW), and the positive derivative of pressure development (dP/dt max) during the time course of an acute hypoxic challenge for non-transgenic (filled circle; n = 3) and transgenic (open circle; n = 3) aged mice. (B) Summarized mean survival data and survival curve showing time to systolic heart failure for 2-year-old non-transgenic (n = 3) and transgenic (n = 3) mice. Values are expressed as mean ± SEM. *P < 0.05.

Nathan J. Palpant, et al. Cardiovasc Res. 2008 November 1;80(2):209-218.
4.
Figure 1

Figure 1. From: Single histidine-substituted cardiac troponin I confers protection from age-related systolic and diastolic dysfunction.

Age-dependent stoichiometric replacement in cardiac troponin I A164H transgenic mice. (A) Sequence alignment showing location of the single histidine substitution originally studied in the slow skeletal isoform of troponin I and subsequently introduced into cardiac troponin I (cTnI A164HFLAG). Expression cassette of cDNA-encoding cardiac troponin I A164H with an SV40 polyadenylation (pA) signal was driven by the 5.5 kb Myh6 promoter. A C-terminal flag epitope was used to aid detection of cardiac troponin I A164H. (B) Immunoblot and bar graph showing expression of native cardiac troponin I (filled square) in non-transgenic mice as well as stoichiometric incorporation of cardiac troponin I A164HFLAG (open square) relative to endogenous cardiac troponin I (filled square) in transgenic mice at 6 months (n = 12) and 2 years (n = 6). Values are expressed as mean ± SEM. *P < 0.05 for 6 month vs. 2 year replacement.

Nathan J. Palpant, et al. Cardiovasc Res. 2008 November 1;80(2):209-218.
5.
Figure 3

Figure 3. From: Single histidine-substituted cardiac troponin I confers protection from age-related systolic and diastolic dysfunction.

In vivo haemodynamic differences between aged non-transgenic and transgenic mice during an acute hypoxic challenge. (A) Two second raw data sweeps derived by conductance micromanometry of left ventricular pressure (LVP), left ventricular pressure derivatives (dP/dt), and left ventricular volume of 2-year-old non-transgenic and transgenic mice during an acute hypoxic challenge (12% O2). (B) Representative pressure–volume loops in vivo of non-transgenic (grey) and transgenic (black) mice during hypoxia. (C) Mean data showing haemodynamic function as well as the delta change (Δ, right side axes) from baseline values for cardiac output (CO), stroke volume (SV), stroke work (SW), end systolic pressure (ESp), and positive pressure derivatives (dP/dt max) derived by Millar catheterization of 2-year-old non-transgenic (filled square; n = 3) and transgenic (open square; n = 3) mice. *P < 0.05. Values are expressed as mean ± SEM. Ntg, nontransgenic; Tg, transgenic.

Nathan J. Palpant, et al. Cardiovasc Res. 2008 November 1;80(2):209-218.
6.
Figure 2

Figure 2. From: Single histidine-substituted cardiac troponin I confers protection from age-related systolic and diastolic dysfunction.

Age-dependent changes in baseline cardiac function by echocardiography and Millar catheterization. (A) Representative M-mode echocardiographic images along the parasternal short axis view showing changes in contractility of non-transgenic and transgenic mice between 4 months and 2 years (scale bar = 0.1 s). White bars delineate systole and diastole. (B) Summarized mean data showing age-related differences in cardiac function as assessed by echocardiography including velocity of circumferential fibre shortening corrected for heart rate (Vcfc), volume at diastole (Vol d), and the ratio of the Mitral E wave to lateral annular E wave (E/Ela) showing changes in cardiac function in non-transgenic (filled square) and transgenic (open square) mice at 4 months (non-transgenic, n = 26; transgenic, n = 32), 1 year (non-transgenic, n = 12; transgenic, n = 13), and 2 years (non-transgenic, n = 13; transgenic, n = 15). Values are expressed as mean ± SEM. Two-way ANOVA main effects: age (double dagger) and genotype (single dagger): Vcfc, Vol d, E/Ela, P < 0.05. ANOVA interaction effects between genotype and age (section symbol): E/Ela, *P < 0.05 for non-transgenic vs. transgenic at 2 years of age. (C) Summarized conductance micromanometry mean data showing age-related differences in haemodynamic function including the ejection fraction (EF), time constant for relaxation (tau g), and heart rate of non-transgenic (filled square) and transgenic (open square) mice at 4 months (n = 12–14) and 2 years (n = 3–4) of age. Values are expressed as mean ± SEM. *P < 0.05 for non-transgenic vs. transgenic at 24 months. ANOVA main effects: genotype (single dagger): tau g, HR, P < 0.05; age (double dagger): EF, P < 0.05. Ntg, nontransgenic; Tg, transgenic.

Nathan J. Palpant, et al. Cardiovasc Res. 2008 November 1;80(2):209-218.

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