TGF-P is a member of transforming growth factor family which has immunomodulatory function. It is secreted primarily by monocytes, macrophages, lymphocytes, and dendritic cells. This cytokine takes part in angiogenesis, stimulates synthesis and degeneration of extracellular matrix proteins, regulates induction of apoptosis and stimulates proliferation of mesenchymal cells.
TGF-P exists in three isoforms coded by different genes p1, p2, p3; best known is TGF- p1 (Bertolino et al., 2005; Orlova et al., 2011) . TGF-P is believed to be the most important ligand in the pathogenesis of fibrotic diseases in the eye. Such ocular fibrotic diseases include scarring in the cornea and conjunctiva, fibrosis in the corneal endothelium, post-cataract surgery fibrosis of the lens capsule, excess scarring of tissue around the extraocular muscles in the strabismus surgery and proliferative vitreoretinopathy (Saika et al., 2009; Sumioka et al., 2011; Hills et al., 2011). Those properties of TGF-ß are confirmed in animal models (Yingchuan et al., 2010; Kowluru et al., 2010) as well as in patients with diabetic retinopathy (George et al., 2009; Abu El-Asrar et al., 2010). It is believed that TGF-ß plays a role in pathogenesis of diabetic retinopathy via hyperglycaemia and inflammation. Kowluru et al., 2010 have reported that both the duration of the initial exposure to high glucose, and normal glucose that follows high glucose, are critical in determining the outcome of the alterations in the inflammatory mediators such as IL-1 beta, NF-kB, VEGF, TNF-a including with TGF-ß in retinal.
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