Cardiac apoptosis induced under high glucose condition involves activation of IGF2R signaling in H9c2 cardiomyoblasts and streptozotocin-induced diabetic rat hearts

Feng, Chih Chung; Pandey, Sudhir; Lin, Ching Yuang; Shen, Chia Yao; Chang, Ruey Lin; Chang, Tung Ti; Chen, Ray Jade; Viswanadha, Vijaya Padma; Huang, Chih‐Yang

doi:10.1016/j.biopha.2017.11.020

Cited by 22 publications

(19 citation statements)

References 39 publications

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“…Ang-II is an important mediator of cardiovascular remodeling processes which not only increases blood pressure but also enhances the generation of reactive oxygen species (ROS) [4]. Our earlier studies have also shown the involvement of IGF-IIR signaling in the development of pathological cardiac changes during stresses via Gαq/PKCα/NFATC3 modulations [5,6]. Recently, β-catenin participation has been implicated in hypertensive heart condition [7].…”

Section: Introductionmentioning

confidence: 99%

β-catenin/LEF1/IGF-IIR Signaling Axis Galvanizes the Angiotensin-II- induced Cardiac Hypertrophy

Lai

Pandey

Day

et al. 2019

IJMS

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Cardiovascular diseases have a high prevalence worldwide and constitute the leading causes of mortality. Recently, malfunctioning of β-catenin signaling has been addressed in hypertensive heart condition. Ang-II is an important mediator of cardiovascular remodeling processes which not only regulates blood pressure but also leads to pathological cardiac changes. However, the contribution of Ang-II/β-catenin axis in hypertrophied hearts is ill-defined. Employing in vitro H9c2 cells and in vivo spontaneously hypertensive rats (SHR) cardiac tissue samples, western blot analysis, luciferase assays, nuclear-cytosolic protein extracts, and immunoprecipitation assays, we found that under hypertensive condition β-catenin gets abnormally induced that co-activated LEF1 and lead to cardiac hypertrophy changes by up-regulating the IGF-IIR signaling pathway. We identified putative LEF1 consensus binding site on IGF-IIR promoter that could be regulated by β-catenin/LEF1 which in turn modulate the expression of cardiac hypertrophy agents. This study suggested that suppression of β-catenin expression under hypertensive condition could be exploited as a clinical strategy for cardiac pathological remodeling processes.

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Section: Introductionmentioning

confidence: 99%

β-catenin/LEF1/IGF-IIR Signaling Axis Galvanizes the Angiotensin-II- induced Cardiac Hypertrophy

Lai

Pandey

Day

et al. 2019

IJMS

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“…All animal experiments were performed in accordance with the Guide for the Care and Use of Laboratory Animals under a protocol approved by the Institutional Animal Care and Use Committee of China Medical University, Taichung, Taiwan (No.102‐71‐N and 104‐222‐N). The metabolic syndrome diseased animal model was used as described in our previous studies . Finally, rats were killed, heart tissues were aseptically collected and analyzed through Western blot analysis as described previously.…”

Section: Methodsmentioning

confidence: 99%

Tid1‐S attenuates LPS‐induced cardiac hypertrophy and apoptosis through ER‐a mediated modulation of p‐PI3K/p‐Akt signaling cascade

Chao

Badrealam

et al. 2019

J of Cellular Biochemistry

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Myocardial dysfunction is clinically relevant? repercussion that follows sepsis. Tid 1 protein has been implicated in many biological process. However, the role of Tid 1 in lipopolysaccharide (LPS)‐induced cardiomyocyte hypertrophy and apoptosis remains elusive. In the current research endeavor, we have elucidated the role of Tid1‐S on LPS‐induced cardiac hypertrophy and apoptosis. Interestingly, we found that overexpression of Tid1‐S suppressed TLR‐4, NFATc3, and BNP protein expression which eventually led to inhibition of LPS‐induced cardiac hypertrophy. Moreover, Tid1‐S overexpression attenuated cellular apoptosis and activated survival proteins p‐PI3K and pser473Akt. Besides this, Tid1‐S overexpression enhanced ER‐a protein expression. Collectively, our data suggest that Tid1‐S plausibly enhance ER‐a protein and further activate p‐PI3K and p ser473Akt survival protein expression; which thereby led to attenuation of LPS‐induced apoptosis in cardiomyoblast cells. Interestingly, our data suggest that Tid1‐S is involved in attenuation of cardiomyoblast cells damages induced by LPS.

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“…H9c2 cardiomyoblasts from the American Type Culture Collection (ATCC,CRL-1446) (Rockville, MD, USA) were cultured in 100-mm or 60-mm culture dishes in Dulbecco's modified Eagles medium (DMEM, Sigma-Aldrich, USA) supplemented with 100 μg/mL penicillin (Gibco, Waltham, MA, USA), 100 μg/mL streptomycin (Gibco), 2 mM glutamine (Gibco), and 10% Clontech fetal bovine serum (Hyclone, GE Healthcare Life Sciences, Pittsburgh, PA, USA) inside humidified air (5% CO 2 ) at 37°C. The control cells were exposed to media containing 5.5 mM D-glucose and for high-glucose challenge the cells were exposed to 33 mM D-glucose according to previous reports [4,7,25].…”

Section: Cell Culture and Treatmentmentioning

confidence: 99%

Tetramethylpyrazine reverses high-glucose induced hypoxic effects by negatively regulating HIF-1α induced BNIP3 expression to ameliorate H9c2 cardiomyoblast apoptosis

et al. 2020

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Background: Diabetic patients are highly vulnerable to hypoxic injury, which is associated with hypoxia induced BNIP3 expression that subsequently activate apoptosis. Our previous research show that Tetramethylpyrazine (TMP), a food flavoring agent, represses the hypoxia induced BNIP3 expression attenuate myocardial apoptosis. In this study, we evaluate the effect of TMP to provide protection against hypoxia aggravated high-glucose associated cellular apoptosis. Methods: The cytoprotective effect of TMP against high glucose induced cellular damages was determined on embryo derived H9c2 cardiomyoblast cells that were subjected to 5% hypoxia for 24 h and subjected to different duration of 33 mM high glucose challenge. Further, the involvement of HIF-1α and BNIP3 in cellular damage and the mechanism of protection of TMP were determined by overexpression and silencing HIF-1α and BNIP3 protein expression. Results: The results show that hypoxic effects on cell viability aggravates with high glucose challenge and this augmentative effect is mediated through BNIP3 in H9c2 cardiomyoblast cells. However, TMP administration effectively reversed the augmented HIF-1α levels and BNIP3 elevation. TMP improved the survival of H9c2 cells and effectively suppressed apoptosis in H9c2 cells. Further comparison on the effects of TMP on H9c2 cells challenged with high glucose and those challenged with hypoxia show that TMP precisely regulated the hypoxic intensified apoptotic effects in high-glucose condition. Conclusion: The results clearly show that flavoring agent-TMP attenuates cytotoxicity amplified by hypoxia challenge in high glucose condition by destabilizing HIF-1α.

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Cardiac apoptosis induced under high glucose condition involves activation of IGF2R signaling in H9c2 cardiomyoblasts and streptozotocin-induced diabetic rat hearts

Cited by 22 publications

References 39 publications

β-catenin/LEF1/IGF-IIR Signaling Axis Galvanizes the Angiotensin-II- induced Cardiac Hypertrophy

β-catenin/LEF1/IGF-IIR Signaling Axis Galvanizes the Angiotensin-II- induced Cardiac Hypertrophy

Tid1‐S attenuates LPS‐induced cardiac hypertrophy and apoptosis through ER‐a mediated modulation of p‐PI3K/p‐Akt signaling cascade

Tetramethylpyrazine reverses high-glucose induced hypoxic effects by negatively regulating HIF-1α induced BNIP3 expression to ameliorate H9c2 cardiomyoblast apoptosis

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