scholarly journals The c-Abl tyrosine kinase controls protein kinase Cδ-induced Fli-1 phosphorylation in human dermal fibroblasts

2011 ◽  
Vol 63 (6) ◽  
pp. 1729-1737 ◽  
Author(s):  
Andreea M. Bujor ◽  
Yoshihide Asano ◽  
Paul Haines ◽  
Robert Lafyatis ◽  
Maria Trojanowska
Keyword(s):  
Protein Kinase ◽  
Tyrosine Kinase ◽  
Dermal Fibroblasts ◽  
Human Dermal Fibroblasts ◽  
Abl Tyrosine Kinase ◽  
Protein Kinase Cδ

scholarly journals Piper retrofractumVahl. Extract, as a PPARδand AMPK Activator, Suppresses UVB-Induced Photoaging through Mitochondrial Biogenesis and MMPs Inhibition in Human Dermal Fibroblasts and Hairless Mice

2018 ◽  
Vol 2018 ◽  
pp. 1-11 ◽  
Author(s):  
Jungon Yun ◽  
Changhee Kim ◽  
Mi-Bo Kim ◽  
Jae-Kwan Hwang
Keyword(s):  
Protein Kinase ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Mouse Skin ◽  
Adenosine Monophosphate ◽  
Dermal Fibroblasts ◽  
Mitogen Activated Protein Kinase ◽  
Peroxisome Proliferator ◽  
Human Dermal Fibroblasts ◽  
Piper Retrofractum

Photoaging occurs by UVB-irradiation and involves production of reactive oxygen species (ROS) and overexpression of matrix metalloproteinases (MMPs), leading to extracellular matrix damage.Piper retrofractumVahl. is used as a traditional medicine for antiflatulence, expectorant, sedative, and anti-irritant; however, its antiphotoaging effect has not yet been studied. The current study investigated the antiphotoaging effect of standardizedPiper retrofractumextract (PRE) on UVB-damaged human dermal fibroblasts and hairless mouse skin. PRE treatment activated the peroxisome proliferator-activated receptor delta (PPARδ) and the adenosine monophosphate-activated protein kinase (AMPK), consequently upregulating mitochondrial synthesis and reducing ROS production. Additionally, PRE inhibited MMPs expression via suppressing mitogen-activated protein kinase (MAPK) and activator protein-1 (AP-1). PRE downregulated UVB-induced inflammatory reactions by inhibiting the nuclear factor-kappa B (NF-κB) activity. PRE also enhanced transforming growth factor-beta (TGF-β) and the Smad signaling pathway, thereby promoting procollagen gene transcription. Furthermore, oral administration of PRE (300 mg/kg/day) similarly regulated the signaling pathways and increased antioxidant enzyme expression, thus attenuating physiological deformations, such as wrinkle formation and erythema response. Collectively, these results suggest that PRE acts as a potent antiphotoaging agent via PPARδand AMPK activation.

Protein kinase C-α levels are inversely associated with growth rate in cultured human dermal fibroblasts

1998 ◽  
Vol 18 (1) ◽  
pp. 54-63 ◽  
Author(s):  
Sung Woo Choi ◽  
Hee-Young Park ◽  
Nelly G. Rubeiz ◽  
Dana Sachs ◽  
Barbara A. Gilchrest
Keyword(s):  
Growth Rate ◽  
Protein Kinase C ◽  
Protein Kinase ◽  
Dermal Fibroblasts ◽  
Human Dermal Fibroblasts ◽  
Kinase C

scholarly journals Protein kinase G increases antioxidant function in lung microvascular endothelial cells by inhibiting the c-Abl tyrosine kinase

2014 ◽  
Vol 306 (6) ◽  
pp. C559-C569 ◽  
Author(s):  
R. Scott Stephens ◽  
Laura E. Servinsky ◽  
Otgonchimeg Rentsendorj ◽  
Todd M. Kolb ◽  
Alexander Pfeifer ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Antioxidant Enzymes ◽  
Protein Kinase ◽  
Tyrosine Kinase ◽  
Protein Kinase G ◽  
Microvascular Endothelial Cells ◽  
Wild Type ◽  
Oxidant Injury ◽  
Abl Tyrosine Kinase ◽  
Microvascular Endothelial

Oxidant injury contributes to acute lung injury (ALI). We previously reported that activation of protein kinase GI(PKGI) posttranscriptionally increased the key antioxidant enzymes catalase and glutathione peroxidase 1 (Gpx-1) and attenuated oxidant-induced cytotoxicity in mouse lung microvascular endothelial cells (MLMVEC). The present studies tested the hypothesis that the antioxidant effect of PKGIis mediated via inhibition of the c-Abl tyrosine kinase. We found that activation of PKGIwith the cGMP analog 8pCPT-cGMP inhibited c-Abl activity and decreased c-Abl expression in wild-type but not PKGI−/−MLMVEC. Treatment of wild-type MLMVEC with atrial natriuretic peptide also inhibited c-Abl activation. Moreover, treatment of MLMVEC with the c-Abl inhibitor imatinib increased catalase and GPx-1 protein in a posttranscriptional fashion. In imatinib-treated MLMVEC, there was no additional effect of 8pCPT-cGMP on catalase or GPx-1. The imatinib-induced increase in antioxidant proteins was associated with an increase in extracellular H2O2scavenging by MLMVEC, attenuation of oxidant-induced endothelial barrier dysfunction, and prevention of oxidant-induced endothelial cell death. Finally, in the isolated perfused lung, imatinib prevented oxidant-induced endothelial toxicity. We conclude that cGMP, through activation of PKGI, inhibits c-Abl, leading to increased key antioxidant enzymes and resistance to lung endothelial oxidant injury. Inhibition of c-Abl by active PKGImay be the downstream mechanism underlying PKGI-mediated antioxidant signaling. Tyrosine kinase inhibitors may represent a novel therapeutic approach in oxidant-induced ALI.

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