CTNNB x WNT3A

Last update 23 Jan 2025

Basic Info

Related Targets

CTNNBWNT3A

Drugs associated with CTNNB x WNT3A

ASCs-exos

Target

CTNNB x WNT3A

Mechanism

CTNNB agonists [+1]

Active Org.

Zhongnan hospital of wuhan university

Originator Org.

Zhongnan hospital of wuhan university

Active Indication

Diabetes Complications

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with CTNNB x WNT3A

100 Translational Medicine associated with CTNNB x WNT3A

0 Patents (Medical) associated with CTNNB x WNT3A

1,741

Literatures (Medical) associated with CTNNB x WNT3A

01 Mar 2025·Journal of Stroke and Cerebrovascular Diseases

Hirudin promotes cerebral angiogenesis and exerts neuroprotective effects in MCAO/R rats by activating the Wnt/β-catenin pathway

Article

Author: Li, Shuangyang ; Yang, Xinyue ; Jiang, Yu ; He, Linrong ; He, Xinying ; Zhao, Xiaoying ; Liu, Ping ; Lei, Ruolan ; Zhang, Dechou

OBJECTIVEHirudin has shown potential in promoting angiogenesis and providing neuroprotection in ischemic stroke; however, its therapeutic role in promoting cerebrovascular angiogenesis remains unclear. In this study, we aimed to investigate whether hirudin exerts neuroprotective effects by promoting angiogenesis through the regulation of the Wnt/β-catenin signaling pathway.METHODSAn in vitro model of glucose and oxygen deprivation/reperfusion (OGD/R) was established using rat brain microvascular endothelial cells (BMECs). The effects of hirudin on OGD/R cell viability were assessed using the cell counting kit-8 (CCK-8) assay. The angiogenic potential of hirudin was evaluated using Transwell and tube formation assays. In vivo, a middle cerebral artery occlusion/reperfusion (MCAO/R) model was created in rats. The neuroprotective effects of hirudin were assessed using the modified neurological severity score (mNSS), Hematoxylin and eosin (H&E) staining, 2,3,5-Triphenyltetrazolium chloride (TTC) staining, and immunofluorescence staining. Dickkopf-1 (DKK1), a specific inhibitor of this pathway, was introduced in order to investigate the role of the Wnt/β-catenin pathway. The effects of hirudin on the Wnt/β-catenin pathway were examined through immunohistochemistry, western blotting, and reverse transcription quantitative polymerase chain reaction (RT-qPCR).RESULTSHirudin significantly improved BMEC survival and enhanced both cell migration and tube formation in the OGD/R model. In the MCAO/R model, hirudin reduced the mNSS score, alleviated pathological damage, decreased infarction volume, and increased the expression of key angiogenic factors, including CD34, vascular endothelial growth factor (VEGF), and angiopoietin-2 (Ang-2). In addition, hirudin activated the Wnt/β-catenin pathway, leading to elevated levels of Wnt3a and β-catenin.CONCLUSIONHirudin has substantial neuroprotective effects associated with the promotion of angiogenesis in the ischemic penumbra. This mechanism is mediated by the regulation of the Wnt/β-catenin pathway.

12 Jan 2025·Neuro-Oncology

Activation of Wnt/β-catenin signaling is critical for the tumorigenesis of choroid plexus

Article

Author: Schwerk, Christian ; Salasova, Alena ; Ishikawa, Hiroshi ; Salio, Chiara ; Hasselblatt, Martin ; Koch, Philipp ; Guida, Catello ; Bernatík, Ondřej ; Angel, Peter ; De Jaime-Soguero, Anchel ; Ivanova, Ekaterina L ; Thomas, Christian ; Sassoè-Pognetto, Marco ; Trapp, Marleen ; Čajánek, Lukáš ; Acebrón, Sergio P ; Jabali, Ammar ; Schroten, Horst ; Ho, Kim Hoa ; Patrizi, Annarita ; Horschitz, Sandra

AbstractBackgroundThe choroid plexus (ChP) is the secretory epithelial structure located in the brain ventricles. Choroid plexus tumors (CPTs) are rare neoplasms predominantly occurring in young patients with intensified malignancy in children. CPT treatment is hindered by insufficient knowledge of tumor pathology and the limited availability of valid models.MethodsGenomic and transcriptomic data from CPT patients were analyzed to identify the putative pathological pathway. Cellular and molecular techniques were employed to validate bioinformatic results in CPT patient samples. Pharmacologic inhibition of Wnt/β-catenin signaling was assessed in CPT cells. Cell-based assays of ChP cell lines were performed following CRISPR-Cas9-derived knockout and overexpression of Wnt/β-catenin pathway genes. A 3D CPT model was generated through CRISPR-Cas9-derived knockout of APC.ResultsWe discovered that Wnt/β-catenin signaling is activated in human CPTs, likely as a consequence of large-scale chromosomal instability events of the CPT genomes. We demonstrated that CPT-derived cells depend on autocrine Wnt/β-catenin signaling for survival. Constitutive Wnt/β-catenin pathway activation, either through knockout of the negative regulator APC or overexpression of the ligand WNT3A, induced tumorigenic properties in ChP 2D in vitro models. Increased activation of the Wnt/β-catenin pathway in ChP organoids, through treatment with a potent GSK3β inhibitor, reduced the differentiation of mature ChP epithelial cells. Remarkably, the depletion of APC was sufficient to induce the oncogenic transformation of ChP organoids.ConclusionsOur research identifies Wnt/β-catenin signaling as a critical driver of CPT tumorigenesis and provides the first 3D in vitro model for future pathological and therapeutic studies of CPT.

01 Jan 2025·International Immunopharmacology

An injectable hydrogel loaded with Icariin attenuates cartilage damage in rabbit knee osteoarthritis via Wnt/β-catenin signaling pathway

Article

Author: Song, Ling ; Zheng, Hanxiao ; Qu, Limin ; Xie, Xianmin ; Xie, Qiuen ; Yang, Lei

Knee osteoarthritis (KOA) is a chronic disease characterized by joint wear and cartilage degeneration. Current clinical treatments are based on symptomatic relief and are not effective in regenerating cartilage, and inflammation-induced cartilage damage accelerates the progression of osteoarthritis, making the protection of articular cartilage important for controlling the development of knee osteoarthritis. In this study, a biodegradable hydrogel (HA-Ca-Alg@Ica) loaded with Icariin (Ica) was prepared by in situ cross-linking of hyaluronic acid-calcium complex (HA-Ca) and sodium alginate (Alg-Na) for local sustained delivery of Ica. The hydrogel promoted chondrocyte proliferation and inhibited the degradation of cartilage matrix by regulating key factors (Wnt3a, β-catenin and GSK-3β) in the Wnt/β-catenin signaling pathway. In addition, the hydrogel reduced the expression of inflammatory factors, including IL-1β, IL-6, TNF-α, COX-2, and MMP13, leading to a reduction in inflammation and pain relief. In summary, this hydrogel containing Icariin has shown significant effects in reducing chondrocyte degradation and promoting chondrocyte proliferation, which can play a role in delaying osteoarthritis by protecting chondrocytes. These findings offer innovative prospects for the therapeutic management of knee osteoarthritis.

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