Journal
JOURNAL OF NEUROSCIENCE RESEARCH
Volume 98, Issue 5, Pages 826-842Publisher
WILEY
DOI: 10.1002/jnr.24557
Keywords
collagen; extracellular matrix; fibronectin; fibrotic scar; glial scar; pericytes; RRID; AB_2082660; RRID; AB_2105706; RRID; AB_2162497; RRID; AB_217595; RRID; AB_2298772; RRID; AB_298179; RRID; AB_305808; RRID; AB_354858; RRID; AB_393571; RRID; AB_467492; RRID; SCR_002798; RRID; SCR_003070; RRID; SCR_010279; stroke
Categories
Funding
- Vetenskapsradet [2015-02468]
- Crafoordska Stiftelsen [2015-02468]
- Stiftelsen Olle Engkvist Byggmastare [2014/184]
- Kungliga Fysiografiska Sallskapet i Lund
- Aners Foundation [FB17-0054]
- Swedish Research Council [2015-02468] Funding Source: Swedish Research Council
- Vinnova [2015-02468] Funding Source: Vinnova
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Scar formation after injury of the brain or spinal cord is a common event. While glial scar formation by astrocytes has been extensively studied, much less is known about the fibrotic scar, in particular after stroke. Platelet-derived growth factor receptor ss-expressing (PDGFR ss(+)) pericytes have been suggested as a source of the fibrotic scar depositing fibrous extracellular matrix (ECM) proteins after detaching from the vessel wall. However, to what extent these parenchymal PDGFR ss(+) cells contribute to the fibrotic scar and whether targeting these cells affects fibrotic scar formation in stroke is still unclear. Here, we utilize male transgenic mice that after a permanent middle cerebral artery occlusion stroke model have a shift from a parenchymal to a perivascular location of PDGFR ss(+) cells due to the loss of regulator of G-protein signaling 5 in pericytes. We find that only a small fraction of parenchymal PDGFR ss(+) cells co-label with type I collagen and fibronectin. Consequently, a reduction in parenchymal PDGFR ss(+) cells by ca. 50% did not affect the overall type I collagen or fibronectin deposition after stroke. The redistribution of PDGFR ss(+) cells to a perivascular location, however, resulted in a reduced thickening of the vascular basement membrane and changed the temporal dynamics of glial scar maturation after stroke. We demonstrate that parenchymal PDGFR ss(+) cells are not the main contributor to the fibrotic ECM, and therefore targeting these cells might not impact on fibrotic scar formation after stroke.
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