Literature DB >> 11329586

Structural immaturity of the heart in congenital diaphragmatic hernia in rats.

N Guarino1, H Shima, P Puri.   

Abstract

PURPOSE: The form and function of the heart are the final result of an integration of cells, tissues, and extracellular material. The extracellular matrix (ECM) is a complex array of different molecular components, and it plays an important role for the transfer of mechanical force in both contraction and relaxation phases in the cardiac cycle. ECM plays also a significant role in the development of the heart. The aim of this study was to evaluate the expression of important ECM components in the heart of rats with induced CDH to test the hypothesis that an alteration of ECM may contribute to the cardiac maldevelopment, which recently has been identified as a contributive factor for the high mortality rate in babies with congenital diaphragmatic hernia (CDH).
METHODS: CDH model was induced in pregnant rats after administration of 100 mg of nitrofen on day 9.5 of gestation (term, 22 days). In control animals the same dose of olive oil was given without nitrofen. Cesarean section was performed on day 21 of gestation. The fetuses were divided into 2 groups: normal control (n = 10) and nitrofen-induced CDH (n = 10). Reverse transcription polymerase chain reaction (RT-PCR) was performed to evaluate the relative amount of tropoelastin and alpha1 (I) procollagen mRNA expression. Elastin protein content was measured using enzyme-linked immunosorbent assay (ELISA).
RESULTS: There was a reduction in tropoelastin mRNA (P <.05) and procollagen mRNA (P <.05) in CDH compared with controls. The cardiac alpha-elastin content also was reduced in CDH (P <.01).
CONCLUSIONS: The reduced cardiac tropoelastin and procollagen gene expression and the reduced alpha-elastin content indicate that the heart in CDH structurally is immature. The reduced production of cardiac ECM may contribute to a contractile dysfunction, which makes the heart unable to respond to the hemodynamic load accompanying persistent pulmonary hypertension (PPH). Copyright 2001 by W.B. Saunders Company.

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Year:  2001        PMID: 11329586     DOI: 10.1053/jpsu.2001.22957

Source DB:  PubMed          Journal:  J Pediatr Surg        ISSN: 0022-3468            Impact factor:   2.545


  4 in total

Review 1.  Electrical and mechanical stimulation of cardiac cells and tissue constructs.

Authors:  Whitney L Stoppel; David L Kaplan; Lauren D Black
Journal:  Adv Drug Deliv Rev       Date:  2015-07-30       Impact factor: 15.470

2.  Expression of Connexin 43 in the hearts of rat embryos exposed to nitrofen and effects of vitamin A on it.

Authors:  Salome Gonzalez-Reyes; Virginia Fernandez-Dumont; Wenceslao M Calonge; Leopoldo Martinez; Juan A Tovar
Journal:  Pediatr Surg Int       Date:  2006-01       Impact factor: 1.827

3.  Altered expression of angiotensin II receptor subtypes and transforming growth factor-beta in the heart of nitrofen-induced diaphragmatic hernia in rats.

Authors:  Honami Teramoto; Masato Shinkai; Prem Puri
Journal:  Pediatr Surg Int       Date:  2004-12-02       Impact factor: 1.827

4.  Increased CaSR and TRPC6 pulmonary vascular expression in the nitrofen-induced model of congenital diaphragmatic hernia.

Authors:  Hiroki Nakamura; Julia Zimmer; Tristan Lim; Prem Puri
Journal:  Pediatr Surg Int       Date:  2017-10-05       Impact factor: 1.827

  4 in total

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