A Point Mutant of Apolipoprotein A-I (V156K) Showed Enhancement of Cellular Insulin Secretion and Potent Activity of Facultative Regeneration in Zebrafish

Title
A Point Mutant of Apolipoprotein A-I (V156K) Showed Enhancement of Cellular Insulin Secretion and Potent Activity of Facultative Regeneration in Zebrafish
Author(s)
조경현윤정혜[윤정혜]
Keywords
HIGH-DENSITY-LIPOPROTEIN; RECONSTITUTED HDL; DIABETES-MELLITUS; HUMAN HEMOGLOBIN; END-PRODUCTS; LIPID-FREE; ANTIOXIDANT; GLYCATION; OXIDATION; SENESCENCE
Issue Date
201206
Publisher
MARY ANN LIEBERT, INC
Citation
REJUVENATION RESEARCH, v.15, no.3, pp.313 - 321
Abstract
Sensitivity of glycation and functional changes were compared between wild-type (WT) and the V156K mutant of apolipoprotein A-I in the reconstituted high-density lipoproteins (rHDL) state. WT-rHDL showed increased production of advanced glycated end (AGE) products with proteolytic fragmentation by fructose treatment (final 5mM) for 48 hr; however, V156K-rHDL was more resistant to the same fructosylation and protein cleavage. Glycated WT-rHDL severely lost antioxidant activity; in contrast, V156K-rHDL showed much less AGE production and retained stronger antioxidant properties in the glycated state. In both native and glycated states, V156K-rHDL showed significantly enhanced stimulation activity for insulin secretion from the rat pancreatic beta-cell, whereas WT-rHDL induced less insulin secretion by glycation. In the zebrafish model, under diabetic and hyperlipidemic diet conditions, injection of native V156K-rHDL caused an approximate five-fold increase in fin regeneration activity compared to native WT-rHDL over 120 hr. Under the same conditions, injection of glycated WT-rHDL caused severe tissue damage in tail fins after 48 hr, whereas glycated V156K-rHDL showed normal regeneration. In conclusion, insulin secretion and tissue rejuvenation activities of WT-rHDL were nearly depleted by fructosylation, but V156K-rHDL did not lose its beneficial activity. These results suggest that V156K-rHDL can be applied to facilitate facultative regeneration in aging-related complications.
URI
http://hdl.handle.net/YU.REPOSITORY/28017http://dx.doi.org/10.1089/rej.2011.1246
ISSN
1549-1684
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생명공학부 > 생명공학부 > Articles
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