PMID- 21306609
OWN - NLM
STAT- MEDLINE
DCOM- 20110722
LR  - 20211203
IS  - 1471-213X (Electronic)
IS  - 1471-213X (Linking)
VI  - 11
DP  - 2011 Feb 9
TI  - Coordinated gene expression during gilthead sea bream skeletogenesis and its 
      disruption by nutritional hypervitaminosis A.
PG  - 7
LID - 10.1186/1471-213X-11-7 [doi]
AB  - BACKGROUND: Vitamin A (VA) has a key role in vertebrate morphogenesis, 
      determining body patterning and growth through the control of cell proliferation 
      and differentiation processes. VA regulates primary molecular pathways of those 
      processes by the binding of its active metabolite (retinoic acid) to two types of 
      specific nuclear receptors: retinoic acid receptors (RARs) and retinoid X 
      receptors (RXRs), which promote transcription of downstream target genes. This 
      process is well known in most of higher vertebrates; however, scarce information 
      is available regarding fishes. Therefore, in order to gain further knowledge of 
      fish larval development and its disruption by nutritional VA imbalance, the 
      relative expression of some RARs and RXRs, as well as several genes involved in 
      morpho- and skeletogenesis such as peroxisome proliferator-activated receptors 
      (PPARA, PPARB and PPARG); retinol-binding protein (RBP); insulin-like growth 
      factors I and II (IGF1 and IGF2, respectively); bone morphogenetic protein 2 
      (Bmp2); transforming growth factor beta-1 (TGFB1); and genes encoding different 
      extracellular matrix (ECM) proteins such as matrix Gla protein (mgp), osteocalcin 
      (bglap), osteopontin (SPP1), secreted protein acidic and rich in cysteine (SPARC) 
      and type I collagen alpha1 chain (COL1A1) have been studied in gilthead sea bream. 
      RESULTS: During gilthead sea bream larval development, specific expression 
      profiles for each gene were tightly regulated during fish morphogenesis and 
      correlated with specific morphogenetic events and tissue development. Dietary 
      hypervitaminosis A during early larval development disrupted the normal gene 
      expression profile for genes involved in RA signalling (RARA), VA homeostasis 
      (RBP) and several genes encoding ECM proteins that are linked to skeletogenesis, 
      such as bglap and mgp. CONCLUSIONS: Present data reflects the specific gene 
      expression patterns of several genes involved in larval fish RA signalling and 
      skeletogenesis; and how specific gene disruption induced by a nutritional VA 
      imbalance underlie the skeletal deformities. Our results are of basic interest 
      for fish VA signalling and point out some of the potential molecular players 
      involved in fish skeletogenesis. Increased incidences of skeletal deformities in 
      gilthead sea bream fed with hypervitaminosis A were the likely ultimate 
      consequence of specific gene expression disruption at critical development 
      stages.
FAU - Fernandez, Ignacio
AU  - Fernandez I
AD  - Unitat de Cultius Experimentals, IRTA Centre de Sant Carles de la Rapita 
      (IRTA-SCR), Crta, del Poble Nou s/n, 43540 - Sant Carles de la Rapita (Spain) 
      ignacio.fernandez@irta.es
FAU - Darias, Maria
AU  - Darias M
FAU - Andree, Karl B
AU  - Andree KB
FAU - Mazurais, David
AU  - Mazurais D
FAU - Zambonino-Infante, Jose Luis
AU  - Zambonino-Infante JL
FAU - Gisbert, Enric
AU  - Gisbert E
LA  - eng
PT  - Journal Article
DEP - 20110209
PL  - England
TA  - BMC Dev Biol
JT  - BMC developmental biology
JID - 100966973
RN  - 0 (Bone Morphogenetic Protein 2)
RN  - 0 (Collagen Type I)
RN  - 0 (Collagen Type I, alpha 1 Chain)
RN  - 0 (Extracellular Matrix Proteins)
RN  - 0 (Peroxisome Proliferator-Activated Receptors)
RN  - 0 (Receptors, Retinoic Acid)
RN  - 0 (Retinoid X Receptors)
RN  - 0 (Retinol-Binding Proteins)
RN  - 0 (Somatomedins)
RN  - 0 (Transforming Growth Factor beta)
RN  - 11103-57-4 (Vitamin A)
RN  - 5688UTC01R (Tretinoin)
SB  - IM
MH  - Animals
MH  - *Bone Development
MH  - Bone Morphogenetic Protein 2/genetics
MH  - Cell Differentiation/drug effects
MH  - Cell Proliferation/drug effects
MH  - Collagen Type I/genetics
MH  - Collagen Type I, alpha 1 Chain
MH  - Extracellular Matrix Proteins/drug effects/genetics
MH  - Gene Expression/*drug effects
MH  - Gene Expression Profiling
MH  - *Gene Expression Regulation, Developmental
MH  - Hypervitaminosis A/genetics
MH  - Morphogenesis
MH  - Peroxisome Proliferator-Activated Receptors/genetics
MH  - Receptors, Retinoic Acid/genetics
MH  - Retinoid X Receptors/genetics
MH  - Retinol-Binding Proteins/genetics
MH  - Reverse Transcriptase Polymerase Chain Reaction
MH  - Sea Bream/*genetics/*growth & development/metabolism
MH  - Somatomedins/genetics
MH  - Transforming Growth Factor beta/genetics
MH  - Tretinoin/*metabolism
MH  - Vitamin A/*administration & dosage
PMC - PMC3045981
EDAT- 2011/02/11 06:00
MHDA- 2011/07/23 06:00
PMCR- 2011/02/09
CRDT- 2011/02/11 06:00
PHST- 2010/09/17 00:00 [received]
PHST- 2011/02/09 00:00 [accepted]
PHST- 2011/02/11 06:00 [entrez]
PHST- 2011/02/11 06:00 [pubmed]
PHST- 2011/07/23 06:00 [medline]
PHST- 2011/02/09 00:00 [pmc-release]
AID - 1471-213X-11-7 [pii]
AID - 10.1186/1471-213X-11-7 [doi]
PST - epublish
SO  - BMC Dev Biol. 2011 Feb 9;11:7. doi: 10.1186/1471-213X-11-7.