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Cyclin-dependent kinase inhibitors enhance the resolution of inflammation by promoting inflammatory cell apoptosis

Apoptosis is essential for clearance of potentially injurious inflammatory cells and subsequent efficient resolution of inflammation. Here we report that human neutrophils contain functionally active cyclin-dependent kinases (CDKs), and that structurally diverse CDK inhibitors induce caspase-depende... Full description

Journal Title: Nature medicine 2006-09, Vol.12 (9), p.1056-1064
Main Author: Rossi, Adriano G
Other Authors: Sawatzky, Deborah A , Walker, Annemieke , Ward, Carol , Sheldrake, Tara A , Riley, Nicola A , Caldicott, Alison , Martinez-Losa, Magdalena , Walker, Trevor R , Duffin, Rodger , Gray, Mohini , Crescenzi, Elvira , Martin, Morag C , Brady, Hugh J , Savill, John S , Dransfield, Ian , Haslett, Christopher
Format: Electronic Article Electronic Article
Language: English
Subjects:
Publisher: United States: Nature Publishing Group
ID: ISSN: 1078-8956
Link: https://www.ncbi.nlm.nih.gov/pubmed/16951685
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title: Cyclin-dependent kinase inhibitors enhance the resolution of inflammation by promoting inflammatory cell apoptosis
format: Article
creator:
  • Rossi, Adriano G
  • Sawatzky, Deborah A
  • Walker, Annemieke
  • Ward, Carol
  • Sheldrake, Tara A
  • Riley, Nicola A
  • Caldicott, Alison
  • Martinez-Losa, Magdalena
  • Walker, Trevor R
  • Duffin, Rodger
  • Gray, Mohini
  • Crescenzi, Elvira
  • Martin, Morag C
  • Brady, Hugh J
  • Savill, John S
  • Dransfield, Ian
  • Haslett, Christopher
subjects:
  • Amino Acid Chloromethyl Ketones - pharmacology
  • Animals
  • Apoptosis
  • Apoptosis - drug effects
  • Apoptosis - physiology
  • Azepines - pharmacology
  • Carrageenan
  • Caspase 3 - physiology
  • Cyclin-Dependent Kinases - antagonists & inhibitors
  • Enzyme Inhibitors - therapeutic use
  • Granulocyte-Macrophage Colony-Stimulating Factor - pharmacology
  • Humans
  • Inflammation - drug therapy
  • Inhibitor drugs
  • Lungs
  • Male
  • Medical treatment
  • Mice
  • Myeloid Cell Leukemia Sequence 1 Protein
  • Neoplasm Proteins - biosynthesis
  • Neutrophils - drug effects
  • Neutrophils - physiology
  • Pharmacology
  • Pleurisy - chemically induced
  • Pleurisy - drug therapy
  • Proteins
  • Proto-Oncogene Proteins c-bcl-2 - biosynthesis
  • Purines - pharmacology
  • Pyrroles - pharmacology
  • Roscovitine
ispartof: Nature medicine, 2006-09, Vol.12 (9), p.1056-1064
description: Apoptosis is essential for clearance of potentially injurious inflammatory cells and subsequent efficient resolution of inflammation. Here we report that human neutrophils contain functionally active cyclin-dependent kinases (CDKs), and that structurally diverse CDK inhibitors induce caspase-dependent apoptosis and override powerful anti-apoptosis signals from survival factors such as granulocyte-macrophage colony-stimulating factor (GM-CSF). We show that the CDK inhibitor R-roscovitine (Seliciclib or CYC202) markedly enhances resolution of established neutrophil-dependent inflammation in carrageenan-elicited acute pleurisy, bleomycin-induced lung injury, and passively induced arthritis in mice. In the pleurisy model, the caspase inhibitor zVAD-fmk prevents R-roscovitine-enhanced resolution of inflammation, indicating that this CDK inhibitor augments inflammatory cell apoptosis. We also provide evidence that R-roscovitine promotes apoptosis by reducing concentrations of the anti-apoptotic protein Mcl-1. Thus, CDK inhibitors enhance the resolution of established inflammation by promoting apoptosis of inflammatory cells, thereby demonstrating a hitherto unrecognized potential for the treatment of inflammatory disorders.
language: eng
source:
identifier: ISSN: 1078-8956
fulltext: no_fulltext
issn:
  • 1078-8956
  • 1546-170X
url: Link


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titleCyclin-dependent kinase inhibitors enhance the resolution of inflammation by promoting inflammatory cell apoptosis
creatorRossi, Adriano G ; Sawatzky, Deborah A ; Walker, Annemieke ; Ward, Carol ; Sheldrake, Tara A ; Riley, Nicola A ; Caldicott, Alison ; Martinez-Losa, Magdalena ; Walker, Trevor R ; Duffin, Rodger ; Gray, Mohini ; Crescenzi, Elvira ; Martin, Morag C ; Brady, Hugh J ; Savill, John S ; Dransfield, Ian ; Haslett, Christopher
creatorcontribRossi, Adriano G ; Sawatzky, Deborah A ; Walker, Annemieke ; Ward, Carol ; Sheldrake, Tara A ; Riley, Nicola A ; Caldicott, Alison ; Martinez-Losa, Magdalena ; Walker, Trevor R ; Duffin, Rodger ; Gray, Mohini ; Crescenzi, Elvira ; Martin, Morag C ; Brady, Hugh J ; Savill, John S ; Dransfield, Ian ; Haslett, Christopher
descriptionApoptosis is essential for clearance of potentially injurious inflammatory cells and subsequent efficient resolution of inflammation. Here we report that human neutrophils contain functionally active cyclin-dependent kinases (CDKs), and that structurally diverse CDK inhibitors induce caspase-dependent apoptosis and override powerful anti-apoptosis signals from survival factors such as granulocyte-macrophage colony-stimulating factor (GM-CSF). We show that the CDK inhibitor R-roscovitine (Seliciclib or CYC202) markedly enhances resolution of established neutrophil-dependent inflammation in carrageenan-elicited acute pleurisy, bleomycin-induced lung injury, and passively induced arthritis in mice. In the pleurisy model, the caspase inhibitor zVAD-fmk prevents R-roscovitine-enhanced resolution of inflammation, indicating that this CDK inhibitor augments inflammatory cell apoptosis. We also provide evidence that R-roscovitine promotes apoptosis by reducing concentrations of the anti-apoptotic protein Mcl-1. Thus, CDK inhibitors enhance the resolution of established inflammation by promoting apoptosis of inflammatory cells, thereby demonstrating a hitherto unrecognized potential for the treatment of inflammatory disorders.
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languageeng
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subjectAmino Acid Chloromethyl Ketones - pharmacology ; Animals ; Apoptosis ; Apoptosis - drug effects ; Apoptosis - physiology ; Azepines - pharmacology ; Carrageenan ; Caspase 3 - physiology ; Cyclin-Dependent Kinases - antagonists & inhibitors ; Enzyme Inhibitors - therapeutic use ; Granulocyte-Macrophage Colony-Stimulating Factor - pharmacology ; Humans ; Inflammation - drug therapy ; Inhibitor drugs ; Lungs ; Male ; Medical treatment ; Mice ; Myeloid Cell Leukemia Sequence 1 Protein ; Neoplasm Proteins - biosynthesis ; Neutrophils - drug effects ; Neutrophils - physiology ; Pharmacology ; Pleurisy - chemically induced ; Pleurisy - drug therapy ; Proteins ; Proto-Oncogene Proteins c-bcl-2 - biosynthesis ; Purines - pharmacology ; Pyrroles - pharmacology ; Roscovitine
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10Gray, Mohini
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12Martin, Morag C
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16Haslett, Christopher
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0Cyclin-dependent kinase inhibitors enhance the resolution of inflammation by promoting inflammatory cell apoptosis
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descriptionApoptosis is essential for clearance of potentially injurious inflammatory cells and subsequent efficient resolution of inflammation. Here we report that human neutrophils contain functionally active cyclin-dependent kinases (CDKs), and that structurally diverse CDK inhibitors induce caspase-dependent apoptosis and override powerful anti-apoptosis signals from survival factors such as granulocyte-macrophage colony-stimulating factor (GM-CSF). We show that the CDK inhibitor R-roscovitine (Seliciclib or CYC202) markedly enhances resolution of established neutrophil-dependent inflammation in carrageenan-elicited acute pleurisy, bleomycin-induced lung injury, and passively induced arthritis in mice. In the pleurisy model, the caspase inhibitor zVAD-fmk prevents R-roscovitine-enhanced resolution of inflammation, indicating that this CDK inhibitor augments inflammatory cell apoptosis. We also provide evidence that R-roscovitine promotes apoptosis by reducing concentrations of the anti-apoptotic protein Mcl-1. Thus, CDK inhibitors enhance the resolution of established inflammation by promoting apoptosis of inflammatory cells, thereby demonstrating a hitherto unrecognized potential for the treatment of inflammatory disorders.
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authorRossi, Adriano G ; Sawatzky, Deborah A ; Walker, Annemieke ; Ward, Carol ; Sheldrake, Tara A ; Riley, Nicola A ; Caldicott, Alison ; Martinez-Losa, Magdalena ; Walker, Trevor R ; Duffin, Rodger ; Gray, Mohini ; Crescenzi, Elvira ; Martin, Morag C ; Brady, Hugh J ; Savill, John S ; Dransfield, Ian ; Haslett, Christopher
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7Martinez-Losa, Magdalena
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abstractApoptosis is essential for clearance of potentially injurious inflammatory cells and subsequent efficient resolution of inflammation. Here we report that human neutrophils contain functionally active cyclin-dependent kinases (CDKs), and that structurally diverse CDK inhibitors induce caspase-dependent apoptosis and override powerful anti-apoptosis signals from survival factors such as granulocyte-macrophage colony-stimulating factor (GM-CSF). We show that the CDK inhibitor R-roscovitine (Seliciclib or CYC202) markedly enhances resolution of established neutrophil-dependent inflammation in carrageenan-elicited acute pleurisy, bleomycin-induced lung injury, and passively induced arthritis in mice. In the pleurisy model, the caspase inhibitor zVAD-fmk prevents R-roscovitine-enhanced resolution of inflammation, indicating that this CDK inhibitor augments inflammatory cell apoptosis. We also provide evidence that R-roscovitine promotes apoptosis by reducing concentrations of the anti-apoptotic protein Mcl-1. Thus, CDK inhibitors enhance the resolution of established inflammation by promoting apoptosis of inflammatory cells, thereby demonstrating a hitherto unrecognized potential for the treatment of inflammatory disorders.
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