FGF-2-induced Negative Inotropism and Cardioprotection are Inhibited by Chelerythrine: Involvement of Sarcolemmal Calcium-independent Protein Kinase C

Padua, Raymond R.; Merle, Pierre-Laurent; Doble, Bradley W.; Yu, Chenxu; Zahradka, Peter; Pierce, Grant N.; Panagia, Vincenzo; Kardami, Elissavet

doi:10.1006/jmcc.1998.0832

Cited by 56 publications

(61 citation statements)

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“…Recombinant rat wild-type (wt) or mutant (mt) FGF-2 produced in Escherichia coli bacteria and purified according to previously published procedures was used (22,31). Water-soluble chelerythrine chloride was purchased from Research Biochemicals International (Natick, MA).…”

Section: Animalsmentioning

confidence: 99%

“…After removal from the animals and arrest in cold buffer, hearts were perfused in the Langendorff mode at 37°C as described previously (31). Briefly, a water-filled compliant balloon, connected to a pressure transducer (Stratham P23 ID) was inserted into the left ventricle via the mitral valve.…”

Section: Animalsmentioning

confidence: 99%

“…In addition to its long-term effects on the circulatory system, FGF-2 affects adult cardiac myocytes directly; these cells express functional FGF-2 receptor 1 (FGFR1) (26) and respond to FGF-2 by changes in contractility (31) and hypertrophy (40). Furthermore, FGF-2 administered to the isolated rat or mouse heart before ischemia is clearly protective against subsequent ischemia and reperfusion injury (31,32,42).…”

mentioning

confidence: 99%

“…Furthermore, FGF-2 administered to the isolated rat or mouse heart before ischemia is clearly protective against subsequent ischemia and reperfusion injury (31,32,42). The acute protective effects of FGF pretreatment are proposed to engage a preconditioning-like mechanism (17,31), and thus one theoretical therapeutic possibility for FGF-2 would be as an agent of primary injury prevention.…”

mentioning

confidence: 99%

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Acute protection of ischemic heart by FGF-2: involvement of FGF-2 receptors and protein kinase C

Jiang

Padua

et al. 2002

American Journal of Physiology-Heart and Circulatory Physiology

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We examined the effect of fibroblast growth factor (FGF)-2 on myocardial resistance to injury when administered after the onset of ischemia , in vivo and ex vivo, and the role of FGF-2 receptors and protein kinase C (PKC). FGF-2 was injected into the left ventricle of rats undergoing permanent surgical coronary occlusion leading to myocardial infarction (MI). After 24 h, FGF-2-treated hearts displayed significantly reduced injury, determined by histological staining and troponin T release, and improved developed pressure compared with untreated controls. An FGF-2 mutant with diminished affinity for the tyrosine kinase FGF-2 receptor 1 (FGFR1) was not cardioprotective. FGF-2-treated hearts retained improved function and decreased damage at 6 wk after MI. In the ex vivo heart, FGF-2 administration during reperfusion after 30-min ischemia improved functional recovery and increased relative levels of PKC subtypes α, ε, and ζ in the particulate fraction, in a chelerythrine-preventable mode; it also decreased loss of energy metabolites. We conclude that intramyocardial FGF-2 administration shortly after the onset of ischemia confers protection from acute and chronic cardiac dysfunction and damage; FGF-2 delivered during reperfusion protects from ischemia-reperfusion injury; and protection by FGF-2 requires intact binding to FGFR1 and is likely mediated by PKC.

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Section: Animalsmentioning

confidence: 99%

Section: Animalsmentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

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Acute protection of ischemic heart by FGF-2: involvement of FGF-2 receptors and protein kinase C

Jiang

Padua

et al. 2002

American Journal of Physiology-Heart and Circulatory Physiology

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“…PKC-d reduction protects heart cells and decreases the number of dead cells. In addition, bFGF has been shown to be related to the MAPK/ERK signaling pathway in heart cell protection, although the mechanism remains unclear (Baines et al, 2002;House et al, 2007;Padua et al, 1998;Rose et al, 2010;Srisakuldee et al, 2014). Akt activates a number of substrates, including members of the B-cell lymphoma 2 (Bcl-2) protein family, glycogen synthase kinase 3 beta (GSK-3) and endothelial nitric oxide synthase (eNOS).…”

Section: Protection Of Heart Tissuementioning

confidence: 99%

The effects of transplanted cells in stem cell therapy for myocardial ischemia

Pham

2016

Biomed Res Ther

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It is known that myocardial infarction (MI) causes damages to the heart tissue and that present medical therapies, such as medication, stenting and coronary artery bypass surgery, cannot recover the injured heart. Fortunately, advances in stem cell research have brought hope of full heart recovery for myocardial ischemia patients. There have been many studies using cell therapies for myocardial ischemia, from preclinical trials to clinical trials. However, the biggest concern is the effect of transplanted cells in myocardial recovery. This review will focus on analyzing both the positive and negative effects of transplanted cells in myocardial recovery to better understand the underlying biological mechanisms and ways to evaluate safety and efficacy of cell transplantation in myocardial ischemia treatment.

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Enrichment of protein–RNA crosslinks from crude UV‐irradiated mixtures for MS analysis by on‐line chromatography using titanium dioxide columns

et al. 2009

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UV crosslinking is an appropriate method to identify proteins that directly contact nucleic acid, e.g., RNA. In combination with modern mass spectrometric (MS) analysis such an approach provides the opportunity to reveal not only the nature of the crosslinked proteins but also to identify the actual crosslinking sites between the protein and the nucleic acid. However, the relatively low yield in UV-induced crosslinking makes it difficult to identify in particular those species by MS that represent peptide-nucleic acid conjugates, as the great excess of noncrosslinked material interferes with their detection in MS. Here, we present an automated enrichment strategy of crosslinked peptide-RNA oligonucleotides derived from crude mixtures of UV-irradiated ribonucleoprotein (RNP) particles that uses TiO(2) columns integrated within a two-dimensional (2D) nanoliquid chromatography (LC) system. The setup combines two C18 precolumns, a TiO(2) enrichment column and a nanoanalytical column. It allows the removal of the noncrosslinked RNA and protein moiety and the specific enrichment of crosslinked peptide-RNA conjugates so that UV-irradiated and subsequently completely hydrolyzed RNP complexes can directly be loaded and analyzed by MS. In this feasibility study, we demonstrate the specific enrichment of peptide-RNA oligonucleotides derived from UV-irradiated native spliceosomal U1 snRNPs and spliceosomal [15.5K-61K-U4atac snRNA] complex reconstituted in vitro.

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FGF-2-induced Negative Inotropism and Cardioprotection are Inhibited by Chelerythrine: Involvement of Sarcolemmal Calcium-independent Protein Kinase C

Cited by 56 publications

References 0 publications

Acute protection of ischemic heart by FGF-2: involvement of FGF-2 receptors and protein kinase C

Acute protection of ischemic heart by FGF-2: involvement of FGF-2 receptors and protein kinase C

The effects of transplanted cells in stem cell therapy for myocardial ischemia

Enrichment of protein–RNA crosslinks from crude UV‐irradiated mixtures for MS analysis by on‐line chromatography using titanium dioxide columns

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