Clarithromycin delays progression of bronchial epithelial cells from G1 phase to S phase and delays cell growth via extracellular signal-regulated protein kinase suppression.

Antimicrobial Agents and Chemotherapy
Masaharu ShinkaiBruce K Rubin

Abstract

The nonsteroidal anti-inflammatory drugs have been shown to support cytoprotection of cells by shifting cells toward a quiescent state (G(0)/G(1)). Extracellular signal-regulated kinase (ERK) is required for cells to pass from G(1) phase into S phase, and macrolide antibiotics can inhibit ERK1/2 phosphorylation. However, previous reports suggest that macrolide antibiotics do not affect cell growth in bronchial epithelial cells. Therefore, we studied normal human bronchial epithelial (NHBE) cells to determine whether clarithromycin (CAM) suppresses ERK, delays bronchial epithelial cells from progressing to S phase, and delays cell growth. Exposure to CAM at 10 microg/ml daily over 4 days irreversibly decreased the cell proliferation with and without growth supplements (P < 0.0001). CAM also inhibited ERK1/2 phosphorylation over the first 90 min of exposure (P < 0.05 for 30 min, P < 0.0001 for 60 min, and P < 0.01 for 90 min) and decreased the ratio of phosphorylated ERK1/2 (pERK1/2) to total ERK1/2 (tERK1/2) (P < 0.0001). Incubation with CAM for 48 h increased the proportion of cells in G(1) phase (means +/- standard deviations) from 63.5% +/- 0.9% to 79.1% +/- 1.4% (P < 0.0001), decreased that in S phase from 19.8% +/- 1.2% to ...Continue Reading

References

Aug 1, 1991·The Journal of Histochemistry and Cytochemistry : Official Journal of the Histochemistry Society·T E Kute, Y Quadri
Oct 1, 1996·Antimicrobial Agents and Chemotherapy·K B PatelC H Nightingale
Jul 22, 1998·Proceedings of the National Academy of Sciences of the United States of America·C P WebbG F Vande Woude
Dec 10, 1999·The Journal of Biological Chemistry·O KranenburgW H Moolenaar
Aug 17, 2000·BioEssays : News and Reviews in Molecular, Cellular and Developmental Biology·K Roovers, R K Assoian
Dec 24, 2002·The Journal of Pharmacy and Pharmacology·Tat Khuen Lee, Ieva Stupans
Jun 24, 2003·American Journal of Physiology. Lung Cellular and Molecular Physiology·Yukihiro KanekoShigeru Kohno
Mar 5, 2004·British Journal of Cancer·S VicentL M Montuenga
Sep 14, 2004·American Journal of Respiratory and Critical Care Medicine·Wan C TsaiTheodore J Standiford
Jan 25, 2005·Molecular Cell·Michele K DoughertyDeborah K Morrison
Apr 7, 2005·Cancer Chemotherapy and Pharmacology·Shu-Zhen ChenYong-su Zhen
Aug 9, 2005·American Journal of Physiology. Lung Cellular and Molecular Physiology·Masaharu ShinkaiBruce K Rubin
Sep 13, 2005·Paediatric Respiratory Reviews·Masaharu Shinkai, Bruce K Rubin

❮ Previous
Next ❯

Citations

Mar 15, 2008·Respirology : Official Journal of the Asian Pacific Society of Respirology·Daisuke InoueMutsuo Yamaya
Mar 11, 2009·Respirology : Official Journal of the Asian Pacific Society of Respirology·Charles Feldman, Ronald Anderson
Jul 9, 2010·Clinical Microbiology Reviews·Soichiro Kanoh, Bruce K Rubin
Jul 11, 2012·Mediators of Inflammation·Helen C SteelCharles Feldman
Feb 16, 2010·Expert Opinion on Investigational Drugs·D M MurphyC Ward
Dec 8, 2009·Archivos de bronconeumología·Daniel Sevilla-SánchezNéstor Soler-Porcar
Feb 22, 2008·Pharmacology & Therapeutics·Masaharu ShinkaiBruce K Rubin
Oct 16, 2007·International Journal of Antimicrobial Agents·Evangelos J Giamarellos-Bourboulis
Mar 19, 2014·Pharmacology & Therapeutics·Michael J ParnhamRobin Vos
Mar 26, 2013·Respiratory Medicine·K Suresh BabuJ B Morjaria
Mar 14, 2012·International Immunopharmacology·Syh-Jae LinPei-Yzu Lee
Feb 7, 2018·Pediatric Pulmonology·Ricardo A MosqueraGiuseppe N Colasurdo
Mar 12, 2009·Current Opinion in Infectious Diseases·Charles Feldman, Ronald Anderson
Apr 3, 2019·Antimicrobial Agents and Chemotherapy·Shigeki NakamuraYoshitsugu Miyazaki

❮ Previous
Next ❯

Related Concepts

Related Feeds

CRISPR Screens in Drug Resistance

CRISPR-Cas system enables the editing of genes to create or correct mutations. This feed focuses on the application of CRISPR-Cas system in high-throughput genome-wide screens to identify genes that may confer drug resistance.