Using the Phoenix MICRON™ IV to examine a potential treatment for disrupted retinal vasculature

Many eye diseases, including age-related macular degeneration, diabetic macular edema, cancer growth, and uveitis, involve disrupted blood vessel growth and leakage. Curing the leakage and growth helps modulate and treat the underlying disease. The Phoenix MICRON™ IV fundus camera allows for clear visualization of the rodent vasculature in bright field and with fluorescein angiography. Mirando et al, in their paper “A collagen IV-derived peptide disrupts α5β1 integrin and potentiates Ang2/Tie2 signaling,” examine the cell signaling pathway that leads to disrupted blood vessel physiology in the eye. In a comprehensive paper that studies the details of the molecule all the way up to the in-vivo mouse eye, they identify a potential target for diseases involving vascular leakage.

Mirando et al thoroughly discuss the angiopoietin (ang)/Tie system in their paper. In an oversimplified summary: Ang1 works with Tie2 in the healthy eye to keep firm endothelial cell junctions with no blood leakage; in the diseased eye, elevated levels of Ang2 destabilize the vasculature and lead to new blood vessels and leakage by antagonizing Ang1. The researchers use a peptide, AXT107, to elegantly use the normally disruptive Ang2 as an agent for stabilizing the vasculature and reducing leakage.

FA Images from Mirando et al paper
Figure 1. AXT107 improves disrupted vasculature as shown with fluorescein angiography and the Phoenix MICRON IV. A: Mice overexpressing Ang2 show excessive blood leakage. B: Mice overexpressing Ang2 and treated with AXT107 have normal looking vasculature. C: Control, wild type mice with no treatment or disorder.

 

The Phoenix MICRON IV live fundus camera is an essential tool for studying vasculature. Crisp, live video and specialized filters allow fluorescein angiography that shows the structure of the blood vessels and leakage. Mirando et al examined the in-vivo effects of AXT107 by using mice with overexpressed Ang2 and subsequently disrupted vasculature (Figure 1, A). When treated with AXT107, the blood vessels appeared normal and had minimal leakage (Figure 1, B), similar to the control, wild type mice (Figure 1, C). The Phoenix MICRON IV shows a stark difference between the diseased and treated mice, demonstrating the promise of AXT107 as a treatment for vasculature-disrupting diseases.

 

Article citation: Mirando, A. C., Shen, J., Silva, R., Chu, Z., Sass, N. C., Lorenc, V. E., Green, J. J., Campochiaro, P. A., Popel, A. S., Pandey, N. B. (2019). A collagen IV-derived peptide disrupts α5β1 integrin and potentiates Ang2/Tie2 signaling. JCI insight4(4), e122043. doi:10.1172/jci.insight.122043