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Goodwin, Anne M.; D’Amore, Patricia A.

doi:10.1023/a:1021563510866

Cited by 159 publications

(70 citation statements)

References 96 publications

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“…Discussion of select genes in this category is limited to abundant genes with known vascular functions. Two soluble naturally occurring Wnt antagonists, frizzled-related proteins, FRP1 and FRP3, are expressed by vascular cells (16). Wnt growth factors function via Frizzled receptors to stimulate angiogenesis (17).…”

Section: Resultsmentioning

confidence: 99%

Transcriptome-wide analysis of blood vessels laser captured from human skin and chronic wound-edge tissue

Roy

Patel

Khanna

et al. 2007

Proc. Natl. Acad. Sci. U.S.A.

105

131

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Chronic wounds represent a substantial public health problem. The development of tools that would enable sophisticated scrutiny of clinical wound tissue material is highly desirable. This work presents evidence enabling rapid specific identification and laser capture of blood vessels from human tissue in a manner which lends itself to successful high-density (U133A) microarray analysis. Such screening of transcriptome followed by real-time PCR and immunohistochemical verification of candidate genes and their corresponding products were performed by using 3 mm biopsies. Of the 18,400 transcripts and variants screened, a focused set of 53 up-regulated and 24 down-regulated genes were noted in woundderived blood vessels compared with blood vessels from intact human skin. The mean abundance of periostin in wound-site blood vessels was 96-fold higher. Periostin is known to be induced in response to vascular injury and its expression is associated with smooth muscle cell differentiation in vitro and promotes cell migration. Forty-fold higher expression of heparan sulfate 6-Oendosulfatase1 (Sulf1) was noted in wound-site vessels. Sulf1 has been recently recognized to be anti-angiogenic. During embryonic vasculogenesis, CD24 expression is down-regulated in human embryonic stem cells. Wound-site vessels had lower CD24 expression. The findings of this work provide a unique opportunity to appreciate the striking contrast in the transcriptome composition in blood vessels collected from the intact skin and from the wound-edge tissue. Sets of genes with known vascular functions but never connected to wound healing were identified to be differentially expressed in wound-derived blood vessels paving the way for innovative clinically relevant hypotheses.angiogenesis ͉ microarray ͉ wound healing

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Section: Resultsmentioning

confidence: 99%

Transcriptome-wide analysis of blood vessels laser captured from human skin and chronic wound-edge tissue

Roy

Patel

Khanna

et al. 2007

Proc. Natl. Acad. Sci. U.S.A.

105

131

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“…Msx2 has also promoted osteogenic differentiation, and it suppresses adipogenesis of vascular myofibroblasts 96. Msx2 enhances Wnt signaling through the upregulation of several Wnt ligands98 and the downregulation of dickkopf homologue 1,99 a canonical Wnt pathway antagonist. Indeed, Msx2 and Wnt seem to regulate each other's expression in a bidirectional way 100, 101.…”

Section: Implication Of Wnt Signaling In Atherosclerotic Calcificationmentioning

confidence: 99%

Atherosclerotic Calcification: Wnt Is the Hint

Albanese

Khan

Barratt

et al. 2018

JAHA

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“…Wnt ligands, receptors, and inhibitors are expressed by vascular cells and participate in both normal and pathologic vessel growth, yet the key players in these processes and their roles are not yet identified (reviewed in Ref. 21). Wnt signaling also participates in hematopoiesis by providing proliferative signals for immature hematopoietic progeni-tors and promoting the self-renewal of hematopoietic stem cells (22,23).…”

Section: Embryonic Stem (Es)mentioning

confidence: 99%

Wnt2 Coordinates the Commitment of Mesoderm to Hematopoietic, Endothelial, and Cardiac Lineages in Embryoid Bodies

Wang

Gilner

Bautch

et al. 2007

Journal of Biological Chemistry

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Our recent gene expression profiling analyses demonstrated that Wnt2 is highly expressed in Flk1؉ cells, which serve as common progenitors of endothelial cells, blood cells, and mural cells. In this report, we characterize the role of Wnt2 in mesoderm development during embryonic stem (ES) cell differentiation by creating ES cell lines in which Wnt2 was deleted. Wnt2؊/؊ embryoid bodies (EBs) generated increased numbers of Flk1؉ cells and blast colony-forming cells compared with wild-type EBs, and had higher Flk1 expression at comparable stages of differentiation. Although Flk1 ؉ cells were increased, we found that endothelial cell and terminal cardiomyocyte differentiation was impaired, but hematopoietic cell differentiation was enhanced and smooth muscle cell differentiation was unchanged in Wnt2 ؊/؊ EBs. Later stage Wnt2 ؊/؊ EBs had either lower or undetectable expression of endothelial and cardiac genes compared with wild-type EBs. Consistently, vascular plexi were poorly formed and neither beating cardiomyocytes nor ␣-actinin-staining cells were detectable in later stage Wnt2 ؊/؊ EBs. In contrast, hematopoietic cell gene expression was upregulated, and the number of hematopoietic progenitor colonies was significantly enhanced in Wnt2 ؊/؊ EBs. Our data indicate that Wnt2 functions at multiple stages of development during ES cell differentiation and during the commitment and diversification of mesoderm: as a negative regulator for hemangioblast differentiation and hematopoiesis but alternatively as a positive regulator for endothelial and terminal cardiomyocyte differentiation. Embryonic stem (ES)2 cells have considerable potential for use in cellular therapies for many human diseases or disorders.However, manipulating the differentiation of pluripotent cells into a desired cell type is difficult to control. Therefore, efforts have been directed toward understanding the molecular and cellular mechanisms for maintaining ES cell pluripotency as well as for ES cell fate determination and lineage specification. Under appropriate culture conditions, ES cells will spontaneously differentiate and form embryoid bodies (EBs) that recapitulate the differentiation program of normal embryonic development. This in vitro experimental model is widely used to study mesoderm development, including the hematopoietic system, vascular endothelial cells, and cardiomyocytes (1-4).Murine hematopoietic and endothelial cell development begins in the yolk sac mesoderm at approximately day 7.5 of gestation and is marked by establishment of blood islands (5, 6). The close physical relationship between these two cell populations within blood islands has led to a widely accepted hypothesis that a common precursor for both hematopoietic and endothelial cells exists, the hemangioblast (7, 8). The receptor for vascular endothelial growth factor (VEGF), fetal liver kinase-1 (Flk1), is an early molecular marker for hemangioblasts (9 -12). Blast colony-forming cells (BLCFCs) derived from EBs can generate hematopoietic and endothelial cell lineag...

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Untitled

Cited by 159 publications

References 96 publications

Transcriptome-wide analysis of blood vessels laser captured from human skin and chronic wound-edge tissue

Transcriptome-wide analysis of blood vessels laser captured from human skin and chronic wound-edge tissue

Atherosclerotic Calcification: Wnt Is the Hint

Wnt2 Coordinates the Commitment of Mesoderm to Hematopoietic, Endothelial, and Cardiac Lineages in Embryoid Bodies

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