| First Author | Tan JC | Year | 2024 |
| Journal | Sci Rep | Volume | 14 |
| Issue | 1 | Pages | 3517 |
| PubMed ID | 38347040 | Mgi Jnum | J:363443 |
| Mgi Id | MGI:7595051 | Doi | 10.1038/s41598-024-53659-z |
| Citation | Tan JC, et al. (2024) Aqueous humor TGFbeta and fibrillin-1 in Tsk mice reveal clues to POAG pathogenesis. Sci Rep 14(1):3517 |
| abstractText | Aqueous humor (AH) and blood levels of transforming growth factor beta (TGFbeta) are elevated in idiopathic primary open angle glaucoma (POAG) representing a disease biomarker of unclear status and function. Tsk mice display a POAG phenotype and harbor a mutation of fibrillin-1, an important regulator of TGFbeta bioavailability. AH TGFbeta2 was higher in Tsk than wild-type (WT) mice (by 34%; p = 0.002; ELISA); similarly, AH TGFbeta2 was higher in human POAG than controls (2.7-fold; p = 0.00005). As in POAG, TGFbeta1 was elevated in Tsk serum (p = 0.01). Fibrillin-1 was detected in AH from POAG subjects and Tsk mice where both had similar levels relative to controls (p = 0.45). 350 kDa immunoblot bands representing WT full-length fibrillin-1 were present in human and mouse AH. A 418 kDa band representing mutant full-length fibrillin-1 was present only in Tsk mice. Lower molecular weight fibrillin-1 antibody-reactive bands were present in similar patterns in humans and mice. Certain bands (130 and 32 kDa) were elevated only in human POAG and Tsk mice (p </= 0.04 relative to controls) indicating discrete isoforms relevant to disease. In addition to sharing a phenotype, Tsk mice and human POAG subjects had common TGFbeta and fibrillin-1 features in AH and also blood that are pertinent to understanding glaucoma pathogenesis. |
