Track topics on Twitter Track topics that are important to you
Astrocytes have emerged as integral partners with neurons in regulating synapse formation and function, but the mechanisms that mediate these interactions are not well understood. Here, we show that Sonic hedgehog (Shh) signaling in mature astrocytes is required for establishing structural organization and remodeling of cortical synapses in a cell type-specific manner. In the postnatal cortex, Shh signaling is active in a subpopulation of mature astrocytes localized primarily in deep cortical layers. Selective disruption of Shh signaling in astrocytes produces a dramatic increase in synapse number specifically on layer V apical dendrites that emerges during adolescence and persists into adulthood. Dynamic turnover of dendritic spines is impaired in mutant mice and is accompanied by an increase in neuronal excitability and a reduction of the glial-specific, inward-rectifying K channel Kir4.1. These data identify a critical role for Shh signaling in astrocyte-mediated modulation of neuronal activity required for sculpting synapses.
This article was published in the following journal.
Peritoneal fibrosis is a devastating complication of peritoneal dialysis. However, its precise mechanism is unclear, and specific treatments have not yet been established. Recent evidence suggests tha...
To explore the changes of Sonic Hedgehog (Shh) signaling pathway in the stomach mucosa during the formation of gastric precancerous lesions.
Impairment of the blood-brain barrier (BBB) has been associated with cognitive decline in many CNS diseases, including HIV-associated neurocognitive disorders (HAND). Recent research suggests an impor...
In the developing cerebellum, Sonic hedgehog (SHH) signaling is required for expansion of cerebellar granule neural progenitors, proposed to be cells-of-origin for the SHH-driven pediatric brain tumor...
Systemic sclerosis (SSc) is characterised by aberrant hedgehog signalling in fibrotic tissues. The hedgehog acyltransferase (HHAT) skinny hedgehog catalyses the attachment of palmitate onto sonic hedg...
Sonic hedgehog (Shh) signaling, including Gli1, is critical to treatment resistance. For optimizing cervical cancer treatment, the pathological prognostic factors determine whether to admi...
The purpose of this study is to demonstrate that orally administered itraconazole, a commonly used antifungal medication, can inhibit Hedgehog pathway signaling in patients with esophageal...
This randomized, controlled clinical trial, triple-blind, split-mouth type was conducted aiming to assess the absolute risk of sensitivity with and without sonic activation of a desensitiz...
Non-small cell lung cancer (NSCLC) accounts for more than two-thirds of lung cancer, which is the leading cause of cancer deaths in Taiwan. The overall prognosis of NSCLC is poor with low ...
A study of the complex genetics of brain development will be undertaken with an emphasis on those genes that cause the most common structural brain anomaly in humans called holoprosencepha...
A frizzled-like, G-protein-coupled receptor that associates with PATCHED RECEPTORS to transduce signals from HEDGEHOG PROTEINS and initiate hedgehog signaling to ZINC FINGER PROTEIN GLI1. It may normally inhibit signaling in the absence of SONIC HEDGEHOG PROTEIN binding to PATCHED RECEPTOR-1.
A transcriptional activator and oncogene protein that contains two CYS2-HIS2 ZINC FINGERS. Two isoforms are expressed; both regulate the expression of specific genes during development of craniofacial features, digits, the CENTRAL NERVOUS SYSTEM; and the GASTROINTESTINAL TRACT. They also regulate SONIC HEDGEHOG PROTEIN signaling and cell proliferation.
A patched receptor for several HEDGEHOG PROTEINS that associates with the SMOOTHENED RECEPTOR to modulate hedgehog signaling. It is also a TUMOR SUPPRESSOR PROTEIN; mutations in the patched-1 gene are associated with BASAL CELL NEVUS SYNDROME; SQUAMOUS CELL CARCNIOMA of the ESOPHAGUS; trichoepitheliomas, and CARCINOMA, TRANSITIONAL CELL of the URINARY BLADDER.
A specific complex of WNT SIGNALING PATHWAY proteins that mediates the phosphorylation-dependent destruction of cytosolic BETA-CATENIN. The complex is disrupted by cell surface binding of WNT PROTEINS, which allows beta-catenin levels to rise to the point where they migrate to the CELL NUCLEUS and activate transcription.
A family of intercellular signaling proteins that play and important role in regulating the development of many TISSUES and organs. Their name derives from the observation of a hedgehog-like appearance in DROSOPHILA embryos with genetic mutations that block their action.