Paradoxical resistance to myocardial ischemia and age-related cardiomyopathy in NHE1 transgenic mice: A role for ER stress?

Cook, Alexandra; Bardswell, Sonya C.; Pretheshan, Subashini; Dighe, Kushal; Kanaganayagam, Gajen; Jabr, Rita I.; Merkle, Sabine; Marber, Michael; Engelhardt, Stefan; Avkiran, Metin

doi:10.1016/j.yjmcc.2008.10.013

Cited by 35 publications

(27 citation statements)

References 51 publications

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“…16 To exclude the possibility that overexpressed Cre protein led to the cardiac abnormalities observed in the present study, we evaluated Atg5-deficient mice in which Cre was knocked-in downstream of the myosin light chain 2v promoter. The resulting mice exhibited phenotypes similar to Atg5 flox/flox ;α-MyHC-Cre + mice (data not shown).…”

Section: Discussionmentioning

confidence: 99%

Inhibition of autophagy in the heart induces age-related cardiomyopathy

Taneike¹,

Yamaguchi²,

Nakai³

et al. 2010

Autophagy

410

326

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Section: Discussionmentioning

confidence: 99%

Inhibition of autophagy in the heart induces age-related cardiomyopathy

Taneike¹,

Yamaguchi²,

Nakai³

et al. 2010

Autophagy

410

326

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“…Several laboratories [43,44] have shown that elevated NHE1 expression is associated with increased calreticulin and protein disulfide isomerase expression, implicating an association of some of these proteins with NHE1 in other tissues. Glucose-regulated proteins were also increased with elevated NHE1 expression in the myocardium [43]. Here, we found an association of 78 kDa glucose-regulated protein with NHE1 (Table 2).…”

Section: Nhe1 and Chaperone Proteinsmentioning

confidence: 99%

Defining the Na+/H+ exchanger NHE1 interactome in triple-negative breast cancer cells

Amith

Vincent

Wilkinson

et al. 2017

Cellular Signalling

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“…98 Interestingly, overexpression of the cardiac sodium/hydrogen exchanger (NHE1) resulted in upregulation of ER stress. 99 It had been previously determined that NHE1 expression is maladaptive during cardiac function but the unexpected increase in the UPR (during NHE1 overexpression), led to enhanced survival of the mouse heart under ischemic conditions. 99 In other systems, such as brain ischemia/reperfusion and tumor growth, there are significant changes in ER stress during the insult.…”

Section: Er Stress: Pathological Versus Physiological?mentioning

confidence: 99%

Biology of Endoplasmic Reticulum Stress in the Heart

Groenendyk

Sreenivasaiah

Kim

et al. 2010

Circulation Research

283

231

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Abstract:The endoplasmic reticulum (ER) is a multifunctional intracellular organelle supporting many processes required by virtually every mammalian cell, including cardiomyocytes. It performs diverse functions, including protein synthesis, translocation across the membrane, integration into the membrane, folding, posttranslational modification including N-linked glycosylation, and synthesis of phospholipids and steroids on the cytoplasmic side of the ER membrane, and regulation of Ca 2؉ homeostasis. Perturbation of ER-associated functions results in ER stress via the activation of complex cytoplasmic and nuclear signaling pathways, collectively termed the unfolded protein response (UPR) (also known as misfolded protein response), leading to upregulation of expression of ER resident chaperones, inhibition of protein synthesis and activation of protein degradation. The UPR has been associated with numerous human pathologies, and it may play an important role in the pathophysiology of the heart. ER stress responses, ER Ca 2؉ buffering, and protein and lipid turnover impact many cardiac functions, including energy metabolism, cardiogenesis, ischemic/reperfusion, cardiomyopathies, and heart failure. ER proteins and ER stress-associated pathways may play a role in the development of novel UPR-targeted therapies for cardiovascular diseases. (Circ Res. 2010;107:1185-1197.) Key Words: endoplasmic reticulum stress Ⅲ misfolded protein response Ⅲ autophagy Ⅲ endoplasmic reticulum-associated degradation Ⅲ cardiac disease T he endoplasmic reticulum (ER) is a centrally located, multifunctional, and multiprocess intracellular organelle supporting many mechanisms required by virtually every mammalian cell, including cardiomyocytes. The membrane performs a remarkable number of diverse functions, including protein synthesis, translocation across the membrane, integration into the membrane, folding, posttranslational modification including N-linked glycosylation, and synthesis of phospholipids and steroids on the cytoplasmic side of the ER membrane, and regulation of Ca 2ϩ homeostasis. 1 Development and maintenance of optimally functioning ER membrane is essential for virtually all cellular activities, from intracellular signaling to control of transcriptional pathways; ion fluxes to control of energy metabolism; protein synthesis to multisubunit assembly; and lipid synthesis to transcriptional regulation of steroid metabolism. One of the major advantages of the centrally located ER network for the cell is the ability to control the composition and the dynamics of the ER luminal environment in an extracellular environmentindependent way. Furthermore, the ER is not an isolated organelle because it has developed sophisticated mechanisms of communication with many other cellular compartments,

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Paradoxical resistance to myocardial ischemia and age-related cardiomyopathy in NHE1 transgenic mice: A role for ER stress?

Cited by 35 publications

References 51 publications

Inhibition of autophagy in the heart induces age-related cardiomyopathy

Inhibition of autophagy in the heart induces age-related cardiomyopathy

Defining the Na+/H+ exchanger NHE1 interactome in triple-negative breast cancer cells

Biology of Endoplasmic Reticulum Stress in the Heart

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