TY - JOUR
T1 - Prohibitin as the Molecular Binding Switch in the Retinal Pigment Epithelium
AU - Sripathi, Srinivas R.
AU - Sylvester, O’Donnell D.
AU - He, Weilue
AU - Moser, Trevor
AU - Um, Ji Yeon
AU - Lamoke, Folami
AU - Ramakrishna, Wusirika
AU - Bernstein, Paul S.
AU - Bartoli, Manuela
AU - Jahng, Wan Jin
N1 - Funding Information:
The authors thank Jeremy Goldman and Mike Gibson for insightful discussions and sharing equipment. Matthew Durocher and Dr. Tristan Purvis are acknowledged for their suggestions and critical reading. This study was supported by the Century II Equipment fund and the Research Excellence Fund from Michigan Technological University, Research Assistantship and Teaching Assistantship from American University of Nigeria.
Publisher Copyright:
© 2015, Springer Science+Business Media New York.
PY - 2016/2/1
Y1 - 2016/2/1
N2 - Previously, our molecular binding study showed that prohibitin interacts with phospholipids, including phosphatidylinositide and cardiolipin. Under stress conditions, prohibitin interacts with cardiolipin as a retrograde response to activate mitochondrial proliferation. The lipid-binding switch mechanism of prohibitin with phosphatidylinositol-3,4,5-triphosphate and cardiolipin may suggest the role of prohibitin effects on energy metabolism and age-related diseases. The current study examined the region-specific expressions of prohibitin with respect to the retina and retinal pigment epithelium (RPE) in age-related macular degeneration (AMD). A detailed understanding of prohibitin binding with lipids, nucleotides, and proteins shown in the current study may suggest how molecular interactions control apoptosis and how we can intervene against the apoptotic pathway in AMD. Our data imply that decreased prohibitin in the peripheral RPE is a significant step leading to mitochondrial dysfunction that may promote AMD progression.
AB - Previously, our molecular binding study showed that prohibitin interacts with phospholipids, including phosphatidylinositide and cardiolipin. Under stress conditions, prohibitin interacts with cardiolipin as a retrograde response to activate mitochondrial proliferation. The lipid-binding switch mechanism of prohibitin with phosphatidylinositol-3,4,5-triphosphate and cardiolipin may suggest the role of prohibitin effects on energy metabolism and age-related diseases. The current study examined the region-specific expressions of prohibitin with respect to the retina and retinal pigment epithelium (RPE) in age-related macular degeneration (AMD). A detailed understanding of prohibitin binding with lipids, nucleotides, and proteins shown in the current study may suggest how molecular interactions control apoptosis and how we can intervene against the apoptotic pathway in AMD. Our data imply that decreased prohibitin in the peripheral RPE is a significant step leading to mitochondrial dysfunction that may promote AMD progression.
KW - Macular degeneration
KW - Mitochondria
KW - Oxidative stress
KW - Prohibitin
KW - Retinal pigment epithelium
UR - http://www.scopus.com/inward/record.url?scp=85013724801&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=85013724801&partnerID=8YFLogxK
U2 - 10.1007/s10930-015-9641-y
DO - 10.1007/s10930-015-9641-y
M3 - Article
C2 - 26661103
AN - SCOPUS:85013724801
VL - 35
JO - Journal of Protein Chemistry
JF - Journal of Protein Chemistry
SN - 0277-8033
IS - 1
ER -