¡¡¡¡DISCUSSION

¡¡¡¡Pterygium is a common disease in the ophthalmology department. It is generally believed that such excessive stimulation of sandstorms, a longª²term soot, dust, sunlight (ultraviolet radiation) and the pollen are factors of pterygium. A variety of the complex factors are involved in the pathologic process with which chronic inflammation of the conjunctiva may also be correlated. Pterygium is a proliferation disease the clinical performance of which is the new tissue kept on hyperplasia and corneal infiltration. Pathological studies show that the major components of pterygium is a large number of proliferate fibroblast, led by corresponding lesions. Recent studies show that cytokines play an important role in the inflammatory response and the fibroblast proliferation [3ª²4]. TGFª²¦Â is one of the important factor. Research has indicated that TGFª²¦Â1 was strong expressed in the primary pterygium tissue. Exogenous TGFª²¦Â1 has mild suppression on cultured normal conjunctival fibroblasts, and promoting effect on the cultured fibroblasts of pterygium in a doseª²dependent manner [5]. TGFª²¦Â may play an important role in the abnormal proliferation of pterygium, but the exact mechanism of positive and negative control and signal transduction pathway research needs to be further confirmed.

¡¡¡¡TGFª²¦Â is a kind of polypeptide that can regulate cell growth and differentiation, can regulate the expression of a variety of target genes in cell differentiation, proliferation, migration and play an important role in the regulation of apoptosis. It can demonstrate promotion or inhabitation of cell proliferation and differentiation based on different target cells. For example it could facilitate fibroblasts, osteoblasts, and other mesenchymal cell to proliferate, but has strong inhibition for many epithelial cells, endothelial cells and lymphoidand[6]. Study of TGFª²¦Â expression in the pterygium will help on the understanding of their sources and mechanisms. Because TGFª²¦Â must bind to specific receptor and through Smads protein which is an intermediary molecule can transduct extra cellular signal to nuclear biological effects. Therefore, studying the role of TGFª²¦Â in the course of the disease at the same time, should also observe the corresponding receptor gene expression levels. TGFª²¦ÂR is a cell surface receptor, including TGFª²¦ÂRI, TGFª²¦ÂRII and TGFª²¦ÂRIII. TGFª²¦ÂRI and TGFª²¦ÂRII are imperative in TGFª²¦Â signaling transduction system, TGFª²¦ÂRIII is the foundation of the action. TGFª²¦ÂRI and TGFª²¦ÂRII are receptors of serine/ threonine kinase receptors and they have common commencement action of TGFª²¦Â in the cytoplasm signal. Then the Smads protein is activated and the signal is transducted to the nuclei and the transcription of objective gene is regulated [7,8].

¡¡¡¡Our research shows that expression of TGFª²¦Â1 and TGFª²¦Â2 in pterygium was higher than that in normal conjunctival tissue. TGFª²¦Â1 in pterygium and normal bulbar conjunctiva was higher than the expression of TGFª²¦Â2 in the corresponding tissues, but the increasing level of TGFª²¦Â2 in pterygium was higher than TGFª²¦Â1, suggesting that TGFª²¦Â may play an important role in the development of pterygium lesions, and that TGFª²¦Â2 may play regulatory role in the development of pterygium. In the pterygium lesions, our research results also suggest that TGFª²¦ÂRI and TGFª²¦ÂRII expression were significantly lower compared with normal tissue. May ultraviolet affect the TGFª²¦Â/Smads signal transduction process, making the secretion of TGFª²¦Â to increase and change its regulation of target cells, to spur the occurrence and development of the pterygium disease. Advanced study the role of TGFª²¦Â/Smads signal transduction process is needed.

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  ¡¡¡¡1 Di Girolamo N, Wakefield D, Coroneo MT.UVBª²mediated induction of cytokines and growth factors in pterygium epithelial cells involves cell surface receptors and intracellular signaling. Invest Ophthalmol Vis Sci 2006;47(6):2430ª²2437

¡¡¡¡2 Kria L, Ohira A, Amemiya T. Immunohistochemical localization of basic fibroblast growth factor, platalet derived growth factor, transforming growth factorª²¦Âand tumor necrosis factorª²¦Áin the pterygium. Acta Histochem 1996;98(2):195ª²201

¡¡¡¡3 Di Girolamo N, Kumar RK, Coroneo MT, Wakefield D. UVBª² mediated induction of interleukinª² 6andª² 8 in pterygia and cultured human pterygium epithelial cells. Invest Ophthalmol Vis Sci 2002;43(11):3430ª²3437

¡¡¡¡4 Di Girolamo N, Chui J, Coroneo MT, Wakefield D. Pathogenesis of pterygia: role of cytokines, growth factors, and matrix metalloproteiª²nases. Prog Retin Eye Res 2004;23(2):195ª²228

¡¡¡¡5 Lee SB, Li DQ, Tan DT,Meller DC,Tseng SC. Suppression of TGFª²beta signaling in both normal conjunctival fibroblasts and pterygial body fibroblasts by amniotic membrane. Curr Eye Res 2000;20(4):325ª²334

¡¡¡¡6 Kottler VB, Junemann AG, Aigner T, Zenke LM, Rummelt L, Schlotzerª²Schrehardt V. Comparative effects of TGFª² beta1 and TGFª² beta2 on extracellularmatrix production, proliferation, and collagen contraction of human Tenon¬ðs Capsulefibroblasts in pseudoexfoliation and primary openª²angle glaucoma. Exp Eye Res 2005;80(1):121ª²134

¡¡¡¡7 Govinden R, Bhoola KD. Genealogy, expression, and cellular function of transforming growth factorª²beta. Pharmacol Ther 2003;98(20):257ª²265

¡¡¡¡8 ten Dijke P, Hill CS£®New insights into TGFª²betaª²Smad signalling. Trends Biochem Scj 2004;29(5):265ª²227

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