Last update 01 Nov 2024

VEGF-A x Tubulin

Last update 01 Nov 2024

Basic Info

Related Targets

VEGF-ATubulin

Drugs associated with VEGF-A x Tubulin

AB-160

Target

Tubulin x VEGF-A

Mechanism

Tubulin inhibitors [+1]

Active Org.-

Originator Org.

Mayo Clinic

Active Indication-

Inactive Indication

Genital Diseases, Female [+1]

Drug Highest PhasePending

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

Clinical Trials associated with VEGF-A x Tubulin

NCT05601323 / RecruitingNot Applicable

A Randomized Controlled Study of Suizenji in Patients With Unresectable Pancreatic Cancer

The purpose of this study is to evaluate the safety and efficacy of standard chemotherapy with or without a novel High Intensity Focused Ultrasound system (Code: Suizenji) in patients with unresectable pancreatic cancer who are refractory or intolerant to first-line chemotherapy.

Start Date31 Jan 2023

Sponsor / Collaborator

Sonire Therapeutics IncStartup

100 Clinical Results associated with VEGF-A x Tubulin

100 Translational Medicine associated with VEGF-A x Tubulin

0 Patents (Medical) associated with VEGF-A x Tubulin

Literatures (Medical) associated with VEGF-A x Tubulin

29 May 2024·Bioscience Reports

sFlt-1 impairs neurite growth and neuronal differentiation in SH-SY5Y cells and human neurons

Article

Author: Karlsson, Linnea ; Barron, Aaron ; Tuulari, Jetro J ; McCarthy, Cathal M ; Karlsson, Hasse ; Barrett, Lauren ; O'Keeffe, Gerard W

AbstractPre-eclampsia (PE) is a hypertensive disorder of pregnancy which is associated with increased risk of neurodevelopmental disorders in exposed offspring. The pathophysiological mechanisms mediating this relationship are currently unknown, and one potential candidate is the anti-angiogenic factor soluble Fms-like tyrosine kinase 1 (sFlt-1), which is highly elevated in PE. While sFlt-1 can impair angiogenesis via inhibition of VEGFA signalling, it is unclear whether it can directly affect neuronal development independently of its effects on the vasculature. To test this hypothesis, the current study differentiated the human neural progenitor cell (NPC) line ReNcell® VM into a mixed culture of mature neurons and glia, and exposed them to sFlt-1 during development. Outcomes measured were neurite growth, cytotoxicity, mRNA expression of nestin, MBP, GFAP, and βIII-tubulin, and neurosphere differentiation. sFlt-1 induced a significant reduction in neurite growth and this effect was timing- and dose-dependent up to 100 ng/ml, with no effect on cytotoxicity. sFlt-1 (100 ng/ml) also reduced βIII-tubulin mRNA and neuronal differentiation of neurospheres. Undifferentiated NPCs and mature neurons/glia expressed VEGFA and VEGFR-2, required for endogenous autocrine and paracrine VEGFA signalling, while sFlt-1 treatment prevented the neurogenic effects of exogenous VEGFA. Overall, these data provide the first experimental evidence for a direct effect of sFlt-1 on neurite growth and neuronal differentiation in human neurons through inhibition of VEGFA signalling, clarifying our understanding of the potential role of sFlt-1 as a mechanism by which PE can affect neuronal development.

01 Apr 2023·Heliyon

VEGFA-modified DPSCs combined with LC-YE-PLGA NGCs promote facial nerve injury repair in rats

Article

Author: Lin, Song ; Xi, Hualei ; Wang, Xiumei ; Piao, Guiyan ; Xu, Wanqiu ; Xu, Xiaohang ; Xue, Bing ; Yao, Lihong ; Cao, Xiaofang

ObjectiveThe aim of this research was to investigate the effect of vascular endothelial growth factor A (VEGFA)-overexpressing rat dental pulp stem cells (rDPSCs) combined with laminin-coated and yarn-encapsulated poly(_l-lactide-co-glycolide) (PLGA) nerve guidance conduit (LC-YE-PLGA NGC) in repairing 10 mm facial nerve injury in rats.Study DesignrDPSCs isolated from rat mandibular central incisor were cultured and identified in vitro and further transfected with the lentiviral vectors (Lv-VEGFA). To investigate the role and mechanisms of VEGFA in neurogenic differentiation in vitro, semaxanib (SU5416), Cell Counting Kit-8 (CCK-8), real-time quantitative polymerase chain reaction (qPCR) and Western blotting were performed. Ten-millimeter facial nerve defect models in rats were established and bridged by LC-YE-PLGA NGCs. The repair effects were detected by transmission electron microscopy (TEM), compound muscle action potential (CMAP), immunohistochemistry and immunofluorescence.ResultsExtracted cells exhibited spindle-shaped morphology, presented typical markers (CD44⁺CD90⁺CD34^-CD45^-), and presented multidirectional differentiation potential. The DPSCs with VEGFA overexpression were constructed successfully. VEGFA enhanced the proliferation and neural differentiation ability of rDPSCs, and the expression of neuron-specific enolase (NSE) and βIII-tubulin was increased. However, these trends were reversed with the addition of SU5416. This suggests that VEGFA mediates the above effects mainly through vascular endothelial growth factor receptor 2 (VEGFR2) binding. The LC-YE-NGC basically meet the requirements of facial nerve repair. For the in vivo experiment, the CMAP latency period was shorter in DPSCS-VEGFA-NGC group in comparison with other experimental groups, while the amplitude was increased. Such functional recovery correlated well with an increase in histological improvement. Further study suggested that VEGFA-modified DPSCs could increase the myelin number, thickness and axon diameter of facial nerve. NSE, βIII-tubulin and S100 fluorescence intensity and immunohistochemical staining intensity were significantly enhanced.ConclusionVEGFA-modified rDPSCs combined with LC-YE-PLGA NGCs have certain advantages in the growth and functional recovery of facial nerves in rats.

01 Jan 2023·Frontiers in genetics

Overview of distinct N6-Methyladenosine profiles of messenger RNA in osteoarthritis.

Article

Author: Xu, Jianzhong ; Li, Yu ; Lu, Shitao ; Yu, Yang

Although N6-methyladenosine (m6A) modification is closely associated with the pathogenesis of osteoarthritis (OA), the mRNA profile of m6A modification in OA remains unknown. Therefore, our study aimed to identify common m6A features and novel m6A-related therapeutic targets in OA. In the present study, we identified 3962 differentially methylated genes (DMGs) and 2048 differentially expressed genes (DEGs) using methylated RNA immunoprecipitation next-generation sequencing (MeRIP-seq) and RNA-sequencing. A co-expression analysis of DMGs and DEGs showed that the expression of 805 genes was significantly affected by m6A methylation. Specifically, we obtained 28 hypermethylated and upregulated genes, 657 hypermethylated and downregulated genes, 102 hypomethylated and upregulated genes, and 18 hypomethylated and downregulated genes. The differential gene expression analysis based on GSE114007 revealed 2770 DEGs. The Weighted Gene Co-expression Network Analysis (WGCNA) based on GSE114007 identified 134 OA-related genes. By taking the intersection of these results, ten novel aberrantly expressed, m6A-modified and OA-related key genes were identified, including SKP2, SULF1, TNC, ZFP36, CEBPB, BHLHE41, SOX9, VEGFA, MKNK2 and TUBB4B. The present study may provide valuable insight into identifying m6A-related pharmacological targets in OA.

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