Belinda Smith
Belinda Smith is a science and technology journalist in Melbourne, Australia.
White blood cells are the janitors of your circulatory system. They mop up debris and invading pathogens – and now, a new study has shown they also perform maintenance on blood vessels.
Researchers from China, led by Southwest University’s Chi Liu, used a laser to zap a blood vessel in a zebrafish brain in two. They then watched as a white blood cell (also called a macrophage) came along, grabbed the broken ends of the blood vessel and stuck them back together, stemming the bleed, before leaving the scene.
The work, published in the journal Immunity, could help develop drugs that help prevent associated conditions such as dementia.
As we age, tiny blood vessels called arterioles in our brain become less stretchy. This stiffness means they’re more prone to rupture, spurting “microbleeds” into brain tissue.
The brain can naturally repair itself, but how it does so has been a bit of a mystery. Microglia, a type of macrophage that resides in the brain, are thought to help stitch up tears and breaks. But are there any maintenance staff in the blood?
To find out, Liu and colleagues used a laser to blast a blood vessel apart in the brain of a live zebrafish, which simulated a human microbleed, then watched what happened with a special microscope.
After around 30 minutes, a macrophage showed up – perhaps attracted by a distress signal in the form of the molecule ATP which spilt out of the broken cells.
Macrophages are usually round, blobby cells. But when this macrophage reached the injury site, it extended two “arms” from its body towards the ends of the blood vessel. The arms exuded special molecules to latch on, then pulled the ends together.
Adhesion molecules produced by the blood vessel’s cells, the researchers suspect, then “glued” the vessel back together. Once the process was complete, which took around three hours, the macrophage left.
“After we confirmed that the macrophage mediates this repair through direct physical adhesion and generation of mechanical traction forces, we were excited,” Liu says.
“This is a previously unexpected role of macrophages.”
They then repeated the experiment, but instead of allowing the macrophage to get on with the job, they blasted it to bits with the same laser.
Another macrophage did eventually arrive at the scene, but simply ate the pieces of its destroyed counterpart and went on its way without tending to the blood vessel. This may be, the researchers suggest, because the ATP molecules which initially draw a macrophage to the injured area may have dissipated.
Macrophages aren’t the only blood vessel repair system, but they do seem to be the fastest.
In animals genetically designed to lack macrophages, Liu and colleagues found they could still fix damaged blood vessels. The damaged ends slowly extended towards each other and knitted together, but the process took around six hours – much slower than macrophage repair.
In situations where a macrophage turned up at a severed blood vessel but didn’t manage to fix it, the blood vessel didn’t heal itself. This may be because the macrophage signals to the blood vessel cells that help’s arrived, which stops any self-extension activity, but when it leaves that healing activity remains switched off.
Even though their experiments were carried out in zebrafish, geneticist and co-author Lingfei Luo believes the same could be seen in humans.
“Several aspects of vascular development and remodelling, associated with macrophages, are conserved in human and zebrafish,” Luo says.
