Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034067 (emphysema)
 11,506 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Apoptosis is important in developmental biology and in remodeling of tissues during repair. Apoptosis also plays important roles in the progression of many diseases. The cellular and molecular mechanisms of apoptosis, in general, have been extensively demonstrated. However, the causes and the roles of apoptosis of various cell types in the lung are not well understood. We have determined that adenosine/homocysteine causes lung vascular endothelial cell apoptosis by inhibition of carboxyl methylation of the small GTPase, Ras, through inhibition of isoprenylcysteine carboxyl methyltransferase(ICMT) activity, leading to inactivation of Ras and the subsequent disruption of focal adhesion complexes, resulting in cell-extracellular matrix detachment and anoikis. Apoptosis can either ameliorate or exacerbate lung injury, depending upon the cell type. Although apoptosis of polymorphonuclear leukocytes in the lung prevents inflammation and the development of acute respiratory distress syndrome during acute lung injury, Fas/FasL-mediated alveolar epithelial cell apoptosis promotes acute lung injury and pulmonary fibrosis. Lung epithelial and endothelial cell apoptosis also contributes to the development of emphysema. This article focuses on elucidating the mechanisms of adenosine/homocysteine-induced endothelial cell apoptosis. We also review the current understanding of the role of lung cell apoptosis in acute lung injury, pulmonary fibrosis and emphysema.
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PMID:Apoptosis and lung injury. 1645 28

C57Bl/6J, DBA/2 and ICR mouse strains are known to possess different susceptibilities to developing emphysema after exposure to cigarette smoke with DBA/2 and C57Bl/6J strains being significantly more susceptible to pulmonary damage than the ICR strain. This study was aimed at analysing the occurrence of systemic oxidative stress in the blood of these different mouse strains after exposure to cigarette smoke. This study did not observe a significant decrease in glutathione in erythrocytes or in plasma cysteine, cysteinylglycine, homocysteine and glutathione in C57Bl/6J or DBA/2 mice, whereas a significant increase in the corresponding oxidized forms was observed in plasma. However, the ICR strain showed a significant increase in glutathione in erythrocytes and a significant decrease in most of the oxidized forms of cysteine, cysteinylglycine, homocysteine and glutathione in plasma after the same exposition. These experiments demonstrate that exposure to cigarette smoking induces systemic oxidative stress only in some mouse strains which are susceptible to developing emphysema.
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PMID:Differential thiol status in blood of different mouse strains exposed to cigarette smoke. 1937 Apr 73