Harmine promotes osteoblast differentiation through bone morphogenetic protein signaling |
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| Authors: | Yonezawa Takayuki Lee Ji-Won Hibino Ayaka Asai Midori Hojo Hironori Cha Byung-Yoon Teruya Toshiaki Nagai Kazuo Chung Ung-Il Yagasaki Kazumi Woo Je-Tae |
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| Institution: | aDepartment of Chemistry and Biochemistry and The Biomolecular Sciences Programme, Laurentian University, Sudbury, ON, Canada P3E 2C6;bDepartment of Medicine, Dartmouth-Hitchcock Medical Center, Lebanon, NH 03766, USA;cDivision of Cardiovascular Disease and Critical Care Medicine, Cooper University Hospital, Robert Wood Johnson Medical School, Camden, NJ 08103, USA;dSection of Critical Care Medicine, University of Manitoba, Winnipeg, MB, Canada R3A 1R9 |
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| Abstract: | Sepsis, the systemic response to infection, is the leading cause of death in the intensive care units worldwide. Septic patients can succumb through the development of early refractory hypotension or late multiple organ dysfunction. Misregulation of apoptosis during sepsis may contribute to cellular dysfunction and multiple organ dysfunction. Utilizing a tissue culture model which mimics the human disease, we demonstrate that the addition of sera derived from septic patients induces apoptosis in human fibroblast cells. Addition of septic sera to 2fTGH cells induced apoptosis by activating caspase 8, caspase 3 and DNA fragmentation factor 40 (DFF 40). Interestingly, the addition of septic sera to cells which lack STAT1 (U3A cells) did not activate DFF 40. U3A cells were also shown to be resistant to septic serum induced apoptosis. These data suggest that DFF 40 mediated apoptosis plays a significant role in mediating sepsis induced cellular dysfunction. |
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| Keywords: | Sepsis Cytokines Apoptosis Caspases DNA fragmentation factor 40 (DFF 40) |
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