CDK14 expression is down-regulated by cigarette smoke in vivo and in vitro
Daniel Pollack1, Yuxuan Xiao1, Vibha Shrivasatava1
1Department of Biology, Stern College, Yeshiva University, New York, NY, USA.
Abstract:
In this study, DNA arrays have been employed to monitor gene expression patterns in testis of mice exposed to tobacco smoke for 24 weeks and compared to control animals. The results of the analysis revealed significant changes in expression of several genes that may have a role in spermatogenesis. Cdk14 was chosen for further characterization because of a suggested role in the testis and in regulation of Wnt signaling. RT-PCR analysis confirmed down regulation of Cdk14 in mice exposed to cigarette smoke (CS). Cdk14 is expressed in all testicular cells; spermatogonia- and Sertoli-derived cell lines treated with cigarette smoke extract (CSE) in vitro showed down-regulation of CDK14 mRNA and protein levels as well as down-regulation of β-catenin levels. CS-induced down-regulation of CDK14 mRNA and protein levels was also observed in several lung epithelium-derived cell lines including primary normal human bronchial epithelial cells (NHBE), suggesting that the effect is not restricted to the testis. Similar to testicular cells, CS-induced down-regulation of CDK14 in lung cells correlated with decreased levels of β-catenin, a finding suggesting impaired Wnt signaling. In the lungs, CDK14 was localized to the alveolar and bronchial epithelium.
Insights
Cigarette smoke exposure down-regulates Cdk14 gene expression in mouse testes and lung cells, impacting Wnt signaling and potentially affecting spermatogenesis and lung epithelium. This study highlights the widespread effects of tobacco smoke on gene regulation.
Area of Science:
- Reproductive biology
- Toxicology
- Molecular biology
Background:
- Tobacco smoke exposure is linked to various health issues, including reproductive dysfunction.
- Gene expression alterations are a key mechanism underlying smoke-induced toxicity.
- The Wnt signaling pathway plays a crucial role in both spermatogenesis and lung development.
Purpose of the Study:
- To investigate the impact of chronic cigarette smoke (CS) exposure on gene expression patterns in the mouse testis.
- To characterize the role of Cyclin-dependent kinase 14 (Cdk14) in response to CS exposure.
- To determine if CS affects Cdk14 expression and Wnt signaling in other tissues, such as the lung.
Main Methods:
- DNA arrays were used to analyze gene expression changes in mouse testes after 24 weeks of CS exposure.
- Reverse transcription-polymerase chain reaction (RT-PCR) was employed to confirm Cdk14 down-regulation.
- In vitro studies utilized spermatogonia, Sertoli, and lung epithelial cell lines treated with cigarette smoke extract (CSE).
Main Results:
- CS exposure significantly altered the expression of several genes involved in spermatogenesis.
- Cdk14 mRNA and protein levels were down-regulated in the testes of CS-exposed mice.
- CS exposure also led to down-regulation of Cdk14 and β-catenin in testicular and lung epithelial cells, indicating impaired Wnt signaling.
Conclusions:
- Cigarette smoke exposure induces down-regulation of Cdk14 in both testicular and lung tissues.
- The observed decrease in Cdk14 and β-catenin suggests that CS impairs Wnt signaling pathways in multiple organs.
- These findings indicate that CS may negatively affect spermatogenesis and lung epithelial cell function through Cdk14-mediated pathways.
More Related Videos
10:47Isolation of Mouse Respiratory Epithelial Cells and Exposure to Experimental Cigarette Smoke at Air Liquid Interface
Published on: February 21, 2011
08:40Optimization of the Wound Scratch Assay to Detect Changes in Murine Mesenchymal Stromal Cell Migration After Damage by Soluble Cigarette Smoke Extract
Published on: December 3, 2015
Related Concept Videos
02:34Inhibition of CDK Activity
02:34Inhibition of Cdk Activity