Skip to main content
. 2020 Sep 24;10:15641. doi: 10.1038/s41598-020-72779-w

Figure 7.

Figure 7

GIMs modulate specific genes responsible for ECM turnover with or without exogenous TGFβ2 in hTM cells. Primary hTM cells were cultured in the presence or absence of 100 nM dexamethasone for 4 weeks in complete growth media. Cells were subsequently removed using 20 mM ammonium hydroxide solution to obtain GIMs and vehicle control matrices (VehMs). Same strain, fresh primary hTM cells were then seeded on these matrices with or without exogenous 5 ng/ml TGFβ2 in 1% fetal bovine serum growth media for 7 days. RNA was extracted for reverse transcription and qPCR. GAPDH was used as an internal control for normalization. Bar graph for the gene expression of (A) Matrix metalloproteinase 1 (MMP1), (B) MMP2, (C) MMP9, (D) MMP14, (E) A disintegrin and metalloproteinase with a thrombospondin motif 4 (ADAMTS4), (F) Tissue inhibitor of matrix metalloproteinase 1 (TIMP1), and (G) TIMP2. Columns and error bars; means and standard error of mean (SEM). One-way ANOVA with the Tukey pairwise comparisons post hoc test was used for statistical analysis. (n = 4 biological replicates. *p < 0.05, **p < 0.01, ***p < 0.001 for the group of interest versus control, VehM. #p < 0.05, ##p < 0.01, ###p < 0.001 for the group of interest versus GIM. †p < 0.05, ††p < 0.01, †††p < 0.001 for VehM + TGFβ2 versus GIM + TGFβ2). hTM, human trabecular meshwork. GAPDH, Glyceraldehyde 3-phosphate dehydrogenase.