Alternations in genes expression of pathway signaling in esophageal tissue with atresia: results of expression microarray profiling
PBN-AR
Instytucja
Wydział Elektroniki (Politechnika Wrocławska)
Informacje podstawowe
Główny język publikacji
eng
Czasopismo
DISEASES OF THE ESOPHAGUS
ISSN
1120-8694
EISSN
Wydawca
DOI
URL
Rok publikacji
2015
Numer zeszytu
nr 3
Strony od-do
229-233
Numer tomu
vol. 28
Link do pełnego tekstu
Identyfikator DOI
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Autorzy
(liczba autorów: 12)
Pozostali autorzy
+ 11
Słowa kluczowe
pol
ekspresja genów
mikromacierze ekspresyjne
atrezja przełyku
SHH
Streszczenia
Język
eng
Treść
Esophageal atresia (EA) is a congenital defect of the esophagus involving the interruption of the esophagus with or without connection to the trachea (tracheoesophageal fistula [TEF]). EA/TEF may occur as an isolated anomaly, may be part of a complex of congenital defects (syndromic), or may develop within the context of a known syndrome or association. The molecular mechanisms underlying the development of EA are poorly understood. It is supposed that a combination of multigenic factors and epigenetic modification of genes play a role in its etiology. The aim of our work was to assess the human gene expression microarray study in esophageal tissue samples. Total RNA was extracted from 26 lower pouches of esophageal tissue collected during thoracoscopic EA repair in neonates with the isolated (IEA) and the syndromic form (SEA). We identified 787 downregulated and 841 upregulated transcripts between SEA and controls, and about 817 downregulated and 765 upregulated probes between IEA and controls. Fifty percent of these genes showed differential expression specific for either IEA or SEA. Functional pathway analysis revealed substantial enrichment for Wnt and Sonic hedgehog, as well as cytokine and chemokine signaling pathways. Moreover, we performed reverse transcription polymerase chain reaction study in a group of SHH and Wnt pathways genes with differential expression in microarray profiling to confirm the microarray expression results. We verified the altered expression in SFRP2 gene from the Wnt pathway as well as SHH, GLI1, GLI2, and GLI3 from the Sonic hedgehog pathway. The results suggest an important role of these pathways and genes for EA/TEF etiology.
Inne
System-identifier
000191364
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