Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020473 (hyperlipidemia)
 15,891 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) was originally identified as a receptor for oxidatively modified low-density lipoprotein. It has been reported that oxidative stress and hyperlipidemia play important roles in the etiology of preeclampsia, and that placental oxidative stress may stimulate syncytiotrophoblast apoptosis in preeclampsia. In this study, we examined the expression of LOX-1 in the human placentas of normal pregnancies and in preeclampsia using immunohistochemistry and Western blot analysis, and proposed that LOX-1 has a role in trophoblast apoptosis. To analyze apoptotic activity, the expression of the specific caspase cleavage site within cytokeratin 18 was assessed immunohistochemically using the monoclonal antibody M30 CytoDeath. Both LOX-1 and M30 immunoreactivity occurred predominantly in syncytiotrophoblasts. A significantly higher number of LOX-1 and M30-positive cells were found in preeclamptic placentas than in normal placentas. The number of M30-positive cells correlated with the apoptotic index of trophoblasts determined by TdT-mediated dUTP nick-end labeling (TUNEL). Syncytiotrophoblasts showing apoptotic activity were immunopositive to LOX-1 by double immunohistochemical fluorescence. We suggest that the functional role of syncytiotrophoblasts in placental dysfunction results from the localization and upregulation of LOX-1 in the preeclamptic placenta, possible implications in upregulation of syncytiotrophoblast apoptotic activity in preeclampsia.
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PMID:Expression of lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) in human preeclamptic placenta: possible implications in the process of trophoblast apoptosis. 1570 24

Burn injury often is associated with the abnormal lipid metabolism, including hyperlipidemia, desensitization to lipolytic responses to catecholamines, and reduction in the size of the white adipose tissue. Understanding the biological mechanisms for the decrease in fat mass despite desensitization to catecholamines is important both for the study of lipid metabolism and for the study of its relationship to concomitant insulin resistance. Using epididymal adipose tissue from adult male Sprague-Dawley rats after burn injury (n = 102) or sham-burn injury (n = 102), we tested the hypothesis that a whole-body burn injury causes apoptosis in that tissue. At 1, 3, and 7 days after 40% to 50% body burn injury to the rat, epidydimal adipose tissue was harvested and studied for apoptotic changes and lipolytic properties. For apoptosis, paraformaldehyde-fixed tissue sections were analyzed by in situ TdT-mediated dUTP-X nick-end labeling (TUNEL) staining, and tissue homogenates were also analyzed for DNA fragmentation by enzyme-linked immunoassay and ligation-mediated polymerase chain reaction ladder assay. Isolated adipocytes were stimulated with isoprotenerol, and glycerol production was measured as a reflector of effectiveness of lipolysis. Epididymal adipose tissue showed increased apoptosis manifested by the positive TUNEL staining and increased DNA fragmentation by enzyme-linked immunoassay at day 3 and 7 after burn injury. The DNA fragmentation was confirmed further by the ligation-mediated polymerase chain reaction ladder assay. This elevated DNA fragmentation persisted in the burned animals from day 3 until day 7 after burn injury, the end of observation period. Increase in apoptosis was correlated with decrease in DNA content and tissue weight in the epidydimis. At the functional level, a significant decrease in isoproterenol-induced lipolytic activity (glycerol production) was observed to almost 50% of control level at day 3 and 7 but was not decreased at day 1. Apoptosis of adipocytes may play a role in the altered lipid metabolism, including hyperlipidemia observed in burned subjects.
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PMID:Adipocyte apoptosis after burn injury is associated with altered fat metabolism. 1667 8