Cigarette Smoke‐Induced Disease

Rennard, Stephen I.; Hepp, Lisa M.; Stockley, Robert A.; Rabe, Klaus F.; Celli, Bartolomé R.

doi:10.1002/9780470755976.ch33

Cited by 5 publications

(5 citation statements)

References 81 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Cigarette smoke is well recognized as the major cause of pulmonary emphysema (Rennard and Daughton, 1998). It is likely that cigarette smoke induces emphysema by a variety of mechanisms.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Prostaglandin E₂ protects human lung fibroblasts from cigarette smoke extract‐induced apoptosis via EP₂ receptor activation

Sugiura

Liu

Togo

et al. 2006

Journal Cellular Physiology

Self Cite

View full text Add to dashboard Cite

Prostaglandin E(2) (PGE(2)) has been shown to have a strong cytoprotective effect, inhibiting apoptosis. In the present study, we evaluated whether PGE(2) has a protective effect on cigarette smoke extract (CSE)-induced apoptosis in human lung fibroblasts. Apoptosis was assessed by various methods, including DNA content analysis. CSE (15%-20%) led to apoptosis and induced imbalance in favor of pro- over anti-apoptotic protein expression and activated caspases. PGE(2) blocked CSE-induced apoptosis and modulated the balance of pro- and anti-apoptotic proteins and decreased the activation of caspases. This anti-apoptotic effect was mediated via EP(2) receptor activation as the EP(2) agonist butaprost mimicked PGE(2) activity and siRNA for the EP(2) receptor blocked it. An adenylyl cyclase inhibitor was found to abolish the PGE(2)-mediated cytoprotective effect. Correspondingly, c-AMP analogs blocked CSE-induced apoptosis. Consistently, the protein kinase A (PKA) inhibitor KT-5720 abolished PGE(2)-mediated protection. PGE(2) and butaprost phosphorylated Bad and KT-5720 blocked phosphorylation. These results suggest that PGE(2) inhibits CSE-induced apoptosis via EP(2) receptor activation and activation of PKA, which leads to an alteration in the balance between pro- and anti-apoptotic factors. Through such a mechanism, PGE(2) may alter survival of cells in the smoke-exposed lungs, thus affecting the pathogenesis of cigarette smoke-induced disease.

show abstract

“…Cigarette smoke is well recognized as the major cause of pulmonary emphysema (Rennard and Daughton, 1998). It is likely that cigarette smoke induces emphysema by a variety of mechanisms.…”

Section: Discussionmentioning

confidence: 99%

“…Cigarette smoke is the major risk factor for the development of chronic obstructive pulmonary disease (COPD) (Rennard and Daughton, 1998) and for the development of lung cancer (Prager et al, 2000). It is likely that several mechanisms contribute to cigarette smoke-induced disease.…”

mentioning

confidence: 99%

Prostaglandin E₂ protects human lung fibroblasts from cigarette smoke extract‐induced apoptosis via EP₂ receptor activation

Sugiura

Liu

Togo

et al. 2006

Journal Cellular Physiology

Self Cite

View full text Add to dashboard Cite

show abstract

“…The accumulation of these mutations in lung structural cells has also been suggested to contribute to COPD (61). A well-recognized toxicity of cigarette smoke is its ability to damage DNA by several mechanisms (62). In the face of this damage, however, cigarette smoke can also inhibit apoptosis (51,63).…”

Section: Repair Functions In Cells In Patients With Copdmentioning

confidence: 99%

Cigarette Smoke Inhibits Alveolar Repair: A Mechanism for the Development of Emphysema

Rennard¹,

Togo²,

Holz³

2006

Proceedings of the American Thoracic Society

112

View full text Add to dashboard Cite

Classically, emphysema has been believed to develop when mediators of tissue injury exceed protective mechanisms within the lung. Evidence also supports the concept that tissue destruction represents a balance between tissue injury and tissue repair. In this context, cigarette smoke is directly toxic to cells within the lung and can impair the repair functions of fibroblasts, epithelial cells, and mesenchymal cells. This may occur in the absence of overt cytotoxicity and may result from alteration of selected biochemical pathways. A variety of repair functions can be affected, including chemotaxis, proliferation, production of extracellular matrix, and remodeling of extracellular matrix. Finally, cigarette smoke can damage DNA but can also compromise apoptosis. As a result, DNA repair mechanisms can be initiated, leading to recovery of cells that potentially contain somatic cell mutations. This pathway may contribute not only to the development of cancer but to the persistent abnormalities in tissue structure that characterize chronic obstructive pulmonary disease. Understanding the mechanisms that mediate normal tissue repair and understanding the bases for altered tissue repair in the face of cigarette smoking offer new opportunities designed to address the structural alterations that characterize chronic obstructive pulmonary disease.

show abstract

“…3,4 Smoking is the main etiological factor to cause COPD followed by occupational dusts, biomass fuels etc. 5,6 Once the disease is diagnosed, patient education, smoking cessation, pharmacological and non-pharmacological methods are required to ameliorate signs and symptoms of COPD. 7,8 The pharmacological treatments include bronchodilators, corticosteroids, immunizations, antibiotics, mucokinetics and others.…”

Section: Introductionmentioning

confidence: 99%

A Cross-Sectional Study of Medication Adherence Pattern and Factors Affecting the Adherence in Chronic Obstructive Pulmonary Disease

Shrestha

Pant

Shrestha

et al. 2015

Kathmandu Univ. Med. J.

View full text Add to dashboard Cite

show abstract

Cigarette Smoke‐Induced Disease

Cited by 5 publications

References 81 publications

Prostaglandin E₂ protects human lung fibroblasts from cigarette smoke extract‐induced apoptosis via EP₂ receptor activation

Prostaglandin E₂ protects human lung fibroblasts from cigarette smoke extract‐induced apoptosis via EP₂ receptor activation

Cigarette Smoke Inhibits Alveolar Repair: A Mechanism for the Development of Emphysema

A Cross-Sectional Study of Medication Adherence Pattern and Factors Affecting the Adherence in Chronic Obstructive Pulmonary Disease

Contact Info

Product

Resources

About

Cigarette Smoke‐Induced Disease

Cited by 5 publications

References 81 publications

Prostaglandin E2 protects human lung fibroblasts from cigarette smoke extract‐induced apoptosis via EP2 receptor activation

Prostaglandin E2 protects human lung fibroblasts from cigarette smoke extract‐induced apoptosis via EP2 receptor activation

Cigarette Smoke Inhibits Alveolar Repair: A Mechanism for the Development of Emphysema

A Cross-Sectional Study of Medication Adherence Pattern and Factors Affecting the Adherence in Chronic Obstructive Pulmonary Disease

Contact Info

Product

Resources

About

Prostaglandin E₂ protects human lung fibroblasts from cigarette smoke extract‐induced apoptosis via EP₂ receptor activation

Prostaglandin E₂ protects human lung fibroblasts from cigarette smoke extract‐induced apoptosis via EP₂ receptor activation