Effects of Short-Term Cigarette Smoke Exposure on Fischer 344 Rats and on Selected Lung Proteins

Abstract

A short-term 5-day cigarette smoke exposure study was conducted in Fischer 344 rats to identify smoke-induced lung protein changes. Groups of 10 male and 10 female rats at 5 weeks of age were randomly assigned to one of four exposure groups. Animals received filtered air (control) or 75, 200, or 400 mg total particulate matter (TPM)/m 3 of diluted Kentucky reference 3R4F cigarette smoke. Nose-only exposures were conducted for 3 hours/day for 5 consecutive days. Mean body weights were significantly reduced only in male rats exposed to 400 mg TPM/m 3 . Body weight gains were significantly reduced in 200-and 400-mg TPM/m 3 -exposed males and in all smoke-exposed females compared with controls. Alveolar histiocytosis increased slightly in all smoke exposed-females and 200-and 400-mg TPM/m 3 -exposed males. Cyclooxygenase-2 staining increased at 400 mg TPM/m 3 . Matrix metalloproteinase-12 staining of alveolar macrophages and bronchiolar epithelia increased in smoke-exposed animals, especially 400-mg TPM/m 3 -exposed females. Protein kinase C-a staining increased in macrophages at 200-and 400-mg TPM/m 3 doses. c-Jun NH 2 -terminal kinases staining decreased in smoke-exposed tissues. The identified changed proteins play roles in inflammation, transformation, proliferation, stress activation, and apoptosis.

Effects of Human Umbilical Cord-Derived Mesenchymal Stem Cells on the Acute Cigarette Smoke-Induced Pulmonary Inflammation Model

“…5 at an average of 108.7 ± 72.8 mg/m 3 during the study period. Consistently, in previous reports, mice were exposed to CS at an average of 90-100 mg/m 3 (Chen et al, 2005;Carter and Misra, 2010;Schweitzer et al, 2011;Siggins et al, 2014).…”

“…Compared with bone marrow-and gingival tissue-derived MSCs, hUC-MSCs have been determined to display the highest immunomodulatory ability (Li et al, 2018). Doses of hUC-MSC between 1 × 10 6 and 4 × 10 6 cells/ml have been deemed effective in a previous study (Chen et al, 2005;Carter and Misra, 2010;Lin et al, 2017). For example, the hUC-MSC concentration of 3 × 10 6 cells/ml was administered in lung disease (Zhang et al, 2018).…”

Identification of nuclear phosphoproteins as novel tobacco markers in mouse lung tissue following short‐term exposure to tobacco smoke

“…Therefore, K8 and K18 may have been upregulated in order to moderate JNK signaling and to suppress inflammation and apoptosis. In contrast, another study in rats that had been exposed to tobacco smoke for 5 days reported that the intensity of staining for JNK in epithelial cells in lung parenchyma and for protein kinase C‐α (PKC‐α) in macrophages were increased, suggesting that PKC‐α is activated by exposure to tobacco smoke and leads to the activation of NF‐κB through the activation of JNK [53]. In addition, another study has reported increased expression of JNK and ERK2 following prolonged (over 1 month) exposure to tobacco smoke [54].…”

Upregulation of Multidrug Resistance-Associated Protein 1 by Allyl Isothiocyanate in Human Bronchial Epithelial Cell: Involvement of c-Jun N-Terminal Kinase Signaling Pathway

“…During the development of COPD, cigarette smoke extract was reported to affect the protective activity of MRP1 on lung tissue [ 24 ]. Additional studies reported that JNK expression in lung parenchyma was increased after tobacco smoke exposure for 5 days in rats and 4–12 weeks in guinea pigs [ 36 , 37 ]. In contrast, upregulation of phosphorylated keratin type 2 cytoskeletal 8 (K8) and keratin type 1 cytoskeletal 18 (K18) is to moderate JNK signaling in lung tissue of rats after a short time of tobacco smoke exposure [ 38 ].…”