Abnormal expression of genes associated with development and inflammation in the heart of mouse maternal phenylketonuria offspring

Reuben Matalon, Sankar Surendran, J. D. McDonald, Anthony Okorodudu, S. K. Tyring, K. Michals-Matalon, P. Harris

Research output: Contribution to journalArticle

11 Citations (Scopus)

Abstract

This study descibes gene expression in the fetus hearts obtained from mouse model for Phenylketonuria. These hearts have cardiovascular disease (CVD). Therefore genes involved in CVD were examined. Several genes associated with heart development and inflammation were found to be altered. In order to investigate whether the abnormal gene expression alters transcription and translation, the levels of troponin mRNA and protein were determined. One step real time RT-PCR showed a reduction in cardiac troponin I, troponin T2 and ryanodine receptor 2. Determination of troponin I and T protein levels showed reduced levels of these proteins. Our results suggest that altered gene expression affects protein production. These changes are likely involved in the cardiovascular defects seen in the mouse.

Original languageEnglish (US)
Pages (from-to)557-565
Number of pages9
JournalInternational Journal of Immunopathology and Pharmacology
Volume18
Issue number3
StatePublished - Jul 2005

Fingerprint

Maternal Phenylketonuria
Inflammation
Gene Expression
Troponin T
Troponin I
Proteins
Cardiovascular Diseases
Ryanodine Receptor Calcium Release Channel
Phenylketonurias
Troponin
Genes
Real-Time Polymerase Chain Reaction
Fetus
Messenger RNA

Keywords

  • Cardiovascular defects
  • Growth factors
  • Inflammation
  • RyR2
  • Troponin I
  • Troponin T

ASJC Scopus subject areas

  • Pharmacology

Cite this

Abnormal expression of genes associated with development and inflammation in the heart of mouse maternal phenylketonuria offspring. / Matalon, Reuben; Surendran, Sankar; McDonald, J. D.; Okorodudu, Anthony; Tyring, S. K.; Michals-Matalon, K.; Harris, P.

In: International Journal of Immunopathology and Pharmacology, Vol. 18, No. 3, 07.2005, p. 557-565.

Research output: Contribution to journalArticle

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