Increase in hypotonic stress-induced endocytic activity in macrophages via ClC-3

• Published in: Molecules and cells Vol. 37; no. 5; pp. 418 - 425
• Main Authors: Yan, Yutao, Ding, Yu, Ming, Bingxia, Du, Wenjiao, Kong, Xiaoling, Tian, Li, Zheng, Fang, Fang, Min, Tan, Zheng, Gong, Feili
• Format: Journal Article
• Language: English
• Published: United States Korean Society for Molecular and Cellular Biology 01.05.2014; 한국분자세포생물학회
• Subjects: Animals; Apoptosis; B7-1 Antigen - metabolism; B7-2 Antigen - metabolism; Cells, Cultured; Chloride Channels - genetics; Chloride Channels - metabolism; Female; Gene Expression; Interleukin-10 - metabolism; Macrophages - physiology; Mice, Inbred C57BL; Osmotic Pressure; Pinocytosis; Stress, Physiological; Tumor Necrosis Factor-alpha - metabolism; 생물학
• ISSN: 1016-8478; 0219-1032
• DOI: 10.14348/molcells.2014.0031

Extracellular hypotonic stress can affect cellular function. Whether and how hypotonicity affects immune cell function remains to be elucidated. Macrophages are immune cells that play key roles in adaptive and innate in immune reactions. The purpose of this study was to investigate the role and underlying mechanism of hypotonic stress in the function of bone marrow-derived macrophages (BMDMs). Hypotonic stress increased endocytic activity in BMDMs, but there was no significant change in the expression of CD80, CD86, and MHC class II molecules, nor in the secretion of TNF-α or IL-10 by BMDMs. Furthermore, the enhanced endocytic activity of BMDMs triggered by hypotonic stress was significantly inhibited by chloride channel-3 (ClC-3) siRNA. Our findings suggest that hypotonic stress can induce endocytosis in BMDMs and that ClC-3 plays a central role in the endocytic process.