Mitochondrial impact on nerve growth factor production in vascular smooth muscle-derived cells.
Ht30</=Ht10>/=Ht5). Cells with reduced mitochondrial activity also showed abnormal responses to the stimulation of NGF output. Thrombin and phorbol ester elevated NGF production from Ht100, Ht30 and Ht10 cells, but not from Ht5 cells. Ht30 cells, despite secreting less NGF basally than Ht100 cells, reached a similar or greater NGF output upon stimulation. Mitogens increased NGF output and NGF mRNA levels with the largest effect on NGF protein in Ht30 cells. Free radical production and the ability of cells to respond to NGF-inducing agents were related. These data suggest that chronic impairment of mitochondrial function associates with disturbances in cellular production of a signaling protein.
Sherer
T B
TB
Center for the Study of Neurodegenerative Disease, Health Science Center, University of Virginia, MR4 Box 5148, Charlottesville, VA 22908, USA.
Neff
P S
PS
Parks
J K
JK
Tuttle
J B
JB
D000818:Animals; D002460:Cell Line; D019069:Cell Respiration; D004996:Ethidium / Q000494:pharmacology; D005609:Free Radicals / Q000032:analysis; D008928:Mitochondria / Q000502:physiology*; D009131:Muscle, Smooth, Vascular / Q000378:metabolism*; D020932:Nerve Growth Factor / Q000096:biosynthesis* / Q000235:genetics; D012333:RNA, Messenger / Q000096:biosynthesis; D051381:Rats; D015398:Signal Transduction / Q000502:physiology; D013755:Tetradecanoylphorbol Acetate / Q000494:pharmacology; D013917:Thrombin / Q000494:pharmacology; D013997:Time Factors
D005609:Free Radicals; D012333:RNA, Messenger; D020932:Nerve Growth Factor; D013917:Thrombin; D004996:Ethidium; D013755:Tetradecanoylphorbol Acetate