MRI Reporter Genes

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FIGURE 1.
Principles of CEST contrast mechanism. Frequency-selective saturation pulse is applied to label amide protons (A, green) or guanidyl protons (C, red) of polypeptide contrast agent. Labeled protons exchange with water protons, which leads to reduction in MRI signal intensity (ΔSI) in frequency-selective manner (B and D). CEST maps of MRI phantoms were acquired with frequency-selective saturation pulses (E) at ±3.7 ppm, which enhances PLL (F); at ±1.8 ppm, which enhances PLA (G); and at ±0.8 ppm, which enhances PLT (H). Merged composition image of maps (F–H) is shown in I. PBS = phosphate-buffered saline. (Modified from McMahon et al. (23) and Gilad et al. (24)).
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FIGURE 2.
MRI detection of endothelial overexpression of H-ferritin in transgenic mice. Expression of ferritin was regulated by vascular endothelial cadherin promoter in double transgenic mice but not in single transgenic siblings. Elevated R² was observed in liver and heart of E13.5 embryos studied in utero (A) and in brain of adult mice (B). TG = transgenic. (Adapted from Cohen et al. (18)).

TABLE 1

Comparison of Existing MR Reporter Genes

Gene	Contrast	Substrate	Advantages	Disadvantages
CK	³¹P-MRS	Endogenous adenosine triphosphate	No background signal in most tissues	Spectroscopic image (low resolution)
Tyrosinase	T2/T2*	Endogenous or exogenous iron	Rapid straightforward gene product	Signal dependent on availability of iron
β-gal	T1	Exogenous EgadMe	Positive contrast	Exogenous agent also gives partial signal without reporter gene
Transferrin receptor	T2/T2*	Exogenous transferrin-MION	High sensitivity	Accessibility and nonspecific uptake of substrate nanoparticles
Ferritin	T2/T2*	Endogenous or exogenous iron	High sensitivity	Delay of change in signal that is dependent on iron availability and ferritin loading factor
Mag A	T2/T2*	Endogenous or exogenous iron	High sensitivity	Delay of change in signal that is dependent on iron availability
LRP	CEST	None	Multicolor detection, on–off switchable	Current low sensitivity