Transmembrane transport of the Gαq protein carboxyl terminus imitation polypeptide GCIP-27

Yang, Hua; Liu, Ya; Lu, Xiaolan; Li, Xiaohui; Zhang, Haigang

doi:10.1016/j.ejps.2013.05.028

Cited by 8 publications

(11 citation statements)

References 42 publications

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“…More recently, the nanoscopic resolution of this technique allowed to detect changes in the plasma membrane surface of neonatal murine CMs induced by administration of aldosterone [8]. Similarly, neonatal rat CMs were treated with GCIP-27, a synthetic polypeptide thought to prevent cardiac hypertrophy, and exhibited an increased surface roughness compared to the not-treated, control group [9]. Another study analysed the cell surface and confirmed the absence of t-tubules in mouse and human embryonic stem cell-derived cardiomyocytes (ESC-CMs), which were compared with adult guinea pig ventricular CMs [10].…”

Section: Afm As Imaging Machine Applied To Cardiomyocytesmentioning

confidence: 99%

Novel insights into cardiomyocytes provided by atomic force microscopy

Borin

Pecorari

Peña

et al. 2018

Seminars in Cell & Developmental Biology

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Cardiovascular diseases (CVDs) are the number one cause of death globally, therefore interest in studying aetiology, hallmarks, progress and therapies for these disorders is constantly growing. Over the last decades, the introduction and development of atomic force microscopy (AFM) technique allowed the study of biological samples at the micro- and nanoscopic level, hence revealing noteworthy details and paving the way for investigations on physiological and pathological conditions at cellular scale. The present work is aimed to collect and review the literature on cardiomyocytes (CMs) studied by AFM, in order to emphasise the numerous potentialities of this approach and provide a platform for researchers in the field of cardiovascular diseases. Original data are also presented to highlight the application of AFM to characterise the viscoelastic properties of CMs.

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Section: Afm As Imaging Machine Applied To Cardiomyocytesmentioning

confidence: 99%

Novel insights into cardiomyocytes provided by atomic force microscopy

Borin

Pecorari

Peña

et al. 2018

Seminars in Cell & Developmental Biology

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“…As a peptide, transport across the cell membrane is critical for GCIP-27 to produce its effects. In this systematic study, we found [ 16 ] that GCIP-27 could be transported through the plasmalemma in a time- and concentration-dependent manner, which was mediated by an energy-dependent endocytosis process. This peptide could preferentially enter myocardial cells and VSMCs, which is especially beneficial for the treatment of cardiac hypertrophy and CHF.…”

Section: Discussionmentioning

confidence: 99%

“…Neonatal rats ventricular myocytes (NRVC) from 1–2 days old Sprague-Dawley rats were isolated and cultured as described previously [ 15 , 16 ]. NRVC were washed twice with D-Hanks' solution after being cultured in serum-free DMEM for 24 h, and incubated for 6 h in a non-serum medium containing 0.1 μmol/L DOX.…”

Section: Methodsmentioning

confidence: 99%

“…Gαq protein carboxyl terminus imitation polypeptide (GCIP)-27 is a synthetic polypeptide that was previously designed and optimized in our laboratory [ 15 ]. Serial studies indicated that the GCIP-27 peptide could be preferentially transported into cardiomyocytes and vascular smooth muscle cells through an energy-dependent endocytosis mechanism [ 16 ], inhibiting cardiomyocyte hypertrophy induced by angiotensin II or norepinephrine in vitro and alleviating left ventricular hypertrophy in various animal models [ 15 – 19 ]. Based on these results, there is little doubt that GCIP-27 could ameliorate CHF by alleviating cardiac hypertrophy.…”

Section: Introductionmentioning

confidence: 99%

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Gαq Protein Carboxyl Terminus Imitation Polypeptide GCIP-27 Improves Cardiac Function in Chronic Heart Failure Rats

Tong

Liu

et al. 2015

PLoS ONE

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BackgroundGαq protein carboxyl terminus imitation polypeptide (GCIP)-27 has been shown to alleviate pathological cardiomyocyte hypertrophy induced by various factors. Pathological cardiac hypertrophy increases the morbidity and mortality of cardiovascular diseases while it compensates for poor heart function. This study was designed to investigate the effects of GCIP-27 on heart function in rats with heart failure induced by doxorubicin.Methods and ResultsForty-eight rats were randomly divided into the following six groups receiving vehicle (control), doxorubicin (Dox), losartan (6 mg/kg, i.g.) and three doses of GCIP-27 (10, 30, 90 μg/kg; i.p., bid), respectively. Heart failure was induced by Dox, which was administered at a 20 mg/kg cumulative dose. After 10 weeks of treatment, we observed that GCIP-27 (30, 90 μg/kg) significantly increased ejection fraction, fraction shortening, stroke volume and sarcoplasmic reticulum Ca2+ ATPase activity of Dox-treated hearts. Additionally, GCIP-27 decreased myocardial injury, heart weight index and left ventricular weight index, fibrosis and serum cardiac troponin-I concentration in Dox-treated mice. Immunohistochemistry, western blotting and real-time PCR experiments indicated that GCIP-27 (10–90 μg/kg) could markedly upregulate the protein expression of myocardial α-myosin heavy chain (MHC), Bcl-2, protein kinase C (PKC) ε and phosphorylated extracellular signal-regulated kinase (p-ERK) 1/2 as well as the mRNA expression of α-MHC, but downregulated the expression of β-MHC, Bax and PKC βII, and the mRNA expression levels of β-MHC in Dox-treated mice. It was also found that GCIP-27 (30, 90 μg/L) decreased cell size and protein content of cardiomyocytes significantly in vitro by comparison of Dox group.ConclusionsGCIP-27 could effectively ameliorate heart failure development induced by Dox. PKC–ERK1/2 signaling might represent the underlying mechanism of the beneficial effects of GCIP-27.

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“…Neonatal rat ventricular myocytes (NRVM) from 1 to 2 days old Sprague-Dawley rats were isolated and cultured as described previously (Yang et al, 2013; Lu et al, 2015). After being cultured in serum-free DMEM for 24 h, the cells were incubated for 24 h in a non-serum medium containing 1 μmol/L AngII.…”

Section: Methodsmentioning

confidence: 99%

Triptolide Upregulates Myocardial Forkhead Helix Transcription Factor p3 Expression and Attenuates Cardiac Hypertrophy

Ding

Liu

et al. 2016

Front. Pharmacol.

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The forkhead/winged helix transcription factor (Fox) p3 can regulate the expression of various genes, and it has been reported that the transfer of Foxp3-positive T cells could ameliorate cardiac hypertrophy and fibrosis. Triptolide (TP) can elevate the expression of Foxp3, but its effects on cardiac hypertrophy remain unclear. In the present study, neonatal rat ventricular myocytes (NRVM) were isolated and stimulated with angiotensin II (1 μmol/L) to induce hypertrophic response. The expression of Foxp3 in NRVM was observed by using immunofluorescence assay. Fifty mice were randomly divided into five groups and received vehicle (control), isoproterenol (Iso, 5 mg/kg, s.c.), one of three doses of TP (10, 30, or 90 μg/kg, i.p.) for 14 days, respectively. The pathological morphology changes were observed after Hematoxylin and eosin, lectin and Masson’s trichrome staining. The levels of serum brain natriuretic peptide (BNP) and troponin I were determined by enzyme-linked immunosorbent assay and chemiluminescence, respectively. The mRNA and protein expressions of α- myosin heavy chain (MHC), β-MHC and Foxp3 were determined using real-time PCR and immunohistochemistry, respectively. It was shown that TP (1, 3, 10 μg/L) treatment significantly decreased cell size, mRNA and protein expression of β-MHC, and upregulated Foxp3 expression in NRVM. TP also decreased heart weight index, left ventricular weight index and, improved myocardial injury and fibrosis; and decreased the cross-scetional area of the myocardium, serum cardiac troponin and BNP. Additionally, TP markedly reduced the mRNA and protein expression of myocardial β-MHC and elevated the mRNA and protein expression of α-MHC and Foxp3 in a dose-dependent manner. In conclusion, TP can effectively ameliorate myocardial damage and inhibit cardiac hypertrophy, which is at least partly related to the elevation of Foxp3 expression in cardiomyocytes.

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Transmembrane transport of the Gαq protein carboxyl terminus imitation polypeptide GCIP-27

Cited by 8 publications

References 42 publications

Novel insights into cardiomyocytes provided by atomic force microscopy

Novel insights into cardiomyocytes provided by atomic force microscopy

Gαq Protein Carboxyl Terminus Imitation Polypeptide GCIP-27 Improves Cardiac Function in Chronic Heart Failure Rats

Triptolide Upregulates Myocardial Forkhead Helix Transcription Factor p3 Expression and Attenuates Cardiac Hypertrophy

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