Lenses of SPARC-null mice exhibit an abnormal cell surface-basement membrane interface

Area of Science:

• Ophthalmology
• Cell Biology
• Biochemistry

Background:

• Secreted protein acidic and rich in cysteine (SPARC) is a matricellular protein crucial for cell-matrix interactions.
• SPARC-deficient mice exhibit early-onset posterior cortical cataracts, progressing to opacity and capsule rupture.

Purpose of the Study:

• To investigate the primary effects of SPARC deficiency on lens ultrastructure.
• To examine the basement membrane (capsule)-lens cell interface in SPARC-null mice.

Main Methods:

• Electron microscopy of SPARC-null and wild-type mouse lenses.
• Immunohistochemistry, including rhodamine-phalloidin labeling for actin filaments.

Main Results:

• SPARC deficiency leads to filopodial projections from basal lens epithelial and fiber cells into the lens capsule.
• These projections increase in size and frequency with cataract progression.
• Actin filaments are present within these basal invasive filopodia.

Conclusions:

• Absence of SPARC in murine lenses induces basal filopodial protrusions into the lens capsule.
• These ultrastructural alterations precede lens opacification in the SPARC-null cataract model.
• Findings support SPARC's role in modulating cell shape and cell-matrix interactions within the lens.