PMID- 12823230
OWN - NLM
STAT- MEDLINE
DCOM- 20040304
LR  - 20190922
IS  - 0301-4681 (Print)
IS  - 0301-4681 (Linking)
VI  - 71
IP  - 4-5
DP  - 2003 Jun
TI  - The dynamic expression of tenascin-C and tenascin-X during early heart 
      development in the mouse.
PG  - 291-8
AB  - One of a family of extracellular matrix proteins, tenascin-C (TNC) is expressed 
      in a spatiotemporally restricted pattern associated with tissue remodeling during 
      embryonic development, wound healing, cancer invasion and tissue regeneration. 
      Another form, tenascin-X (TNX), is found in most tissues but most predominantly 
      in heart and muscle, often complementarily to TNC. The present analysis 
      demonstrated their expression during early heart development, using mouse lines 
      containing the lacZ gene targeted to the TNC locus, by RT-PCR, 
      immunohistochemistry, and in situ hybridization. TNC was transiently expressed at 
      important steps during heart development: (1) precardiac mesodermal cells 
      differentiating to cardiomyocytes and endocardial cells at E 7.5 - 8.5; (2) 
      cardiomyocytes in the outflow tract at E 8.5 - 12; (3) endocardial cells forming 
      cushion tissue at E 9.5 - 13; and (4) mesenchymal cells in the proepicardial 
      organ (PEO), the precursors of coronary vessels, at E 9.5. When PEO cells were 
      transferred onto the heart surface, the expression of TNC was downregulated, 
      while TNX was upregulated at E 11. Initially, epicardial cells around the AV 
      groove and atrium started to express TNX. TNX-positive cells then gradually 
      spread all over the entire surface of the heart and invaded and formed primitive 
      vascular channels in the myocardium. Despite restricted expression at important 
      sites and steps during cardiogenesis, the hearts of TNC deficient mice developed 
      normally. No difference in the expression pattern of TNX were observed in TNC 
      knockout and wild mice. These results suggest; (1) TNC could play important roles 
      in the differentiation of cardiomyocytes and the early morphogenesis of the 
      heart; (2) TNX could be involved in coronary vasculogenesis; (3) TNX does not 
      compensate for the loss of TNC.
FAU - Imanaka-Yoshida, Kyoko
AU  - Imanaka-Yoshida K
AD  - Department of Pathology, Mie University School of Medicine, 2-174 Edobashi, Tsu, 
      Mie 514-8507 Japan. imanaka@doc.medic.mie-u.ac.jp
FAU - Matsumoto, Kenn-ichi
AU  - Matsumoto K
FAU - Hara, Mari
AU  - Hara M
FAU - Sakakura, Teruyo
AU  - Sakakura T
FAU - Yoshida, Toshimichi
AU  - Yoshida T
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - Differentiation
JT  - Differentiation; research in biological diversity
JID - 0401650
RN  - 0 (Tenascin)
RN  - 0 (tenascin X)
SB  - IM
MH  - Animals
MH  - Cell Differentiation/physiology
MH  - Endocardium/embryology/metabolism
MH  - Heart/*embryology
MH  - Mesoderm/metabolism
MH  - Mice
MH  - Mice, Knockout
MH  - Myocardium/*metabolism
MH  - Myocytes, Cardiac/metabolism
MH  - Neovascularization, Physiologic/physiology
MH  - Tenascin/biosynthesis/*genetics
EDAT- 2003/06/26 05:00
MHDA- 2004/03/05 05:00
CRDT- 2003/06/26 05:00
PHST- 2003/06/26 05:00 [pubmed]
PHST- 2004/03/05 05:00 [medline]
PHST- 2003/06/26 05:00 [entrez]
AID - 7104-506 [pii]
AID - 10.1046/j.1432-0436.2003.7104506.x [doi]
PST - ppublish
SO  - Differentiation. 2003 Jun;71(4-5):291-8. doi: 10.1046/j.1432-0436.2003.7104506.x.