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Quantitative proteomics: TGFβ₂ signaling in trabecular meshwork cells
Kathryn E Bollinger1, John S Crabb, Xianglin Yuan
1Cole Eye Institute, Cleveland Clinic Foundation, Cleveland, Ohio 44195, USA.
Investigative Ophthalmology & Visual Science
|September 16, 2011
Summary
Transforming growth factor beta 2 (TGFβ₂) alters proteins in the trabecular meshwork (TM), offering new insights into primary open-angle glaucoma (POAG) pathogenesis. This study identifies novel TGFβ₂-affected proteins, potentially revealing new glaucoma biomarkers.
Area of Science:
- Ophthalmology
- Proteomics
- Cell Biology
Background:
- Transforming growth factor beta 2 (TGFβ₂) is elevated in primary open-angle glaucoma (POAG) patients' aqueous humor and trabecular meshwork (TM).
- TGFβ₂ is implicated in POAG pathogenesis and intraocular pressure (IOP) elevation.
Purpose of the Study:
- To investigate TGFβ₂-induced proteomic changes in human TM cells.
- To identify proteins involved in TGFβ₂ signaling within the TM.
Main Methods:
- Human TM cells from four donors were cultured.
- Cells were treated with TGFβ₂ (5 ng/mL) for 48 hours.
- Proteomic analysis was performed using liquid chromatography-mass spectrometry iTRAQ.
Main Results:
- A total of 853 proteins were quantified, with 47 significantly altered by TGFβ₂.
- Over half of the elevated proteins relate to extracellular matrix remodeling and cytoskeletal interactions.
- Altered mitochondrial and regulatory proteins suggest TGFβ₂-induced mitochondrial dysfunction and impacts on cellular processes.
Conclusions:
- The study expands the known proteins involved in TGFβ₂ signaling.
- New molecular insights into POAG pathogenesis are provided.
- A quantitative proteomics database of TM proteins is established, including potential glaucoma biomarkers.
