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Canonical Wnt Signaling Pathway

Canonical Wnt Signaling Pathway

The gene encoding the main signaling molecules of the Wnt signaling pathways (the Wnt proteins) was discovered almost four decades ago by Nüsslein-Volhard and Wieschaus. They identified and originally named the gene "wingless" (wg) after a phenotype discovered during their landmark genetic screen in Drosophila for body pattern defects. At around the same time, another researcher named Harold Varmus found that a murine tumor virus activates the mammalian wg homolog, Int-1, which results in tumor...

Canonical Wnt Signaling Pathway

Canonical Wnt Signaling Pathway

The gene encoding the main signaling molecules of the Wnt signaling pathways (the Wnt proteins) was discovered almost four decades ago by Nüsslein-Volhard and Wieschaus. They identified and originally named the gene "wingless" (wg) after a phenotype discovered during their landmark genetic screen in Drosophila for body pattern defects. At around the same time, another researcher named Harold Varmus found that a murine tumor virus activates the mammalian wg homolog, Int-1, which results in tumor...

The JAK-STAT Signaling Pathway

The JAK-STAT Signaling Pathway

Several cytokine receptors have tightly bound Janus kinase or JAK proteins attached at their cytosolic tail. Small signaling molecules such as cytokines, growth hormones, or prolactins bind to the cytokine receptors and initiate their dimerization. The dimerization brings the cytosolic JAKs together that trans-phosphorylate and activates each other. The activated JAKs now phosphorylate cytosolic tails of the cytokine receptors, which serve as binding sites for adaptor proteins such as SH2...

Regulation of Angiogenesis and Blood Supply

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Non-Canonical Wnt Signaling Pathways

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Wnt is a zygotic effect gene that is expressed during very early embryonic development. It regulates various processes in animals starting from early development through the adult stage, such as organogenesis in the embryo and maintenance of neuronal and blood stem cells. Wnt proteins can induce a wide variety of intracellular pathways depending upon the specific abilities of different Wnt ligands to form a complex with shared and cognate receptors in the presence of different co-receptors. The...

Non-Canonical Wnt Signaling Pathways

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Wnt is a zygotic effect gene that is expressed during very early embryonic development. It regulates various processes in animals starting from early development through the adult stage, such as organogenesis in the embryo and maintenance of neuronal and blood stem cells. Wnt proteins can induce a wide variety of intracellular pathways depending upon the specific abilities of different Wnt ligands to form a complex with shared and cognate receptors in the presence of different co-receptors. The...

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Related Experiment Video

Updated: Jul 8, 2026

Modeling Paracrine Noncanonical Wnt Signaling In Vitro

Modeling Paracrine Noncanonical Wnt Signaling In Vitro

Published on: December 10, 2021

SPI1 Promotes Intracranial Aneurysm Formation by Inhibiting Wnt5a Transcription.

ZengShi Li^1,2, WeiChen Wang², Wei Li²

¹School of Medicine, Hunan Normal University, 410000 Changsha, Hunan, China.

Frontiers in Bioscience (Landmark Edition)

|July 7, 2026

Summary

This summary is machine-generated.

SPI1 promotes intracranial aneurysm (IA) formation by suppressing Wnt5a, leading to vascular smooth muscle cell changes. SPI1 inhibition in mice reduced IA development and inflammation, suggesting SPI1/Wnt5a as a therapeutic target.

Keywords:

SPI1 Wnt5a intracranial aneurysm phenotypic switching vascular smooth muscle cells

Related Experiment Videos

Last Updated: Jul 8, 2026

Modeling Paracrine Noncanonical Wnt Signaling In Vitro

Modeling Paracrine Noncanonical Wnt Signaling In Vitro

Published on: December 10, 2021

Area of Science:

Vascular Biology
Molecular Medicine
Genetics

Background:

SPI1 is a hub gene implicated in intracranial aneurysms (IA) and is upregulated in IA tissues.
The precise functional role of SPI1 in the pathogenesis of IA remains to be elucidated.

Purpose of the Study:

To investigate the functional impact of SPI1 on the development of intracranial aneurysms.
To elucidate the underlying molecular mechanisms by which SPI1 influences IA formation.

Main Methods:

Established an in vitro IA cell model using Platelet-Derived Growth Factor BB (PDGF-BB)-stimulated vascular smooth muscle cells (VSMCs).
Utilized sh-SPI1 plasmids for SPI1 silencing to assess VSMC phenotypic switching and Wnt pathway modulation.
Employed chromatin immunoprecipitation (ChIP) assays to confirm SPI1 binding to the Wnt5a promoter and in vivo studies using an IA mouse model.

Main Results:

PDGF-BB treatment increased SPI1, synthetic markers (MMP3/9), and Wnt pathway proteins (β-catenin, c-Myc), while decreasing contractile markers (α-SMA, SM22α) and Wnt5a.
SPI1 silencing reversed these effects, and ChIP confirmed SPI1 directly binds the Wnt5a promoter.
In vivo SPI1 knockdown mitigated vascular wall thickening, elastic fiber loss, and inflammation in IA mice, promoting Wnt5a expression and restoring VSMC phenotype.

Conclusions:

SPI1 promotes IA formation by inhibiting Wnt5a transcription, activating the Wnt/β-catenin pathway, and driving VSMC synthetic phenotype.
SPI1 knockdown alleviates vascular injury and inflammation in vivo.
The SPI1/Wnt5a signaling axis presents a potential therapeutic target for intracranial aneurysms.