Expression of Laminin α1, α2, α4, and α5 Chains, Fibronectin, and Tenascin-C in Skeletal Muscle of Dystrophic 129ReJdy/dyMice

Ringelmann, Birgit; Röder, Christine; Hallmann, Rupert; Maley, Moira; Davies, Marilyn; Grounds, Miranda D.; Sorokin, Lydia

doi:10.1006/excr.1998.4244

Cited by 116 publications

(125 citation statements)

References 57 publications

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“…Double or triple whole-mount immunohistochemistry was performed in retinas fixed 2 h on ice in 4% PFA or in MeOH at À 20°C. After fixation, retinas were blocked for 2 h in 1% BSA with 0.3% Triton X-100 and incubated overnight or for 2 h with isolectin B4 (Vector Labs, 1:50) and the following primary antibodies: rat anti-VE-cadherin (BD Biosciences, 1:200), rat anti-Integrin b1 (Chemicon, 1:200), rabbit anti-laminin a4 (serum 377, 1:1,000) 61 For labelling of proliferating cells, 100 mg of EdU (Life Technologies) per pup was injected intraperitoneally 4 h before killing. Following isolectin B4 staining, retinas were isolated and processed as described before 60 .…”

Section: Discussionmentioning

confidence: 99%

Integrin β1 controls VE-cadherin localization and blood vessel stability

et al. 2015

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Angiogenic blood vessel growth requires several distinct but integrated cellular activities. Endothelial cell sprouting and proliferation lead to the expansion of the vasculature and give rise to a highly branched, immature plexus, which is subsequently reorganized into a mature and stable network. Although it is known that integrin-mediated cell-matrix interactions are indispensable for embryonic angiogenesis, little is known about the function of integrins in different steps of vascular morphogenesis. Here, by investigating the integrin b1-subunit with inducible and endothelial-specific gene targeting in the postnatal mouse retina, we show that b1 integrin promotes endothelial sprouting but is a negative regulator of proliferation. In maturing vessels, integrin b1 is indispensable for proper localization of VE-cadherin and thereby cell-cell junction integrity. The sum of our findings establishes that integrin b1 has critical functions in the growing and maturing vasculature, and is required for the formation of stable, non-leaky blood vessels.

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Section: Discussionmentioning

confidence: 99%

Integrin β1 controls VE-cadherin localization and blood vessel stability

et al. 2015

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“…Primary antibodies were: rabbit anti-Prox1 (11,002, AngioBio, 1:200), rabbit anti-Lyve1 (11-034, AngioBio, 1:400), rabbit anti-laminin α5 (Ringelmann et al, 1999) (1:1000), rat anti-VE-cadherin (clone 11D4.1, 555289, BD Biosciences, 1:100), goat anti-Vegfr3 (AF743, R&D Systems, 1:100), hamster anti-podoplanin (Developmental Studies Hybridoma Bank, University of Iowa, 1:1000) and Cy3-conjugated αSMA (clone 1A4, C6198, Sigma-Aldrich, 1:400); Alexa Fluor 488-conjugated phalloidin was used to stain actin (A12379, Life Technologies, 1:200). …”

Section: Whole-mount Immunofluorescence Staining and Image Acquisitionmentioning

confidence: 99%

Syndecan 4 controls lymphatic vasculature remodeling during mouse embryonic development

Wang¹,

Baeyens²,

Corti³

et al. 2016

Journal of Cell Science

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The role of fluid shear stress in vasculature development and remodeling is well appreciated. However, the mechanisms regulating these effects remain elusive. We show that abnormal flow sensing in lymphatic endothelial cells (LECs) caused by Sdc4 or Pecam1 deletion in mice results in impaired lymphatic vessel remodeling, including abnormal valve morphogenesis. Ablation of either gene leads to the formation of irregular, enlarged and excessively branched lymphatic vessels. In both cases, lymphatic valve-forming endothelial cells are randomly oriented, resulting in the formation of abnormal valves. These abnormalities are much more pronounced in Sdc4 −/− ; Pecam1 −/− double-knockout mice, which develop severe edema. In vitro, SDC4 knockdown human LECs fail to align under flow and exhibit high expression of the planar cell polarity protein VANGL2. Reducing VANGL2 levels in SDC4 knockdown LECs restores their alignment under flow, while VANGL2 overexpression in wild-type LECs mimics the flow alignment abnormalities seen in SDC4 knockdown LECs. SDC4 thus controls flow-induced LEC polarization via regulation of VANGL2 expression.

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“…(20,21) Primary antibodies against CD24a (Biolegend, San Diego, CA), CD81, CD44, CD45 (Pharmingen, Franklin Lakes, NJ), TrkB (R&D, Minneapolis, MN), CD200 (Serotec, Dü sseldorf, Germany), Igf2r, Fgfr3 (Santa Cruz Biotechnology, Inc., Santa Cruz, CA, USA), or Pthr1 (Abcam, Cambridge, UK) were incubated on sections and detected by secondary antibodies conjugated with Alexa or Cy-dyes (Molecular Probes, Jackson, West Grove, PA, USA). Incubations of sections with secondary antibodies only were used as negative controls.…”

Section: Immunohistochemistrymentioning

confidence: 99%

Sorting of growth plate chondrocytes allows the isolation and characterization of cells of a defined differentiation status

Belluoccio¹,

Etich²,

Rosenbaum³

et al. 2010

Journal of Bone and Mineral Research

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Axial growth of long bones occurs through a coordinated process of growth plate chondrocyte proliferation and differentiation. This maturation of chondrocytes is reflected in a zonal change in gene expression and cell morphology from resting to proliferative, prehypertrophic, and hypertrophic chondrocytes of the growth plate followed by ossification. A major experimental limitation in understanding growth plate biology and pathophysiology is the lack of a robust technique to isolate cells from the different zones, particularly from small animals. Here, we report on a new strategy for separating distinct chondrocyte populations from mouse growth plates. By transcriptome profiling of microdissected zones of growth plates, we identified novel, zone-specific cell surface markers and used these for flow cytometry and immunomagnetic cell separation to quantify, enrich, and characterize chondrocytes populations with respect to their differentiation status. This approach provides a novel platform to study cartilage development and characterize mouse growth plate chondrocytes to reveal unique cellular phenotypes of the distinct subpopulations within the growth plate. ß

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Expression of Laminin α1, α2, α4, and α5 Chains, Fibronectin, and Tenascin-C in Skeletal Muscle of Dystrophic 129ReJdy/dyMice

Cited by 116 publications

References 57 publications

Integrin β1 controls VE-cadherin localization and blood vessel stability

Integrin β1 controls VE-cadherin localization and blood vessel stability

Syndecan 4 controls lymphatic vasculature remodeling during mouse embryonic development

Sorting of growth plate chondrocytes allows the isolation and characterization of cells of a defined differentiation status

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