PEDF and PEDF-derived peptide 44mer protect cardiomyocytes against hypoxia-induced apoptosis and necroptosis via anti-oxidative effect

Gao, Xiao; Zhang, Hao; Zhuang, W.; Yuan, Guangda; Sun, Tao; Jiang, Xia; Zhang, Zhou; Yuan, Honghua; Zhang, Zhongming; Dong, Hongyan

doi:10.1038/srep05637

Cited by 60 publications

(62 citation statements)

References 33 publications

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“…That study has revealed that PEDF could upregulate SOD, GPx and CAT activities, thus promote clearing of ROS [4]. As this study has demonstrated, PEDF attenuates hypoxia-induced apoptosis and necrosis by restraining MOMP and MPTP opening via PEDF.…”

Section: Discussionmentioning

confidence: 53%

PEDF attenuates hypoxia-induced apoptosis and necrosis in H9c2 cells by inhibiting p53 mitochondrial translocation via PEDF-R

Wang

Zhang

et al. 2015

Biochemical and Biophysical Research Communications

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Section: Discussionmentioning

confidence: 53%

PEDF attenuates hypoxia-induced apoptosis and necrosis in H9c2 cells by inhibiting p53 mitochondrial translocation via PEDF-R

Wang

Zhang

et al. 2015

Biochemical and Biophysical Research Communications

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“…In many cases, segmental functional peptides play part of the biological function similar to their precursor proteins [41][42][43]. We selected 9 protein precursors closely related to cardiomyocyte structure or AMI from the 119 precursor proteins identified, and listed the differentially expressed peptides that were derived from functional domains in these proteins.…”

Section: Discussionmentioning

confidence: 99%

Peptidomic Analysis of Cultured Cardiomyocytes Exposed to Acute Ischemic-Hypoxia

et al. 2017

Cell Physiol Biochem

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Background: Acute Myocardial Infarction (AMI) is a life-threatening cardiovascular disease involving disruption of blood flow to the heart, consequent tissue damage, and sometimes death. Peptidomics, an emerging branch of proteomics, has attracted wide attention. Methods: A comparative peptidomic profiling was used to explore changes induced by acute ischemichypoxia in primary cultured neonatal rat myocardial cells. Analysis of six-plex tandem mass tag (TMT) labelled peptides was performed using nanoflow liquid chromatography coupled online with an LTQ-Orbitrap Velos mass spectrometer. Results: A total of 220 differentially expressed peptides originating from 119 proteins were identified, of which 37 were upregulated and 183 were downregulated in cardiomyocytes exposed to hypoxia/ischemia conditions. Many of the identified peptides were derived from functional domains of proteins closely associated with cardiomyocyte structure or AMI. Conclusion: Numerous peptides may be involved in process of AMI. These results pave the way for future functional studies of the identified peptides.

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“…It is expressed in multiple tissues and exerts diverse physiological activities, for instance blocking angiogenesis and tumor growth, anti-inflammatory and anti-oxidation [12,13,14]. Our previous studies have declared that PEDF inhibits left ventricular remodeling and improves cardiac function in rats with acute myocardial infarction, and PEDF protects against hypoxia-induced apoptosis and necroptosis via an anti-oxidative effect [15,16]. However, it is not known whether PEDF inhibits the activation of the NLRP3 inflammasome to protect against myocardial cell death in hypoxia cardiomyocytes.…”

Section: Introductionmentioning

confidence: 99%

PEDF Inhibits the Activation of NLRP3 Inflammasome in Hypoxia Cardiomyocytes through PEDF Receptor/Phospholipase A2

Zhang

Wang

Guan

et al. 2016

IJMS

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The nucleotide-binding oligomerization domain-like receptor protein 3 (NLRP3) inflammasome has been linked to sterile inflammation, which is involved in ischemic injury in myocardial cells. Pigment epithelium-derived factor (PEDF) is a multifunctional secreted glycoprotein with many biological activities, such as anti-inflammatory, antioxidant and anti-angiogenic properties. However, it is not known whether and how PEDF acts to regulate the activation of the NLRP3 inflammasome in cardiomyocytes. In the present study, we used the neonatal cardiomyocytes models of ischemia-like conditions to evaluate the mitochondrial fission and the activation of the NLRP3 inflammasome. We also determined the mechanism by which PEDF inhibits hypoxia-induced activation of the NLRP3 inflammasome. We found that PEDF decreased the activation of the NLRP3 inflammasome in neonatal cardiomyocytes through pigment epithelial-derived factor receptor/calcium-independent phospholipase A2 (PEDFR/iPLA2). Meanwhile, PEDF reduced Drp1-induced mitochondrial fission and mitochondrial fission-induced mitochondrial DNA (mtDNA), as well as mitochondrial reactive oxygen species (mtROS) release into cytosol through PEDFR/iPLA2. We also found that PEDF inhibited mitochondrial fission-induced NLRP3 inflammasome activation. Furthermore, previous research has found that endogenous cytosolic mtDNA and mtROS can serve as activators of NLRP3 inflammasome activity. Therefore, we hypothesized that PEDF can protect against hypoxia-induced activation of the NLRP3 inflammasome by inhibiting mitochondrial fission though PEDFR/iPLA2.

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PEDF and PEDF-derived peptide 44mer protect cardiomyocytes against hypoxia-induced apoptosis and necroptosis via anti-oxidative effect

Cited by 60 publications

References 33 publications

PEDF attenuates hypoxia-induced apoptosis and necrosis in H9c2 cells by inhibiting p53 mitochondrial translocation via PEDF-R

PEDF attenuates hypoxia-induced apoptosis and necrosis in H9c2 cells by inhibiting p53 mitochondrial translocation via PEDF-R

Peptidomic Analysis of Cultured Cardiomyocytes Exposed to Acute Ischemic-Hypoxia

PEDF Inhibits the Activation of NLRP3 Inflammasome in Hypoxia Cardiomyocytes through PEDF Receptor/Phospholipase A2

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