Role for the α7β1 integrin in vascular development and integrity

Flintoff-Dye, Nichole L.; Welser, Jennifer V.; Rooney, Jachinta E.; Scowen, Paul; Tamowski, Susan; Hatton, William J.; Burkin, Dean J.

doi:10.1002/dvdy.20462

Cited by 79 publications

(92 citation statements)

References 54 publications

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“…VSMCs are known to switch to a less differentiated state after vascular damage [42]. Loss of α7 integrin results in fewer differentiated and contractile VSMCs leading to cerebral vascular hemorrhaging [25]. To explore if a similar mechanism occurred within the placentae of α7 integrin null mice, we examined smooth muscle cell differentiation by examining expression of smooth muscle cell markers within the placenta.…”

Section: Discussionmentioning

confidence: 99%

“…The loss of one integrin in vascular smooth muscle has been shown to cause altered expression of other integrins [25]. In addition, extracellular matrix deposition can be altered by loss of the α7 integrin [28;30].…”

Section: Discussionmentioning

confidence: 99%

“…Expression of the α7 integrin promoter was detected by β-galactosidase staining. β-galactosidase staining of wild-type and α7 integrin null placentae was performed following a previously published protocol [25].…”

Section: Histological Stainingmentioning

confidence: 99%

“…In addition, the α7β1 integrin can regulate the expression of other integrin chains [25]. To determine if loss of the α7 integrin altered the deposition of extracellular matrix proteins, immunofluorescence was used to detect fibronectin and laminin-1 in wild-type and α7 integrin null placentae.…”

Section: Loss Of the α7 Integrin Affects The Deposition Of Extracellumentioning

confidence: 99%

“…Loss of the α7 integrin causes partial embryonic lethality in which 44% of the α7 integrin null embryos die before birth [24;25]. We have recently demonstrated that loss of the α7 integrin chain leads to cerebral vascular defects which may contribute to the partial embryonic lethality observed in α7 integrin null mice [25]. Studies have shown α7 integrin expression increases in vascular smooth muscle cells (VSMCs) isolated from rats treated with allylamine to induce vascular damage [26].…”

Section: Introductionmentioning

confidence: 99%

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Placental Defects in α7 Integrin Null Mice

et al. 2007

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The α7β1 integrin is a heterodimeric transmembrane receptor that links laminin in the extracellular matrix to the cell cytoskeleton. Loss of the α7 integrin chain results in partial embryonic lethality. We have previously shown that α7 integrin null embryos exhibit vascular smooth muscle cell defects that result in cerebral vascular hemorrhaging. Since the placenta is highly vascularized, we hypothesized that placental vascular defects in α7 integrin null embryos may contribute to the partial embryonic lethality. Placentae from embryonic day (ED) 9.5 and 13.5 α7 integrin knockout embryos showed structural defects including infiltration of the spongiotrophoblast layer into the placental labyrinth, a reduction in the placental labyrinth and loss of distinct placental layers. Embryos and placentae that lacked the α7 integrin weighed less compared to wild-type controls. Blood vessels within the placental labyrinth of α7 integrin null embryos exhibited fewer differentiated vascular smooth muscle cells compared to wild-type. Loss of the α7 integrin resulted in altered extracellular matrix deposition and reduced expression of α5 integrin. Together our results confirm a role for the α7β1 integrin in placental vascular development and demonstrate for the first time that loss of the α7 integrin results in placental defects.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Histological Stainingmentioning

confidence: 99%

Section: Loss Of the α7 Integrin Affects The Deposition Of Extracellumentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Placental Defects in α7 Integrin Null Mice

et al. 2007

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Cell biology of embryonic migration

Kurosaka¹,

Kashina²

2008

Birth Defects Research Pt C

111

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Cell migration is an evolutionarily conserved mechanism that underlies the development and functioning of uni-and multicellular organisms and takes place in normal and pathogenic processes, including various events of embryogenesis, wound healing, immune response, cancer metastases, and angiogenesis. Despite the differences in the cell types that take part in different migratory events, it is believed that all of these migrations occur by similar molecular mechanisms, whose major components have been functionally conserved in evolution and whose perturbation leads to severe developmental defects. These mechanisms involve intricate cytoskeleton-based molecular machines that can sense the environment, respond to signals, and modulate the entire cell behavior. A big question that has concerned the researchers for decades relates to the coordination of cell migration in situ and its relation to the intracellular aspects of the cell migratory mechanisms. Traditionally, this question has been addressed by researchers that considered the intra-and extracellular mechanisms driving migration in separate sets of studies. As more data accumulate researchers are now able to integrate all of the available information and consider the intracellular mechanisms of cell migration in the context of the developing organisms that contain additional levels of complexity provided by extracellular regulation. This review provides a broad summary of the existing and emerging data in the cell and developmental biology fields regarding cell migration during development.

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The basal chorionic trophoblast cell layer: An emerging coordinator of placenta development

2016

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During gestation, fetomaternal exchange occurs in the villous tree (labyrinth) of the placenta. Development of this structure depends on tightly coordinated cellular processes of branching morphogenesis and differentiation of specialized trophoblast cells. The basal chorionic trophoblast (BCT) cell layer that localizes next to the chorioallantoic interface is of critical importance for labyrinth morphogenesis in rodents. Gcm1-positive cell clusters within this layer initiate branching morphogenesis thereby guiding allantoic fetal blood vessels towards maternal blood sinuses. Later these cells differentiate and contribute to the syncytiotrophoblast of the fetomaternal barrier. Additional cells within the BCT layer sustain continued morphogenesis, possibly through a repopulating progenitor population. Several mouse mutants highlight the importance of a structurally intact BCT epithelium, and a growing number of studies addresses its patterning and epithelial architecture. Here, we review and discuss emerging concepts in labyrinth development focussing on the biology of the BCT cell layer.

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Role for the α7β1 integrin in vascular development and integrity

Cited by 79 publications

References 54 publications

Placental Defects in α7 Integrin Null Mice

Placental Defects in α7 Integrin Null Mice

Cell biology of embryonic migration

The basal chorionic trophoblast cell layer: An emerging coordinator of placenta development

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