1. Pro-apoptotic low-density lipoprotein subfractions in type II diabetes
Chao-yuh Yang, Hsin-Hung Chen, Max T. Huang, Joe L. Raya, Jun-Hai Yang, Chu-Huang Chen, John W. Gaubatz, Henry J. Pownall, Addison A. Taylor, Christie M. Ballantyne, Floor A. Jenniskens, Charles V. Smith 
Atherosclerosis 
Volume 193, Issue 2, Pages (August 2007)
DOI: /j.atherosclerosis
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2. Fig. 1
FPLC elution profiles: as described in Section 2, 100mg of (A) N- and (B) D-LDL were eluted from a UnoQ12 column, and effluents monitored at 280nm at two AUFS. The gradient profile was isocratic at 0% B for 10min, 0–15% B 10min, 15–20% B 30min, isocratic at 20% B 10min, 20–40% B 25min, 40–100% B 10min, isocratic at 100% B 10min, returned to 0% B in 5min. Five fractions were collected, as indicated.
Atherosclerosis  , DOI: ( /j.atherosclerosis )
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3. Fig. 2
Effects of fractions of D- and N-LDL on apoptosis in BAEC. (A) BAECs were incubated at 37°C for 18h with 50μg/ml of N- or D-LDL fractions, as indicated. Examples of apoptosis in cultured BAEC induced by N- and D-L5 are presented in the figure. (B) Dose-dependent effects on apoptosis of BAEC were evaluated for D-L4 and D-L5. (C) Protective effects of z-VAD-fmk, a pan-caspase inhibitor against apoptosis induced by D-L5. Cells were treated with or without z-VAD-fmk prior to administering D-L5 (75μg/ml). After 18h, cells were stained for 10min with Hoechst and nuclear morphologies assessed. Cells exhibiting condensed, fragmented nuclei by epifluorescence microscopy were considered to be undergoing apoptosis. Data are expressed as means±S.E.M., n=3 for normal and n=3–6 for diabetic LDL, and were assessed by two-way (A and B) or one-way (C) ANOVA with Student–Newman–Keuls tests post hoc, with differences attributed at p<0.05. (A) Effects of subject and fraction, with no interaction. *Different from the respective subfraction from N-LDL. aData sharing common superscripts are homogeneous subsets, i.e., not different from each other. (B) Effects of subfraction and concentration, with no interaction. (C) *Different from other subgroups.
Atherosclerosis  , DOI: ( /j.atherosclerosis )
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4. Fig. 3
Characterization of FPLC subfractions. Subfractions of LDL from normal (N-LDL) and diabetic (D-LDL) subjects were separated and collected, as described in Section 2. (A) Subfractions were treated with TNBSA, and reactivities calculated. Data are means±S.E.M. from six normal and eight diabetic subjects. Effects of subject and fraction and a significant interaction were observed. *Different from corresponding fraction of N-LDL. (B) Two micrograms of LDL protein, or the indicated reference standards, were separated on 4–20% linear gradient gels at 30mA/gel for 1h and stained with Coomassie. Bands were identified by comparisons with known protein standards. N-LDL: lanes 1–5 are N-L1 to N-L5, respectively; D-LDL: lanes 1–5 are D-L1–L5, respectively; S is marker standards. Molecular weights of markers and apolipoprotein standards are labeled. (C) Lp-PLA2 contents were measured by ELISA, as described in Methods. Data are means±S.E.M. of LDL subfractions from seven normal and four diabetic subjects, respectively. Main effect of sample number, but no effect of subject and no interaction. (D) Non-esterified fatty acid (NEFA) contents of LDL subfractions measured as described in Section 2 are presented as means+S.E.M. Effects of subject and fraction, but no interaction. aData with common superscripted letters form homogeneous subsets.
Atherosclerosis  , DOI: ( /j.atherosclerosis )
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5. Fig. 4
Copper-catalyzed oxidation of LDL subfractions in vitro. LDL subfractions were eluted through PD10 columns with phosphate-buffered saline, to remove EDTA, diluted in PBS to protein concentrations of 100μg/ml and oxidized at 37°C in the presence of 5μM Cu2+. Reactions were monitored at 234nm for 4h. Representative oxidation curves for N and D subjects are depicted in (A) and (B), and ●, ▴ and ■ represent L1, L3 and L5, respectively. The propagation rates for N and D subjects are depicted in (C) and (D), respectively. The data from LDL from four normal and four diabetic subjects are presented as means+S.D. Data were assessed by two-way ANOVA, with SNK post hoc, and differences noted at p<0.05. All data showed main effects of subject and fraction. Lag time and time at peak rate data indicated significant interactions, whereas peak rates and final absorbances did not. *Different from all other data sets in the column. aData sharing a common superscripted letter are homogeneous subsets.
Atherosclerosis  , DOI: ( /j.atherosclerosis )
Copyright © 2006 Elsevier Ireland Ltd Terms and Conditions