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Multiplexed high content screening reveals that cigarette smoke condensate-altered cell signaling pathways are accentuated through FAK inhibition in human bronchial cells.
Int J Toxicol. 2012 Jun; 31(3):257-66.IJ

Abstract

The mechanisms by which cigarette smoke condensate (CSC) disrupts F-actin and decreases cell motility in human bronchial (BEAS-2B) cells were assessed. The hypothesis that CSC activated focal adhesion kinase (FAK), mitogen-activated protein kinases (MAPKs), and paxillin in BEAS-2B cells was tested. When BEAS-2B cells were treated with 20 to 100 μg/mL CSC for 1 hour, FAK increased. The CSC caused F-actin disruption, while FAK inhibition alone caused actin aggregates to collapse to the cell periphery, but FAK inhibition combined with CSC caused actin aggregates to distribute throughout the cells. The CSC treatment of BEAS-2B cells showed a dose-dependent increase in the activation of the MAPKs, c-Jun, JNK, ERK, p38, and heat shock protein 27 (Hsp27) and paxillin. Focal adhesion kinase phosphorylation inhibition combined with CSC treatment increased p38 and ERK at 1 hour and 24 hours along with decreased cell number and motility compared with CSC treatment alone. CSC exerts changes in BEAS-2B cells by altering morphology and activating MAPK pathways.

Authors+Show Affiliations

Life Sciences, AW Spears Research Center, Greensboro, NC, USA. charleatacarter@yahoo.com

Pub Type(s)

Journal Article

Language

eng

PubMed ID

22550048

Citation

Carter, Charleata A.. "Multiplexed High Content Screening Reveals That Cigarette Smoke Condensate-altered Cell Signaling Pathways Are Accentuated Through FAK Inhibition in Human Bronchial Cells." International Journal of Toxicology, vol. 31, no. 3, 2012, pp. 257-66.
Carter CA. Multiplexed high content screening reveals that cigarette smoke condensate-altered cell signaling pathways are accentuated through FAK inhibition in human bronchial cells. Int J Toxicol. 2012;31(3):257-66.
Carter, C. A. (2012). Multiplexed high content screening reveals that cigarette smoke condensate-altered cell signaling pathways are accentuated through FAK inhibition in human bronchial cells. International Journal of Toxicology, 31(3), 257-66. https://doi.org/10.1177/1091581812440890
Carter CA. Multiplexed High Content Screening Reveals That Cigarette Smoke Condensate-altered Cell Signaling Pathways Are Accentuated Through FAK Inhibition in Human Bronchial Cells. Int J Toxicol. 2012;31(3):257-66. PubMed PMID: 22550048.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Multiplexed high content screening reveals that cigarette smoke condensate-altered cell signaling pathways are accentuated through FAK inhibition in human bronchial cells. A1 - Carter,Charleata A, Y1 - 2012/05/01/ PY - 2012/5/3/entrez PY - 2012/5/3/pubmed PY - 2012/10/4/medline SP - 257 EP - 66 JF - International journal of toxicology JO - Int J Toxicol VL - 31 IS - 3 N2 - The mechanisms by which cigarette smoke condensate (CSC) disrupts F-actin and decreases cell motility in human bronchial (BEAS-2B) cells were assessed. The hypothesis that CSC activated focal adhesion kinase (FAK), mitogen-activated protein kinases (MAPKs), and paxillin in BEAS-2B cells was tested. When BEAS-2B cells were treated with 20 to 100 μg/mL CSC for 1 hour, FAK increased. The CSC caused F-actin disruption, while FAK inhibition alone caused actin aggregates to collapse to the cell periphery, but FAK inhibition combined with CSC caused actin aggregates to distribute throughout the cells. The CSC treatment of BEAS-2B cells showed a dose-dependent increase in the activation of the MAPKs, c-Jun, JNK, ERK, p38, and heat shock protein 27 (Hsp27) and paxillin. Focal adhesion kinase phosphorylation inhibition combined with CSC treatment increased p38 and ERK at 1 hour and 24 hours along with decreased cell number and motility compared with CSC treatment alone. CSC exerts changes in BEAS-2B cells by altering morphology and activating MAPK pathways. SN - 1092-874X UR - https://www.unboundmedicine.com/medline/citation/22550048/Multiplexed_high_content_screening_reveals_that_cigarette_smoke_condensate_altered_cell_signaling_pathways_are_accentuated_through_FAK_inhibition_in_human_bronchial_cells_ L2 - https://journals.sagepub.com/doi/10.1177/1091581812440890?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -