Differential expression of ribosomal L31, Zis, gas-5 and mitochondrial mRNAs following oxidant induction of proliferative vascular smooth muscle cell phenotypes

K. P. Lu, N. F. Alejandro, K. M. Taylor, M. Joyce, T. E. Spencer, Kenneth Ramos

Research output: Contribution to journalArticle

21 Citations (Scopus)

Abstract

Treatment of cultured vascular smooth muscle cells (vSMCs) with benzo(a)pyrene (BaP), a prooxidant present in the particulate phase of tobacco smoke, induces highly proliferative (i.e. atherogenic) phenotypes. Critical early target genes in vSMCs have been identified, but patterns of gene expression following repeated cycles of carcinogen treatment in vivo have yet to be evaluated. In the present study, male Sprague-Dawley rats (175-200 g) were given weekly injections of BaP (10 mg/kg) for 8 weeks to induce atherogenic phenotypes. At the end of this atherogenic regimen, vSMCs were established in serial culture and monitored for patterns of proliferative activity and gene expression. vSMCs isolated from BaP-treated animals (hence forth referred to as BaP cells) exhibited constitutively increased growth rates, and marked enhancement of proliferation in response to serum mitogens. Differential display polymerase chain reaction (DD-PCR) and Northern blot analyses revealed that mRNAs for ribosomal protein L31 and Zis genes were suppressed, while gas-5 and mitochondrial mRNAs were overexpressed in BaP cells relative to control mRNA populations. In situ hybridization experiments in vascular tissue confirmed these alterations in vivo. This is the first report linking expression of these genes to proliferative dysregulation during the course of experimentally-induced atherogenesis.

Original languageEnglish (US)
Pages (from-to)273-280
Number of pages8
JournalAtherosclerosis
Volume160
Issue number2
DOIs
StatePublished - 2002
Externally publishedYes

Fingerprint

Galectin 3
Benzo(a)pyrene
Vascular Smooth Muscle
Oxidants
Smooth Muscle Myocytes
Gases
Phenotype
Gene Expression
Messenger RNA
Mitogens
Smoke
Northern Blotting
Carcinogens
Genes
Tobacco
In Situ Hybridization
Blood Vessels
Sprague Dawley Rats
Atherosclerosis
mitochondrial messenger RNA

Keywords

  • Benzo(a)pyrene
  • Chemical atherogenesis
  • Differential gene expression
  • Gas-5
  • Mitochondrial and ribosomal mRNAs
  • Vascular smooth muscle cells
  • Zis

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

Cite this

Differential expression of ribosomal L31, Zis, gas-5 and mitochondrial mRNAs following oxidant induction of proliferative vascular smooth muscle cell phenotypes. / Lu, K. P.; Alejandro, N. F.; Taylor, K. M.; Joyce, M.; Spencer, T. E.; Ramos, Kenneth.

In: Atherosclerosis, Vol. 160, No. 2, 2002, p. 273-280.

Research output: Contribution to journalArticle

@article{b158eb6e4c704ad3b8f01ed899368584,
title = "Differential expression of ribosomal L31, Zis, gas-5 and mitochondrial mRNAs following oxidant induction of proliferative vascular smooth muscle cell phenotypes",
abstract = "Treatment of cultured vascular smooth muscle cells (vSMCs) with benzo(a)pyrene (BaP), a prooxidant present in the particulate phase of tobacco smoke, induces highly proliferative (i.e. atherogenic) phenotypes. Critical early target genes in vSMCs have been identified, but patterns of gene expression following repeated cycles of carcinogen treatment in vivo have yet to be evaluated. In the present study, male Sprague-Dawley rats (175-200 g) were given weekly injections of BaP (10 mg/kg) for 8 weeks to induce atherogenic phenotypes. At the end of this atherogenic regimen, vSMCs were established in serial culture and monitored for patterns of proliferative activity and gene expression. vSMCs isolated from BaP-treated animals (hence forth referred to as BaP cells) exhibited constitutively increased growth rates, and marked enhancement of proliferation in response to serum mitogens. Differential display polymerase chain reaction (DD-PCR) and Northern blot analyses revealed that mRNAs for ribosomal protein L31 and Zis genes were suppressed, while gas-5 and mitochondrial mRNAs were overexpressed in BaP cells relative to control mRNA populations. In situ hybridization experiments in vascular tissue confirmed these alterations in vivo. This is the first report linking expression of these genes to proliferative dysregulation during the course of experimentally-induced atherogenesis.",
keywords = "Benzo(a)pyrene, Chemical atherogenesis, Differential gene expression, Gas-5, Mitochondrial and ribosomal mRNAs, Vascular smooth muscle cells, Zis",
author = "Lu, {K. P.} and Alejandro, {N. F.} and Taylor, {K. M.} and M. Joyce and Spencer, {T. E.} and Kenneth Ramos",
year = "2002",
doi = "10.1016/S0021-9150(01)00581-0",
language = "English (US)",
volume = "160",
pages = "273--280",
journal = "Atherosclerosis",
issn = "0021-9150",
publisher = "Elsevier Ireland Ltd",
number = "2",

}

TY - JOUR

T1 - Differential expression of ribosomal L31, Zis, gas-5 and mitochondrial mRNAs following oxidant induction of proliferative vascular smooth muscle cell phenotypes

AU - Lu, K. P.

AU - Alejandro, N. F.

AU - Taylor, K. M.

AU - Joyce, M.

AU - Spencer, T. E.

AU - Ramos, Kenneth

PY - 2002

Y1 - 2002

N2 - Treatment of cultured vascular smooth muscle cells (vSMCs) with benzo(a)pyrene (BaP), a prooxidant present in the particulate phase of tobacco smoke, induces highly proliferative (i.e. atherogenic) phenotypes. Critical early target genes in vSMCs have been identified, but patterns of gene expression following repeated cycles of carcinogen treatment in vivo have yet to be evaluated. In the present study, male Sprague-Dawley rats (175-200 g) were given weekly injections of BaP (10 mg/kg) for 8 weeks to induce atherogenic phenotypes. At the end of this atherogenic regimen, vSMCs were established in serial culture and monitored for patterns of proliferative activity and gene expression. vSMCs isolated from BaP-treated animals (hence forth referred to as BaP cells) exhibited constitutively increased growth rates, and marked enhancement of proliferation in response to serum mitogens. Differential display polymerase chain reaction (DD-PCR) and Northern blot analyses revealed that mRNAs for ribosomal protein L31 and Zis genes were suppressed, while gas-5 and mitochondrial mRNAs were overexpressed in BaP cells relative to control mRNA populations. In situ hybridization experiments in vascular tissue confirmed these alterations in vivo. This is the first report linking expression of these genes to proliferative dysregulation during the course of experimentally-induced atherogenesis.

AB - Treatment of cultured vascular smooth muscle cells (vSMCs) with benzo(a)pyrene (BaP), a prooxidant present in the particulate phase of tobacco smoke, induces highly proliferative (i.e. atherogenic) phenotypes. Critical early target genes in vSMCs have been identified, but patterns of gene expression following repeated cycles of carcinogen treatment in vivo have yet to be evaluated. In the present study, male Sprague-Dawley rats (175-200 g) were given weekly injections of BaP (10 mg/kg) for 8 weeks to induce atherogenic phenotypes. At the end of this atherogenic regimen, vSMCs were established in serial culture and monitored for patterns of proliferative activity and gene expression. vSMCs isolated from BaP-treated animals (hence forth referred to as BaP cells) exhibited constitutively increased growth rates, and marked enhancement of proliferation in response to serum mitogens. Differential display polymerase chain reaction (DD-PCR) and Northern blot analyses revealed that mRNAs for ribosomal protein L31 and Zis genes were suppressed, while gas-5 and mitochondrial mRNAs were overexpressed in BaP cells relative to control mRNA populations. In situ hybridization experiments in vascular tissue confirmed these alterations in vivo. This is the first report linking expression of these genes to proliferative dysregulation during the course of experimentally-induced atherogenesis.

KW - Benzo(a)pyrene

KW - Chemical atherogenesis

KW - Differential gene expression

KW - Gas-5

KW - Mitochondrial and ribosomal mRNAs

KW - Vascular smooth muscle cells

KW - Zis

UR - http://www.scopus.com/inward/record.url?scp=0036176815&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0036176815&partnerID=8YFLogxK

U2 - 10.1016/S0021-9150(01)00581-0

DO - 10.1016/S0021-9150(01)00581-0

M3 - Article

C2 - 11849648

AN - SCOPUS:0036176815

VL - 160

SP - 273

EP - 280

JO - Atherosclerosis

JF - Atherosclerosis

SN - 0021-9150

IS - 2

ER -