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Role for the α7β1 integrin in vascular development and integrity
Author(s) -
FlintoffDye Nichole L.,
Welser Jennifer,
Rooney Jachinta,
Scowen Paul,
Tamowski Susan,
Hatton William,
Burkin Dean J.
Publication year - 2005
Publication title -
developmental dynamics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.634
H-Index - 141
eISSN - 1097-0177
pISSN - 1058-8388
DOI - 10.1002/dvdy.20462
Subject(s) - biology , integrin , vascular smooth muscle , microbiology and biotechnology , muscle hypertrophy , myosin , laminin , myocyte , receptor , endocrinology , extracellular matrix , genetics , smooth muscle
The α7β1 integrin is a laminin receptor that has been implicated in muscle disease and the development of neuromuscular and myotendinous junctions. Studies have shown the α7β1 integrin is also expressed in nonskeletal muscle tissues. To identify the expression pattern of the α7 integrin in these tissues during embryonic development, α7 integrin chain knockout mice were generated by a LacZ knockin strategy. In these mice, expression from the α7 promoter is reported by β‐galactosidase. From embryonic day (ED) 11.5 to ED14.5, β‐galactosidase was detected in the developing central and peripheral nervous systems and vasculature. The loss of the α7 integrin gene resulted in partial embryonic lethality. Several α7 null embryos were identified with cerebrovascular hemorrhages and showed reduced vascular smooth muscle cells and cerebral vascularization. The α7 null mice that survived to birth exhibited vascular smooth muscle defects, including hyperplasia and hypertrophy. In addition, altered expression of α5 and α6B integrin chains was detected in the cerebral arteries of α7 null mice, which may contribute to the vascular phenotype. Our results demonstrate for the first time that the α7β1 integrin is important for the recruitment or survival of cerebral vascular smooth muscle cells and that this integrin plays an important role in vascular development and integrity. Developmental Dynamics 234:11–21, 2005. © 2005 Wiley‐Liss, Inc.