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Bls 1 frá 137 niðurstöður
Phorbol ester induces photoreceptor-specific degeneration in a Drosophila mutant.
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In the retinal degeneration B (rdgB) mutant of Drosophila, the major class of photoreceptors degenerate when the fly is raised in the light for several days; raising the fly in the dark largely prevents the degeneration. Thus, the rdgB is a conditional mutant that requires the operation of some
Altered regulation of L-type channels by protein kinase C and protein tyrosine kinases as a pathophysiologic effect in retinal degeneration.
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The effect of protein tyrosine kinases (PTK) on L-type calcium channels in cultured retinal pigmented epithelium (RPE) from rats with retinal dystrophy was investigated. Barium currents through Bay K 8644 (10(-6) M) sensitive L-type channels were measured using the patch-clamp technique. The current
Toxicity of Jatropha curcas phorbol esters in mice.
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Phorbol esters are the main toxins in Jatropha curcas seed and oil. The aim of this study was to assess the acute toxicity of phorbol esters given by intragastric administration and to determine the LD50 for Swiss Hauschka mice. The LD50 and 95% confidence limits for male mice were 27.34 mg/kg body
Phorbol 12-myristate 13-acetate induced cell death of porcine peripheral blood polymorphonuclear leucocytes.
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Polymorphonuclear leucocytes (PMNs) circulating in mammalian peripheral blood are terminally differentiated cells, and once isolated in serum-free medium, they undergo apoptosis within 1 or 2 days. In this study, we studied the effects of phorbol myristate acetate (PMA) on the viability of porcine
Pentoxifylline rescue preserves lung function in isolated canine lungs injured with phorbol myristate acetate.
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OBJECTIVE
We hypothesized that pentoxifylline, administered after phorbol myristate acetate (PMA), would diminish the severity of lung injury.
METHODS
Animal research laboratory.
METHODS
Comparative study.
METHODS
Mongrel dogs (n = 33).
METHODS
Baseline measurements were obtained from the isolated
Matrix Degradative Enzymes and Their Inhibitors during Annular Inflammation: Initial Step of Symptomatic Intervertebral Disc Degeneration.
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OBJECTIVE
Symptomatic disc degeneration develops from inflammatory reactions in the annulus fibrosus (AF). Although inflammatory mediators during annular inflammation have been studied, the roles of matrix metalloproteinases (MMPs) and their inhibitors have not been fully elucidated. In this study,
Triamcinolone acetonide modulates permeability and intercellular adhesion molecule-1 (ICAM-1) expression of the ECV304 cell line: implications for macular degeneration.
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Whilst animal studies and a pilot clinical trial suggest that intravitreal triamcinolone acetonide (TA) may be useful in the treatment of age-related macular degeneration (AMD), its mode of action remains to be fully elucidated. The present study has investigated the capacity of TA to modulate the
Alteration of protein kinase C activity in the postischemic rat brain areas using in vitro [3H]phorbol 12,13-dibutyrate autoradiography.
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Chronological changes of protein kinase C (PKC) activity were measured using in vitro [3H]phorbol 12,13-dibutyrate (PDBu) autoradiography to investigate the postischemic alteration of this second messenger system in the rat brain. Transient ischemia was induced by the occlusion of the middle
Induction of protein degradation in skeletal muscle by a phorbol ester involves upregulation of the ubiquitin-proteasome proteolytic pathway.
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Although muscle atrophy is common to a number of disease states there is incomplete knowledge of the cellular mechanisms involved. In this study murine myotubes were treated with the phorbol ester 12-O-tetradecanoylphorbol-13-acetate (TPA) to evaluate the role of protein kinase C (PKC) as an
Induction of Ca2+/calmodulin-stimulated cyclic AMP phosphodiesterase (PDE1) activity in Chinese hamster ovary cells (CHO) by phorbol 12-myristate 13-acetate and by the selective overexpression of protein kinase C isoforms.
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The cAMP phosphodiesterase (PDE) activity of CHO cells was unaffected by the addition of Ca2+ +calmodulin (CaM), indicating the absence of any PDE1 (Ca2+/CaM-stimulated PDE) activity. Treatment with the tumour promoting phorbol ester phorbol 12-myristate 13-acetate (PMA) led to the rapid transient
Involvement of phosphorylation in doxorubicin-mediated myofibril degeneration. An immunofluorescence microscopy analysis.
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Loss of myofilaments has been observed in both adaptive cardiac responses (i.e., hypertrophy) as well as in chemotheraputic use of antineoplastic drugs with cardiotoxic side effects (i.e., doxorubicin). An understanding of the degenerative process is a prerequisite for determining approaches to
Cyclic AMP, but not basic FGF, increases the in vitro survival of mesencephalic dopaminergic neurons and protects them from MPP(+)-induced degeneration.
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We studied how stimulation of protein kinase C and cAMP-dependent protein kinases affect the development of mesencephalic dopaminergic neurons in primary cell cultures derived from fetal rats at embryonic day E14. The effects of compounds which activate these second messenger systems were compared
Effects of phorbol ester-sensitive PKC (c/nPKC) activation on the production of adiponectin in 3T3-L1 adipocytes.
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PPARgamma plays a key role in adipocyte specific gene expression. In this study, we assessed the effects of phorbol ester (TPA)-sensitive PKC (c/nPKC) activation on the expression of adipocyte specific genes and inflammation related genes. Treatment with both TPA and TNFalpha decreased mRNA levels
Survival-promoting and protein kinase C-regulating roles of basic FGF for hippocampal neurons exposed to phorbol ester, glutamate and ischaemia-like conditions.
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Recent evidence suggests that protein kinase C (PKC) is involved in the pathophysiology of neurodegenerative diseases. We examined the effect of basic fibroblast growth factor (bFGF) on the survival of cultured rat hippocampal neurons exposed to conditions in which PKC is likely to play a role. bFGF
Acute airsacculitis in turkeys inoculated with phorbol myristate acetate.
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Phorbol myristate acetate (PMA), which induces acute pulmonary injury in mammals, induced acute airsacculitis in turkeys after intra-airsac inoculation of 0.1 mg/kg. Grossly, air sacs contained multifocal to diffuse hemorrhage and edema at postinoculation hours (PIH) 3 and 6. Microscopically, there
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