Post-translational modifications disclose a dual role for redox stress in cardiovascular pathophysiology

Victorino, Vanessa Jacob; Mencalha, André Luiz

doi:10.1016/j.lfs.2014.11.008

Cited by 27 publications

(15 citation statements)

References 94 publications

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“…Previous studies indicated that mild oxidative stress displays neuro-protection in ischemia through activating nuclear factor erythroid 2-related factor (Nrf2) in astrocytes [15]. ROS and hypoxic preconditioning also show the cardio-protective effects [16,17]. These results suggest that SDT may have a potential cardioprotection and inhibit cardiac fibrosis through modulating intracellular ROS levels.…”

Section: Introductionmentioning

confidence: 83%

Sonodynamic Therapy Inhibits Fibrogenesis in Rat Cardiac Fibroblasts Induced by TGF-β1

Guo

Dong²,

Shi³

et al. 2016

Cell Physiol Biochem

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Key Words SDT • Cardiac fibroblast • TGF-β1 • GSK3β • AKT Abstract Background/Aims: Sonodynamic therapy (SDT) is a localized ultrasound-activated therapy for atherosclerosis when combined with a sonosensitizer, 5-aminolevulinic acid (ALA), but whether it can prevent cardiac fibrosis has not been studied. In the present study, we evaluated the effects SDT on fibrogenesis in rat cardiac fibroblasts. Methods: The primary cardiac fibroblasts were isolated from rats, and induced to fibrogenesis with TGF-β1. With this in vitro model, we tested the preventive effects of SDT on fibrogenesis and further the underlying mechanism. Results: TGF-β1 stimulation up-regulated α-SMA and COLI/III protein levels in cardiac fibroblasts, and enhanced the progression of cells from the G0/G1 phase to the S phase. SDT inhibited the TGF-β1 mediated cell proliferation and decreased the levels of α-SMA and COLI/III by activating AKT/GSK3β pathway and blocking TGF-β1/SMAD3 signaling. Conclusion: Our studies demonstrate an antifibrotic effect of SDT in rat cardiac fibroblasts, suggesting that SDT may intervene cardiac fibrogenesis by regulating myocardial fibrotic remodeling.

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Section: Introductionmentioning

confidence: 83%

Sonodynamic Therapy Inhibits Fibrogenesis in Rat Cardiac Fibroblasts Induced by TGF-β1

Guo

Dong²,

Shi³

et al. 2016

Cell Physiol Biochem

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“…Oxidative stress is described as a leading cause of adverse cardiac remodeling, since it can interfere on myocardial contractile activity and function, propelling the severity of a large spectrum of cardiovascular disorders. [50][51][52] We showed that preserving α-cardiac actin in the SRF HKO hearts lead to a reduction of DNA breaks and protein carbonylation that are usual features of deleterious oxidative stress. Further studies should address the identification of those specific proteins targeted by oxidation.…”

Section: Discussionmentioning

confidence: 99%

Cardioprotective effects of α‐cardiac actin on oxidative stress in a dilated cardiomyopathy mouse model

et al. 2019

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Abbreviations: ANF, atrial natriuretic factor; ARP-WASP, actin-related protein-Wiskott-Aldrich syndrome protein; CAG, Synthetic promoter constructed from the cytomegalovirus (CMV) early enhancer element, chicken beta-actin promoter and the splice acceptor of the rabbit beta-globin set enrichment analysis; HEK293, human embryonic kidney 293 cells; HW/BW, heart weight/body weight; LoxP, locus of X-over P1 which is a binding site of Cre recombinase; LV, left ventricle; MADS, MCM1-AGAMOUS-DEFICIENS-SRF; MCK, muscle creatine kinase; Mer, mutated estrogen receptor; MHC, myosin heavy chain; MHz, Megahertz; Myl, myosin light chain; NADPH, nicotinamide adenine dinucleotide phosphate hydrogen; NOX, nicotinamide adenine dinucleotide phosphate oxidase; NT, untreated cells; PAGE, polyacrylamide gel electrophoresis; PBS, phosphate buffer solution; PCR, polymerase chain reaction; PI3K/AKT, phosphatidylinositol-3-kinase and protein kinase B; PolyA, polyadenylation signal; PS, penicillin-streptomycin; RT-qPCR, real-time quantitative polymerase chain reaction; LVFWd, left ventricle free wall diastolic; LVFWs, left ventricle free wall systolic; ROS, reactive oxygen species; RV, right ventricle; Sa, systolic velocity at mitral annulus; SDS, sodium dodecyl sulfate; Sf, SRF-floxed locus; SOD2, superoxide dismutase 2; Spw, systolic velocity posterior wall; SRF, serum response factor; SRF HKO /CA, SRF heart-specific knock-out and -cardiac actin transgen overexpression; STARS, STriated muscle activator of rho signaling/actin-binding rho activating protein; SYBR, an asymmetrical cyanine dye binding to DNA; TGCRE, transgenic mouse expressing-MHC-MerCreMer; TGCA, transgenic mouse expressing-Cardiac Actin; Tg-r-ACTC1, transgenic mouse expressing rat -cardiac actin (ACTC1); UTC, urea-thiourea-chap buffer; Vcfc, shortening of velocity of circumferential fibers corrected for heart rate; VDAC, voltage-dependent anion channel. AbstractThe expression of α-cardiac actin, a major constituent of the cytoskeleton of cardiomyocytes, is dramatically decreased in a mouse model of dilated cardiomyopathy triggered by inducible cardiac-specific serum response factor (Srf) gene disruption that could mimic some forms of human dilated cardiomyopathy. To investigate the consequences of the maintenance of α-cardiac actin expression in this model, we developed a new transgenic mouse based on Cre/LoxP strategy, allowing together the induction of SRF loss and a compensatory expression of α-cardiac actin. Here, we report that maintenance of α-cardiac actin within cardiomyocytes temporally preserved cytoarchitecture from adverse cardiac remodeling through a positive impact on both structural and transcriptional levels. These protective effects were accompanied in vivo by the decrease of ROS generation and protein carbonylation and the downregulation of NADPH oxidases NOX2 and NOX4. We also show that ectopic expression of α-cardiac actin protects HEK293 cells against oxidative stress induced by H 2 O 2 . Oxidative stress plays an important role in the development of c...

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“…In healthy cells and tissues, PTMs induced by chemical/ enzymatic modification of protein side chains represent a common mechanism of altering protein function, whereas PTMs generated by nonenzymatic or spontaneous chemical processes are associated with the initiation and progression of disease processes (including inflammation, oxidative stress, proteostasic imbalance, and proteinopathy; Halim et al, 2015;Van Kasteren et al, 2007;Victorino, Mencalha, & Panis, 2014). The protein chemical modifications that take place in vivo can occur either spontaneously (e.g., deamidation and racemization), via nonenzymatic chemical reactions (e.g., oxidation and carbamylation), or due to enzymatic activity (Gillery & Jaisson, 2014;Mommen et al, 2014).…”

Section: Nonenzymatic Degenerative Protein Modifications (Dpms) and Pmentioning

confidence: 99%

Uncovering Neurodegenerative Protein Modifications via Proteomic Profiling

Gallart‐Palau¹,

Serra²,

Sze³

2015

International Review of Neurobiology

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Post-translational modifications disclose a dual role for redox stress in cardiovascular pathophysiology

Cited by 27 publications

References 94 publications

Sonodynamic Therapy Inhibits Fibrogenesis in Rat Cardiac Fibroblasts Induced by TGF-β1

Sonodynamic Therapy Inhibits Fibrogenesis in Rat Cardiac Fibroblasts Induced by TGF-β1

Cardioprotective effects of α‐cardiac actin on oxidative stress in a dilated cardiomyopathy mouse model

Uncovering Neurodegenerative Protein Modifications via Proteomic Profiling

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