Local InsP₃-dependent perinuclear Ca²⁺ signaling in cardiac myocyte excitation-transcription coupling
J. Clin. Invest. Xu Wu, et al. 116:675 doi:10.1172/JCI27374 [Go to this article.]

Figure 4
HDAC5 nuclear export is Ca²⁺ dependent but not activated by global Ca²⁺ transients. (A) Adenoviral HDAC5-GFP–infected myocytes were also loaded with Rhod-2 to measure [Ca²⁺]_i. Rhod-2 is more concentrated in the nucleus (nuc), complicating Ca²⁺ transient calibration there. (B) HDAC5 remained nuclear when myocytes were field stimulated at 0.5 Hz (n = 5) or 1 Hz (n = 7) for 60 minutes or even at 2 Hz (not shown). (C) In permeabilized myocytes, internal [Ca²⁺] was increased from 100 nM to 500 nM (at 60 minutes) (n = 7). 2,3 butanedione monoxime (5 mM) was used to prevent contraction. (D) Expected local [Ca²⁺] gradient around the mouth of an InsP₃R Ca²⁺ channel: [Ca2+]_i = [Ca2+]_Init + q/(2πDr) × erfc{r/(2√Dr)}, where q = single channel current (0.1 pA), D = diffusion coefficient (600 μm²/s), [Ca2+]_Init = 100 nM, erfc = complementary error function, and r = radial distance from the channel mouth for hemispheric diffusion. This is the steady state, achieved in approximately 10 μs without buffering and much less than 1 ms when local Ca²⁺ buffering is included (26).