Abstract

Uveitis is a major cause of blindness in the United States. Pars planitis is a well- defined disease subset of uveitis. The cause of pars planitis, as well as other forms of uveitis, is frequently unknown. The PI has identified a 36 kDa protein (p-36) which is markedly increased in the peripheral blood of patients with active pars planitis. Recent results from the laboratory suggest that p-36 is a part of a larger protein which is approximately 95 kD (p-95) in size. The identification of proteins which may contribute to the pathogenesis of pars planitis would be a major advance toward its treatment and possible cure.
The specific aims of this proposal are: A. To correlate levels of p-36 and p-95 with clinical disease in pars planitis. B. To determine the structure of p-95. C. To study the tissue distribution of p-95. Quantitative assessment of p-36 and p-95 levels in patients; blood may be of value in both monitoring disease activity and guiding treatment. The PI hopes that the proposed studies will allow the uncovering of important information concerning the mechanism of ocular inflammation in pars planitis, and possibly, to design more effective treatment for this disease.

  Funding Agency

Agency
National Institute of Health (NIH)
Institute
National Eye Institute (NEI)
Type
Research Project (R01)
Project #
2R01EY009730-04A1
Application #
2624577
Study Section
Visual Sciences A Study Section (VISA)
Project Start
1994-08-01
Project End
2001-03-31
Budget Start
1998-04-01
Budget End
1999-03-31
Support Year
4
Fiscal Year
1998
Total Cost
Indirect Cost

  Institution

Name
Washington University
Department
Ophthalmology
Type
Schools of Medicine
DUNS #
062761671
City
Saint Louis
State
MO
Country
United States
Zip Code
63130

  Publications

Jha, Purushottam; Sohn, Jeong-Hyeon; Xu, Qin et al. (2006) Suppression of complement regulatory proteins (CRPs) exacerbates experimental autoimmune anterior uveitis (EAAU). J Immunol 176:7221-31
Bora, Puran S; Sohn, Jeong-Hyeon; Cruz, Jose M C et al. (2005) Role of complement and complement membrane attack complex in laser-induced choroidal neovascularization. J Immunol 174:491-7
Bora, Nalini S; Sohn, Jeong-Hyeon; Bora, Puran S et al. (2005) Anti-inflammatory effects of specific cyclooxygenase 2,5-lipoxygenase, and inducible nitric oxide synthase inhibitors on experimental autoimmune anterior uveitis (EAAU). Ocul Immunol Inflamm 13:183-9
Bora, Nalini S; Sohn, Jeong-Hyeon; Kang, Shin-Goo et al. (2004) Type I collagen is the autoantigen in experimental autoimmune anterior uveitis. J Immunol 172:7086-94
Sohn, Jeong-Hyeon; Bora, Puran S; Suk, Hye-Jung et al. (2003) Tolerance is dependent on complement C3 fragment iC3b binding to antigen-presenting cells. Nat Med 9:206-12
McLaughlin, Barbara J; Fan, Wei; Zheng, Jing Juan et al. (2003) Novel role for a complement regulatory protein (CD46) in retinal pigment epithelial adhesion. Invest Ophthalmol Vis Sci 44:3669-74
Li, Jianjun; Hu, Weimin; Baldassare, Joseph J et al. (2003) The ethanol metabolite, linolenic acid ethyl ester, stimulates mitogen-activated protein kinase and cyclin signaling in hepatic stellate cells. Life Sci 73:1083-96
Oruc, S; Duffy, B F; Mohanakumar, T et al. (2001) The association of HLA class II with pars planitis. Am J Ophthalmol 131:657-9
Sohn, J H; Kaplan, H J; Suk, H J et al. (2000) Complement regulatory activity of normal human intraocular fluid is mediated by MCP, DAF, and CD59. Invest Ophthalmol Vis Sci 41:4195-202
Sohn, J H; Kaplan, H J; Suk, H J et al. (2000) Chronic low level complement activation within the eye is controlled by intraocular complement regulatory proteins. Invest Ophthalmol Vis Sci 41:3492-502

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