Effect of Propranolol on Hyphae Formation Signal in Candida albicans

• Published in: Biological & Pharmaceutical Bulletin Vol. 32; no. 1; pp. 129 - 131
• Main Authors: Ueno, Yukihiro, Maruyama, Naoko, Kanno, Mika, Watanabe, Toshihiko, Ogasawara, Ayako, Mikami, Takeshi, Matsumoto, Tatsuji
• Format: Journal Article
• Language: English; Japanese
• Published: Japan The Pharmaceutical Society of Japan 01.01.2009; Pharmaceutical Society of Japan; Japan Science and Technology Agency
• Subjects: Adrenergic beta-Antagonists - pharmacology; agglutinin like sequence 3; agglutinin like sequence 8; Candida albicans; Candida albicans - drug effects; EFG1; Fungal Proteins - genetics; Fungal Proteins - metabolism; Gene Expression Regulation, Fungal - drug effects; Hyphae - drug effects; Hyphae - physiology; propranolol; Propranolol - pharmacology; RNA, Messenger - metabolism; Signal Transduction - drug effects; Time Factors
• ISSN: 0918-6158; 1347-5215
• DOI: 10.1248/bpb.32.129

Candida albicans (C. albicans) is known as an opportunistic pathogen that changes from a yeast form to a hyphae form in response to various outside environmental signals. The addition of propranolol inhibited hyphae formation of C. albicans. Propranolol inhibited the expression of agglutinin like sequence 3 (ALS3) and ALS8mRNA, which are regulated by the cAMP-EFG1 pathway in C. albicans. Propranolol did not affect the expression of CST20, HST7 or CPH1mRNA, which are components of the mitogen-activated protein (MAP) kinase cascade in C. albicans. The expression of CYR1mRNA, which encodes adenylate cyclase of C. albicans, was not affected by propranolol. These findings indicated that the interruption of hyphae formation by propranolol is caused by inhibition of the cAMP-EFG1 pathway, but not effects on the MAP kinase cascade.