Apelin/APJ signaling in IGF-1-induced acute mitochondrial and antioxidant effects in spontaneously hypertensive rat myocardium.

IF 3.7 3区 生物学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY Journal of physiology and biochemistry Pub Date : 2024-10-25 DOI:10.1007/s13105-024-01055-6
Alejandra M Yeves, Joshua Godoy Coto, Erica V Pereyra, Andrés J Medina, Luisa F González Arbelaez, Fiorella A Cavalli, Irene L Ennis
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Abstract

IGF-1 and apelin are released in response to exercise training with beneficial effects. Previously we demonstrated that a swimming routine is effective to convert pathological into physiological cardiac hypertrophy, and that IGF-1 improves contractility and the redox state, in spontaneously hypertensive rats (SHR). Now, we hypothesize that the apelinergic pathway is involved in the cardioprotective effects of IGF-1 in the SHR. We assessed the redox state and mitochondrial effects of IGF-1 or apelin in the presence/absence of AG1024 or ML221 [pharmacological antagonists of IGF1 (IGF1R) and apelin (APJ) receptors, respectively] in SHR isolated cardiomyocytes or perfused hearts. Acute IGF-1 (10 nmol/L) significantly: -reduced H2O2 production (IGF-1:62 ± 6; control:100 ± 8.1, %), -increased the activity of superoxide dismutase (IGF-1:193 ± 17, control: 100 ± 13,%), -prevented H2O2-induced ΔΨm loss (TMREF10min/F0 min: IGF-1:0.93 ± 0.017, control: 0.72 ± 0.029), -reduced mitochondrial permeability transition pore (mPTP) opening estimated by the calcium retention capacity (nmol/mg protein, IGF-1:251 ± 34, control:112 ± 5), and -increased P-AMPK (IGF-1:129 ± 0.9, control: 100 ± 2%) and P-AKT (IGF-1:143 ± 17 control:100 ± 6, %). These effects were suppressed not only by the antagonism of IGF1R but also of APJ. Moreover, IGF-1 significantly increased APJ (IGF-1:198 ± 29 control:100 ± 15,%) and apelin mRNAs (IGF-1:251 ± 48, control:100 ± 6,%). On the other hand, an equipotent dose of exogenous apelin (50 nmol/L) emulated IGF-1 effects being cancelled by the antagonism of APJ however not by AG1024. IGF-1/IGF1R stimulates the apelinergic pathway, improving the redox balance and mitochondria status in the pathologically hypertrophied myocardium of the SHR.

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自发性高血压大鼠心肌中 IGF-1 诱导的急性线粒体和抗氧化效应中的凋亡素/APJ 信号传导。
运动训练会释放 IGF-1 和 apelin,并产生有益的影响。在此之前,我们曾证实游泳训练能有效地将自发性高血压大鼠(SHR)的病理性心肌肥厚转变为生理性心肌肥厚,而且 IGF-1 能改善收缩力和氧化还原状态。现在,我们假设凋亡素能途径参与了 IGF-1 在 SHR 中的心脏保护作用。我们评估了 IGF-1 或凋亡素在 AG1024 或 ML221(分别是 IGF1(IGF1R)和凋亡素(APJ)受体的药理拮抗剂)存在/不存在的情况下对 SHR 离体心肌细胞或灌注心脏的氧化还原状态和线粒体效应。急性 IGF-1(10 nmol/L)可显著:-减少 H2O2 生成(IGF-1:62 ± 6;对照组:100 ± 8.1,%);-增加超氧化物歧化酶活性(IGF-1:193 ± 17;对照组:100 ± 13,%);-防止 H2O2 诱导的 ΔΨm 损失(TMREF10min/F0 min:IGF-1:0.93 ± 0.017;对照组:0.72 ± 0.IGF-1:0.93 ± 0.017,对照组:0.72 ± 0.029),通过钙滞留能力(nmol/mg 蛋白,IGF-1:251 ± 34,对照组:112 ± 5)估计的线粒体通透性转换孔(mPTP)开放减少,P-AMPK(IGF-1:129 ± 0.9,对照组:100 ± 2%)和 P-AKT(IGF-1:143 ± 17,对照组:100 ± 6,%)增加。这些效应不仅受到 IGF1R 的抑制,也受到 APJ 的抑制。此外,IGF-1 还能明显增加 APJ(IGF-1:198 ± 29,对照组:100 ± 15%)和 apelin mRNAs(IGF-1:251 ± 48,对照组:100 ± 6%)。另一方面,同等剂量的外源性凋亡素(50 nmol/L)仿效了 IGF-1 的效应,APJ 的拮抗作用取消了 IGF-1 的效应,但 AG1024 的拮抗作用没有取消。IGF-1/IGF1R可刺激凋亡素能途径,改善SHR病理性肥厚心肌的氧化还原平衡和线粒体状态。
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来源期刊
Journal of physiology and biochemistry
Journal of physiology and biochemistry 生物-生化与分子生物学
CiteScore
6.60
自引率
0.00%
发文量
86
审稿时长
6-12 weeks
期刊介绍: The Journal of Physiology and Biochemistry publishes original research articles and reviews describing relevant new observations on molecular, biochemical and cellular mechanisms involved in human physiology. All areas of the physiology are covered. Special emphasis is placed on the integration of those levels in the whole-organism. The Journal of Physiology and Biochemistry also welcomes articles on molecular nutrition and metabolism studies, and works related to the genomic or proteomic bases of the physiological functions. Descriptive manuscripts about physiological/biochemical processes or clinical manuscripts will not be considered. The journal will not accept manuscripts testing effects of animal or plant extracts.
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