Skip to main content
. 2020 Jan 31;11:630. doi: 10.1038/s41467-020-14466-y

Fig. 6. Working model for the role of fibrinogen on SVZ NSPCs in CNS disease.

Fig. 6

In the healthy brain, NSPCs of the SVZ continuously generate mobile DCX+ neuroblasts that migrate through the rostral migratory stream to the olfactory bulb to become newborn neurons. Cortical injury results in increased SVZ vasculature permeability and fibrinogen deposition into the SVZ stem cell niche environment. Fibrinogen activates BMP receptor signaling via its αC domain inducing NSPC differentiation into neuroprotective astrocytes, which migrate towards the cortical lesion area and secrete Thbs4. Local provisional fibrinogen thus activates BMP signaling in NSPCs inducing their differentiation into astrocytes at sites of vascular permeability in the CNS. CSF cerebrospinal fluid, NSPCs neural stem/precursor cells, RGD Arg–Gly-Asp sequence (integrin binding site), SVZ subventricular zone. The Astrocyte image was adapted from http://togotv.dbcls.jp/ja/togopic.2011.17.html, under Creative Commons Attribution 4.0 International (CC BY 4.0) license. The original astrocyte image was designed by Hiromasa Ono. The Brain image was adapted from https://icon-icons.com/de/symbol/Gehirn/39333, under Creative Commons Attribution 4.0 International (CC BY 4.0) license. The original brain image was designed by Lorc, Delapouite & contributors.