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[Decrease of cyclin D1 and CDK4 protein and their related factors induced by quartz in human embryonic lung
Fu-Hai Shen1, Xue-Yun Fan, Bing-Ci Liu
1National Institute of Occupation Health and Poison Control, Chinese Center for Disease Control and Prevention, Beijing 100050, China.
Summary
Quartz exposure decreases cyclin D1 and cyclin-dependent kinase 4 (CDK4) protein levels in lung fibroblasts. Extracellular signal-regulated kinases (ERKs) and c-Jun N-terminal kinases (JNKs) mediate this effect via the AP-1 pathway.
Area of Science:
- Cell biology
- Molecular biology
- Toxicology
Context:
- Quartz inhalation is a significant occupational hazard.
- Understanding cellular responses to crystalline quartz is crucial for mitigating lung disease.
- Cyclin D1 and CDK4 are key regulators of the cell cycle.
Purpose:
- To investigate the impact of crystalline quartz on cyclin D1 and CDK4 protein expression in human embryonic lung fibroblasts (HELF).
- To elucidate the role of mitogen-activated protein kinase (MAPK) and AP-1 signaling pathways in quartz-induced changes in cyclin D1-CDK4 expression.
Summary:
- Exposure of HELF to crystalline quartz for 2 hours significantly decreased cyclin D1 and CDK4 protein expression.
- Inhibitors of extracellular signal-regulated protein kinase (ERK) and c-Jun N-terminal kinase (JNK) pathways, but not p38, prevented this decrease.
- AP-1 signaling was implicated in the reduction of CDK4, but not cyclin D1, expression.
Impact:
- Identifies specific MAPK pathways (ERK, JNK) and the AP-1 transcription factor as mediators of quartz-induced cell cycle regulator downregulation.
- Provides insights into the molecular mechanisms underlying quartz toxicity in lung fibroblasts.
- Suggests potential targets for therapeutic interventions against quartz-induced lung injury.
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