Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.7.11.13 (protein kinase C)
 49,245 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Solar UV radiation damages human skin, affecting skin tone and resiliency, and leading to premature ageing (photoageing). Skin damage by oxidants may lead to activation of PKC, thus increasing matrix metalloproteinase (MMPs) expression and collagen degradation. Administration of Chlorella has been shown to play some biochemical functions as well as in vitro inhibition of MMP1 activity. MMP1 secretion was evaluated following PMA treatment or UVB irradiation in the presence of Resilient Factor (RF, aqueous extract fraction of Chlorella), vitamin C, or vitamin E in human skin fibroblasts. Expression levels of MMP1 and elastin protein and of MMP1, TIMP1, and pro-collagen mRNA were also investigated. PMA-induced MMP1 production, protein, and gene expression were suppressed in the presence of RF. Elastin protein diminished after UVB exposure and RF treatment appeared able to counteract the effect of UVB irradiation. Our results also suggest that RF may increase pro-collagen mRNA expression following UVB exposure. This study shows that application of RF prevents MMP1 production via the inhibition of protein and gene expression. In addition, RF prevents the UVB-suppressed elastin protein and pro-collagen gene expression. These findings indicate that RF may exert a protective effect against UVB irradiation-induced damage in the skin.
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PMID:Potential protective effect of fresh grown unicellular green algae component (resilient factor) against PMA- and UVB-induced MMP1 expression in skin fibroblasts. 1847 60

A number of treatments are being investigated for vocal fold (VF) scar, including designer implants. The aim of the present study was to validate a 3D model system for probing the effects of various bioactive moieties on VF fibroblast (VFF) behavior toward rational implant design. We selected poly(ethylene glycol) diacrylate (PEGDA) hydrogels as our base-scaffold due to their broadly tunable material properties. However, since cells encapsulated in PEGDA hydrogels are generally forced to take on rounded/stellate morphologies, validation of PEGDA gels as a 3D VFF model system required that the present work directly parallel previous studies involving more permissive scaffolds. We therefore chose to focus on hyaluronan (HA), a polysaccharide that has been a particular focus of the VF community. Toward this end, porcine VFFs were encapsulated in PEGDA hydrogels containing consistent levels of high Mw HA (HA(HMW)), intermediate Mw HA (HA(IMW)), or the control polysaccharide, alginate, and cultured for 7 and 21 days. HA(HMW) promoted sustained increases in active ERK1/2 relative to HA(IMW). Furthermore, VFFs in HA(IMW) gels displayed a more myofibroblast-like phenotype, higher elastin production, and greater protein kinase C (PkC) levels at day 21 than VFFs in HA(HMW) and alginate gels. The present results are in agreement with a previous 3D study of VFF responses to HA(IMW) relative to alginate in collagen-based scaffolds permissive of cell elongation, indicating that PEGDA hydrogels may serve as an effective 3D model system for probing at least certain aspects of VFF behavior.
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PMID:Probing vocal fold fibroblast response to hyaluronan in 3D contexts. 1971 86

Arterial stiffness, which increases with aging and hypertension, is an independent cardiovascular risk factor. While stiffer substrates are known to affect single endothelial cell morphology and migration, the effect of substrate stiffness on endothelial monolayer function is less understood. The objective of this study was to determine if substrate stiffness increased endothelial monolayer reactive oxygen species (ROS) in response to protein kinase C (PKC) activation and if this oxidative stress then impacted adherens junction integrity. Porcine aortic endothelial cells were cultured on varied stiffness polyacrylamide gels and treated with phorbol 12-myristate 13-acetate (PMA), which stimulates PKC and ROS without increasing actinomyosin contractility. PMA-treated endothelial cells on stiffer substrates increased ROS and adherens junction loss without increased contractility. ROS scavengers abrogated PMA effects on cell-cell junctions, with a more profound effect in cells on stiffer substrates. Finally, endothelial cells in aortae from elastin haploinsufficient mice (Eln+/-), which were stiffer than aortae from wild-type mice, showed decreased VE-cadherin colocalization with peripheral actin following PMA treatment. These data suggest that oxidative stress may be enhanced in endothelial cells in stiffer vessels, which could contribute to the association between arterial stiffness and cardiovascular disease.
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PMID:Stiff Substrates Enhance Endothelial Oxidative Stress in Response to Protein Kinase C Activation. 3111 May 59


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