AMPK Methods and Protocols

(Rick Simeone) #1

  1. Longer time points could potentially skew interpretation given
    the metabolism of lipids into which^3 H-acetate has been
    incorporated. This may not reflect only synthesis.

  2. At this point, the chloroform (lipid-containing) phase can be
    evaporated to dryness under a stream of nitrogen gas for TLC
    separation or saponified with KOH to extract^3 H-containing
    fatty acid and sterols, as described in other chapters of this
    issue.

  3. To calculate the nmol incorporation of^3 H-acetate into choles-
    terol, use the molar amount of sodium acetate and the radio-
    activity in the initial media to determine specific activity.

  4. If cell debris is present in tubes, this can be pelleted by cen-
    trifuging at 12,000gfor 5 min and the supernatant trans-
    ferred into a fresh 1.5 mL tube.

  5. It is important to note that the uptake of Dil-acLDL can be
    assessed under any permutation of lipid-loaded and AMPK
    activation treatments. The protocol detailed above assesses
    Dil-acLDL uptake in basal BMDM. Past work has demon-
    strated that there is no difference between wild-type and
    AMPKβ1-deficient macrophages in the presence or absence
    of A-769662 treatment.

  6. Each respective plate should be done in triplicate independent
    of how many technical replicates within treatment groups. One
    plate is to be used to assess HDL-mediated efflux, one for
    ApoA-І-mediated efflux, and basal efflux (used to calculate
    the percent-specific efflux).

  7. During the equilibration treatments, AMPK activators may be
    added to “prime” the system prior to the efflux phase of the
    experiment. Shorter equilibration times may be used ranging
    from 2 to 18 h.

  8. It is important to consider that AMPK activator treatment and
    AMPK deficiency can and do alter total cellular cholesterol
    pools. For example, if A-769662 is added to macrophages
    during the initial lipid-loading phase, there is a significant
    reduction in total cholesterol content, which confounds the
    assessment of^3 H-cholesterol. For this reason, it is critical to
    also measure total cellular cholesterol pools when introducing
    new AMPK genetic models or pharmacological activators/
    inhibitors. To this point, timing of AMPK activator treatment
    can also be tailored to suit investigations into transcriptional
    vs. acute posttranslational effects by modulating overall
    treatment time.

  9. Kinetics of cholesterol efflux in response to various AMPK
    activators can be observed by including numerous time points.

  10. Scintillation vials can be left to equilibrate overnight and
    should be counted after at least 24 h.


Assessing Macrophage Cholesterol Homeostasis 491
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