Oxidized low density lipoproteins and lactosylceramide both stimulate the expression of proliferating cell nuclear antigen and the proliferation of aortic smooth muscle cells

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Abstract

We have previously shown that oxidized low density lipoproteins (Ox-LDL) at low concentrations (10μg/ml) via activating a UDP-galactose: glucosylceramide, β1→4 galactosyl-transferase (GalT-2) and producing lactosylceramide can stimulate the proliferation of aortic smooth muscle cells. In this report, we present evidence that Ox-LDL and LacCer, both can induce the expression of proliferating cell nuclear antigen (cyclin). Ox-LDL and LacCer both exerted a time-dependent stimulation of cyclin expression. Maximum increase (3-fold) in cyclin expression occurred between 30-120 min after Ox-LDL/LacCer addition and decreased thereafter. D-threo-1-phenyldecanoylamino-3-morpholino-1-propanol (D-PDMP), an inhibitor of GalT-2, inhibited cell proliferation as well as cyclin expression. This inhibitor also abrogated the Ox-LDL mediated expression of proliferating cell nuclear antigen (cyclin). In contrast, the L-enantiomer of PDMP (L-PDMP) stimulated the expression of cyclin and augmented the Ox-LDL mediated expression of cyclin in these cells. Maximum increase in the expression of cyclin ocurred with 20μmole of L-PDMP and 10 μg of Ox-LDL. This overall pattern of Ox-LDL and LacCer mediated regulation is similar to that of the c-fos protooncogenes reported previously by us. We hypothesize that the early induction of GalT-2 may serve as an "Immediate early gene" that plays a role in the signalling cascade by LacCer and involves the kinase c-fos induction and subsequent expression of cyclins. Thus, GalT-2 may play a role in the proliferative response in aortic smooth muscle cells by Ox-LDL.

Original languageEnglish (US)
Pages (from-to)56-60
Number of pages5
JournalIndian journal of biochemistry & biophysics
Volume34
Issue number1-2
StatePublished - Feb 1997

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Cyclins
Proliferating Cell Nuclear Antigen
Smooth Muscle Myocytes
Muscle
Cells
Enantiomers
Uridine Diphosphate Galactose
Glucosylceramides
CDw17 antigen
oxidized low density lipoprotein
1-Propanol
Morpholinos
Immediate-Early Genes
Cell proliferation
Transferases
Phosphotransferases
Genes
Cell Proliferation
glucosylceramide beta-1-4-galactosyltransferase

ASJC Scopus subject areas

  • Biochemistry
  • Biophysics

Cite this

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title = "Oxidized low density lipoproteins and lactosylceramide both stimulate the expression of proliferating cell nuclear antigen and the proliferation of aortic smooth muscle cells",
abstract = "We have previously shown that oxidized low density lipoproteins (Ox-LDL) at low concentrations (10μg/ml) via activating a UDP-galactose: glucosylceramide, β1→4 galactosyl-transferase (GalT-2) and producing lactosylceramide can stimulate the proliferation of aortic smooth muscle cells. In this report, we present evidence that Ox-LDL and LacCer, both can induce the expression of proliferating cell nuclear antigen (cyclin). Ox-LDL and LacCer both exerted a time-dependent stimulation of cyclin expression. Maximum increase (3-fold) in cyclin expression occurred between 30-120 min after Ox-LDL/LacCer addition and decreased thereafter. D-threo-1-phenyldecanoylamino-3-morpholino-1-propanol (D-PDMP), an inhibitor of GalT-2, inhibited cell proliferation as well as cyclin expression. This inhibitor also abrogated the Ox-LDL mediated expression of proliferating cell nuclear antigen (cyclin). In contrast, the L-enantiomer of PDMP (L-PDMP) stimulated the expression of cyclin and augmented the Ox-LDL mediated expression of cyclin in these cells. Maximum increase in the expression of cyclin ocurred with 20μmole of L-PDMP and 10 μg of Ox-LDL. This overall pattern of Ox-LDL and LacCer mediated regulation is similar to that of the c-fos protooncogenes reported previously by us. We hypothesize that the early induction of GalT-2 may serve as an {"}Immediate early gene{"} that plays a role in the signalling cascade by LacCer and involves the kinase c-fos induction and subsequent expression of cyclins. Thus, GalT-2 may play a role in the proliferative response in aortic smooth muscle cells by Ox-LDL.",
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T1 - Oxidized low density lipoproteins and lactosylceramide both stimulate the expression of proliferating cell nuclear antigen and the proliferation of aortic smooth muscle cells

AU - Chatterjee, Subroto B

PY - 1997/2

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N2 - We have previously shown that oxidized low density lipoproteins (Ox-LDL) at low concentrations (10μg/ml) via activating a UDP-galactose: glucosylceramide, β1→4 galactosyl-transferase (GalT-2) and producing lactosylceramide can stimulate the proliferation of aortic smooth muscle cells. In this report, we present evidence that Ox-LDL and LacCer, both can induce the expression of proliferating cell nuclear antigen (cyclin). Ox-LDL and LacCer both exerted a time-dependent stimulation of cyclin expression. Maximum increase (3-fold) in cyclin expression occurred between 30-120 min after Ox-LDL/LacCer addition and decreased thereafter. D-threo-1-phenyldecanoylamino-3-morpholino-1-propanol (D-PDMP), an inhibitor of GalT-2, inhibited cell proliferation as well as cyclin expression. This inhibitor also abrogated the Ox-LDL mediated expression of proliferating cell nuclear antigen (cyclin). In contrast, the L-enantiomer of PDMP (L-PDMP) stimulated the expression of cyclin and augmented the Ox-LDL mediated expression of cyclin in these cells. Maximum increase in the expression of cyclin ocurred with 20μmole of L-PDMP and 10 μg of Ox-LDL. This overall pattern of Ox-LDL and LacCer mediated regulation is similar to that of the c-fos protooncogenes reported previously by us. We hypothesize that the early induction of GalT-2 may serve as an "Immediate early gene" that plays a role in the signalling cascade by LacCer and involves the kinase c-fos induction and subsequent expression of cyclins. Thus, GalT-2 may play a role in the proliferative response in aortic smooth muscle cells by Ox-LDL.

AB - We have previously shown that oxidized low density lipoproteins (Ox-LDL) at low concentrations (10μg/ml) via activating a UDP-galactose: glucosylceramide, β1→4 galactosyl-transferase (GalT-2) and producing lactosylceramide can stimulate the proliferation of aortic smooth muscle cells. In this report, we present evidence that Ox-LDL and LacCer, both can induce the expression of proliferating cell nuclear antigen (cyclin). Ox-LDL and LacCer both exerted a time-dependent stimulation of cyclin expression. Maximum increase (3-fold) in cyclin expression occurred between 30-120 min after Ox-LDL/LacCer addition and decreased thereafter. D-threo-1-phenyldecanoylamino-3-morpholino-1-propanol (D-PDMP), an inhibitor of GalT-2, inhibited cell proliferation as well as cyclin expression. This inhibitor also abrogated the Ox-LDL mediated expression of proliferating cell nuclear antigen (cyclin). In contrast, the L-enantiomer of PDMP (L-PDMP) stimulated the expression of cyclin and augmented the Ox-LDL mediated expression of cyclin in these cells. Maximum increase in the expression of cyclin ocurred with 20μmole of L-PDMP and 10 μg of Ox-LDL. This overall pattern of Ox-LDL and LacCer mediated regulation is similar to that of the c-fos protooncogenes reported previously by us. We hypothesize that the early induction of GalT-2 may serve as an "Immediate early gene" that plays a role in the signalling cascade by LacCer and involves the kinase c-fos induction and subsequent expression of cyclins. Thus, GalT-2 may play a role in the proliferative response in aortic smooth muscle cells by Ox-LDL.

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