K
Kannan Kunchithapautham
Researcher at Medical University of South Carolina
Publications - 27
Citations - 1421
Kannan Kunchithapautham is an academic researcher from Medical University of South Carolina. The author has contributed to research in topics: Complement system & Alternative complement pathway. The author has an hindex of 18, co-authored 27 publications receiving 1274 citations. Previous affiliations of Kannan Kunchithapautham include University of South Carolina.
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Journal ArticleDOI
A targeted inhibitor of the alternative complement pathway reduces angiogenesis in a mouse model of age-related macular degeneration.
Ba¨rbel Rohrer,Qin Long,Beth Coughlin,R. Brooks Wilson,Yuxiang Huang,Fei Qiao,Peter H. Tang,Kannan Kunchithapautham,Gary S. Gilkeson,Stephen Tomlinson +9 more
TL;DR: In therapeutically relevant paradigms involving delayed treatment after injury, CR2-fH was effective in reducing CNV and provided approximately 60% of the amount of protection of that seen in factor B-deficient mice that lacked functional AP.
Journal ArticleDOI
Oxidative stress renders retinal pigment epithelial cells susceptible to complement-mediated injury.
Joshua M. Thurman,Brandon Renner,Kannan Kunchithapautham,Viviana P. Ferreira,Michael K. Pangburn,Zsolt Ablonczy,Stephen Tomlinson,V. Michael Holers,Bärbel Rohrer +8 more
TL;DR: It is demonstrated that oxidative stress reduces regulation of complement on the surface of ARPE-19 cells, increasing complement activation and linking oxidative stress, complement activation, and apical VEGF release, which have all been associated with the pathogenesis of AMD.
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Apoptosis and autophagy in photoreceptors exposed to oxidative stress.
TL;DR: It is confirmed that cells that normally die by apoptosis will execute cell death by necrosis if the normal pathway is blocked, and the up-stream regulators of autophagy need to be identified as potential therapeutic targets in photoreceptor degeneration.
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Smoke exposure causes endoplasmic reticulum stress and lipid accumulation in retinal pigment epithelium through oxidative stress and complement activation.
TL;DR: In this paper, the effects of smoke exposure on the retinal pigment epithelium (RPE) were examined by biochemical, molecular, and histological measures, and the results provided clear evidence that smoke exposure results in oxidative stress and complement activation via the alternative pathway, resulting in ER stress-mediated lipid accumulation.
Journal ArticleDOI
Eliminating complement factor D reduces photoreceptor susceptibility to light-induced damage.
TL;DR: Results suggest that rod degeneration in the CL-damaged retina involves the activity of the alternative complement pathway and that eliminating the alternative pathway is neuroprotective, and the light damage albino mouse model may be a good model to study complement-mediated photoreceptor degeneration.