Key result
CT-1-expressing myoblast transplantation improves fractional shortening by ~35% and alleviates LV dilation in hypertensive rats.
Why the study?
Although skeletal myoblast transplantation is a therapeutic candidate for chronic HF, little is known about its efficiency in nonischemic HF.
Does transplantation of cardiotrophin-1-expressing myoblasts alleviate the transition to heart failure in Dahl salt-sensitive hypertensive rats?
Does transplantation of cardiotrophin-1-expressing myoblasts alleviate the transition to heart failure in Dahl salt-sensitive hypertensive rats?
Transplantation of skeletal myoblasts combined with CT-1-gene transfer provides cardioprotective effects against ventricular remodeling in a rat model of hypertensive heart failure.
Answers are grounded in this paper and cite their sources.
May support preclinical testing of myoblast-CT-1 therapy in hypertensive HF; leaves open clinical translation.
OBJECTIVES: We investigated whether autologous transplantation of skeletal myoblasts (MB) transferred with cardiotrophin-1 (CT-1) gene could retard the transition to heart failure (HF) in Dahl salt-sensitive (DS) hypertensive rats. BACKGROUND: Although MB is a therapeutic candidate for chronic HF, little is known about the efficiency of this strategy when applied in nonischemic HF. Cardiotrophin-1 has potent hypertrophic and survival effects on cardiac myocytes. We hypothesized that transplantation of CT-1-expressing myoblasts could provide cardioprotective effects against ventricular remodeling in DS hypertensive rats. METHODS: The DS rats were fed a high salt diet for 6 weeks and developed left ventricular (LV) hypertrophy at 11 weeks. At this stage, animals underwent MB to the myocardium with skeletal myoblasts transferred with CT-1 gene using retrovirus (transplantation of CT-1-expressing myoblasts [MB + CT], n = 31) or myoblasts alone (MB, n = 31). The sham group rats were injected with phosphate-buffered saline (n = 24). RESULTS: At 17 weeks, MB and MB + CT groups showed a significant alleviation of LV dilation and contractile dysfunction compared with the sham group. The degree of alleviation was significantly greater in the MB + CT group than the MB group (LV end-diastolic dimension: sham 7.06 +/- 0.14 mm, MB 6.51 +/- 0.16 mm, MB + CT 6.24 +/- 0.07 mm; fractional shortening: sham 32.1 +/- 1.4%, MB 38.5 +/- 1.5%, MB + CT 43.2 +/- 0.8%). Histological examination revealed that the myocyte size was 20% larger in the MB + CT group at 17 weeks than in the age-matched sham group. Upregulation of renin-angiotensin and endothelin systems during the transition to HF was attenuated by myoblast transplantation, and this effect was enhanced in the MB + CT group. CONCLUSIONS: Transplantation of skeletal myoblasts combined with CT-1-gene transfer could be a useful therapeutic strategy for HF.
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Toh et al. (2004) studied Heart failure in hypertensive rats (n=86). Transplantation of CT-1-expressing myoblasts vs. Myoblasts alone or phosphate-buffered saline (sham) was evaluated on Fractional shortening. Transplantation of CT-1-expressing myoblasts significantly improved fractional shortening (43.2% vs 32.1% in sham) and alleviated LV dilation in hypertensive rats.
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