Original Research-Basic Science
Scar formation and lack of regeneration in adult and neonatal liver after stromal injury
Article first published online: 10 DEC 2012
© 2012 by the Wound Healing Society
Wound Repair and Regeneration
Volume 21, Issue 1, pages 122–130, January-February 2013
How to Cite
Masuzaki, R., Zhao, S. R., Csizmadia, E., Yannas, I. and Karp, S. J. (2013), Scar formation and lack of regeneration in adult and neonatal liver after stromal injury. Wound Repair and Regeneration, 21: 122–130. doi: 10.1111/j.1524-475X.2012.00868.x
- Issue published online: 8 JAN 2013
- Article first published online: 10 DEC 2012
- Manuscript Accepted: 25 SEP 2012
- Manuscript Received: 9 FEB 2012
- Center for Integration of Medicine and Innovative Technology at the Massachusetts Institute of Technology
- Transplant Center of the Beth Israel Deaconess Medical Center
- Vanderbilt University Medical Center
Figure S1. Collagen deposition over time in response to stromal injury. Immunohistochemistry shows no collagen deposition 6 hours after injury (A). By 48 hours after injury, diffuse staining for collagen I is present (arrow, B), which becomes more intense by 4 days in a double line pattern flanking the injury (arrows, C). By 7 days, the double line has coalesced into a single line (arrows, D) and the parenchyma contracts (circle, D). The pattern persists at 28 days (E). Magnification 100×.
Figure S2. Sirius Red staining over time in response to stromal injury. Sirius Red staining shows no fibrosis 6 or 24 hours after injury (A,B). By 4 days, there is a double line pattern (C), which coalesces into a single line by 7 days (D) and 28 days (E). This pattern is similar to collagen I staining. Magnification 100×
Figure S3. Proliferation around the area of injury after stromal injury. BrdU incorporation reveals no proliferating cells 6 hours after injury (A). By 48 hours, many cells in the area stain for BrdU (B, brown nuclear staining), which continues at 4 days after injury (C). By 7 days and continuing to 14 days, there are few proliferating cells (D,E). Magnification 400×.
Figure S4. Granulocyte response to stromal injury. Immunohostochemistry for GR-1 shows no neutrophils prior to injury (A). Six hours after injury, neutrophils have infiltrated the area of injury (B). These persist through 48 hours and 4 days (C,D) and are gone by 14 days (E). Magnification 400×.
Figure S5. Quiescent stellate cells after injury. Immunohistochemistry for the quiescent stellate cell marker GFAP. Between 0 and 14 days after injury, staining remains diffuse. Magnification 200×.
Figure S6. Stellate cell activation in response to stromal injury. Immunohostochemistry for SM-22 shows low level staining prior to injury (A). Six hours after injury, stellate cells become activated (B, brown staining), which becomes more intense at the edge of the injury by 48 and hours and 4 days after the injury (C,D). By 14 days after the injury, activated cells are gone (E). Magnification 400×.
Figure S7. Stellate cell activation in response to stromal injury using vimentin. Immunohostochemistry for the stellate cell activation marker vimentin shows a similar pattern to SM-22. There is occasional staining at baseline (A), which increases by 48 hours and 4 days (B–D) and which takes on a linear pattern at 14 days (E). Magnification 400×.
Please note: Wiley Blackwell is not responsible for the content or functionality of any supporting information supplied by the authors. Any queries (other than missing content) should be directed to the corresponding author for the article.