| First Author | Roth M | Year | 2020 |
| Journal | J Neurosci Res | Volume | 98 |
| Issue | 5 | Pages | 826-842 |
| PubMed ID | 31758600 | Mgi Jnum | J:284549 |
| Mgi Id | MGI:6390232 | Doi | 10.1002/jnr.24557 |
| Citation | Roth M, et al. (2019) Parenchymal pericytes are not the major contributor of extracellular matrix in the fibrotic scar after stroke in male mice. J Neurosci Res |
| abstractText | 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 (PDGFRss(+) ) 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 PDGFRss(+) 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 PDGFRss(+) cells due to the loss of regulator of G-protein signaling 5 in pericytes. We find that only a small fraction of parenchymal PDGFRss(+) cells co-label with type I collagen and fibronectin. Consequently, a reduction in parenchymal PDGFRss(+) cells by ca. 50% did not affect the overall type I collagen or fibronectin deposition after stroke. The redistribution of PDGFRss(+) 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 PDGFRss(+) cells are not the main contributor to the fibrotic ECM, and therefore targeting these cells might not impact on fibrotic scar formation after stroke. |
