Cigarette smoke exposure has been shown to upregulate IL-17 expression in human lung tissue [36] and in mice [37].
In the adult, glucocorticoids have been shown to upregulate beta-adrenergic control of adenylate cyclase by a variety of mechanisms; glucocorticoids are also thought to play a role in development of cardiac adrenergic function.
Other teleosts such as the killifish have been shown to upregulate telomerase during fin regeneration [12].
Androgens have been shown to upregulate SCAP expression, subsequently increasing SREBP-2 activation [32].
Pro-inflammatory cytokines have been shown to upregulate CD98 expression in IECs [14], [40].
NF-κB activation by API2-MALT1 has been shown to upregulate anti-apoptotic genes [25], [27].
Several additional KSHV genes have also been shown to upregulate cytokine levels.
Ifi205 has been shown to upregulate the cell cycle inhibitor P21 by interacting with p53 [31].
IL-10 has previously been shown to upregulate NO production in activated macrophages in a dose dependent manner [36].
In vitro, a variety of proinflammatory and atherogenic factors including cytokines and oxidized low-density lipoproteins has been shown to upregulate MMP-9 expression in monocytes [24], [40].
AMPK activation via AICAR treatment has previously been shown to upregulate PGC-1α mRNA and protein expression in skeletal muscle [9], [27] [29].
