Purpose.: Hevin is a matricellular protein and the result of a gene duplication of SPARC. SPARC-null mice have lower intraocular pressure (IOP). The function of hevin in trabecular meshwork (TM) is unknown. The authors hypothesized that hevin is expressed in TM and has a functional consequence on IOP.

Methods.: Reverse transcriptase-polymerase chain reaction (RT-PCR) and immunoblotting were performed to identify transcription and protein expression in TM and cultured TM cells. Toluidine blue stain was performed to compare anterior segments in wild-type (WT) and hevin-null mice. Confocal microscopy localized the structural distribution of hevin in human TM and hevin/SPARC in mouse anterior segments. IOP was measured in WT (C57BL6× 129SvJ) and hevin-null mice using both rebound tonometry and cannulation tonometry. Central corneal thickness (CCT) was measured by ocular coherence tomography. Cultured TM cells were treated with TGF-β2 because TGF-β2 is associated with primary open-angle glaucoma.

Results.: Hevin mRNA and protein were expressed in TM tissues but not in cultured TM cells. No structural differences were observed in anterior segments of WT and hevin-null mice. IOP between hevin-null (n= 46) and WT (n= 44) mice was equivalent (15.3±1.92 mm Hg and 15.9±2.01 mm Hg, respectively; P= 0.15). CCT was similar between hevin-null and WT mice (107.95±5.06 μm and 106.76±3.46 μm, respectively; P= 0.11). TGF-β2 did not induce hevin, whereas SPARC expression was induced in a dose-dependent manner in human TM cell cultures.

Conclusions.: Hevin does not appear to be critical to regulating IOP. Hevin is expressed in TM but, in contrast to SPARC, does not appear to be regulated by TGF-β2.