China
Africa
Explore chapters and articles related to this topic
Overview of Angiogenesis: Molecular and Structural Features
Published in Robert J. Gropler, David K. Glover, Albert J. Sinusas, Heinrich Taegtmeyer, Cardiovascular Molecular Imaging, 2007
Arye Elfenbein, Michael Simons
It follows that ephrins mediate spatially-determined functions, including intercellular contact, cell adhesion and migration (38,39). Additionally, their importance in the vasculature is vastly extended by their contributions to vessel development. In particular, EphB4 has been shown to mark developing veins, while ephrin-B2 is specifically associated with the arterial system (40,41). These findings, combined with the directional duality of ephrin signals, have led to an emerging model of forward signaling in one vessel type that inhibits signaling of the other (30). In this way, arterial sprouting might be enhanced while simultaneously inhibiting the formation of veins in a particular vascular bed. The ability of ephrins to function in the guidance of these forming vessels and to facilitate the formation of arterio-venous junctions consequently represents an active field of investigation.
Nanotechnology-Mediated Strategy for the Treatment of Neuropathic Pain
Published in Cherry Bhargava, Amit Sachdeva, Nanotechnology, 2020
Pankaj Prashar, Ankita Sood, Anamika Gautam, Pardeep Kumar Sharma, Bimlesh Kumar, Indu Melkani, Sakshi Panchal, Sachin Kumar Singh, Monica Gulati, Narendra Kumar Pandey, Linu Dash, Anupriya, Varimadugu Bhanukirankumar Reddy
Eph receptor tyrosine kinases and their ligands include ephrins in many areas of growth, such as patterning of the tissue, angiogenesis, and formation of synapses. The laminae I-III and the tiny and mid-sized DRG nerves are found in many Eph and ephrin-receptor proteins. EphB receptors and ephrins amplify the neuronal behavior of the spinal cord, thus inducing sensory disturbances of NMDA-dependent pain disorders indicating a significant role of ephrin in spinal cords physiologic and pathological pain regulation. Eph B2 and Eph B1 isoforms in neurons of the spinal cord are increased in spinal nerve damage (Li-Na Yu et al. 2017). Administration of Eph B2 siRNA decreased production of Eph B2 and inhibited mechanical allodynia caused by nerve damage. Activation of the EphB1 and ephrin B2 signaling pathway may also be suspected in NP. There is a link between the production of hyperalgesia in CCI and dorsal rhizotomy (DR) models that is due to an increase in the expression of Eph B1 and EphB receptor proteins in DRG neurons and the dorsal horn. After nerve damage, NP is caused by the stimulation and transmission of EphB receptors in DRG and dorsal horn (Khangura et al. 2019). EphB-receptor antagonists’ intrathecal administration has also been shown to prevent the induction and maintenance of a mechanical allodynia and thermal hyperalgesia due to nerve injury. Also, EphB antagonists blocked hyperactivity of nociceptive small DRG neurons and dorsal horn neurons. In addition, intrathecal injection of EphB activator in non-injured animals caused thermal hypersensitivity and decreased the long-term potentiation (LTP) threshold. Therefore, the increased regulation of ephrinB1 and EphB1 receptor proteins after nerve injury will enhance the excitability and plasticity of the neurons at spinal level that contribute to NP induction. Increased EphrinB1/EphB signaling results in increased PKCμ, NMDA, MAPK, P13 K, and p-AKT phosphorylation. All of these leads to enhanced excitability of nociceptive neurons and synaptic plasticity that are basic pathways of NP induction (Lombardi 2017).
Review on the current treatment status of vein of Galen malformations and future directions in research and treatment
Published in Expert Review of Medical Devices, 2021
Panagiotis Primikiris, Georgios Hadjigeorgiou, Maria Tsamopoulou, Alessandra Biondi, Christina Iosif
In the study of Duran et al. [137], the reported EPHB4 missense mutations altered some of the amino acid residues in the tyrosine kinase domain of the vein-specific EPHB4 receptor [109,137]. Interestingly, all patients affected by EPHB4 mutations suffered from choroidal VOGM. There were also seven non-VOGM family members who carried these mutations and three of them presented a cutaneous vascular pathology (port-wine stain and capillary malformations). The above findings suggest a mechanism of incomplete penetrance and variable expressivity for EPHB4 mutations. Duran et al. also reported mutations in the CLDN14 gene (P= 6.44 × 10−7) in approximately 5% of VOGM. The CLDN14 gene encodes the tight junction protein, Claudin-14. It is also to point out that non-VOGM family members of CLDN14-mutated probands were also diagnosed with cutaneous vascular pathology. Using Ingenuity Pathway Analysis, which analyzes common shared signaling pathways, it was also identified in this study that the most commonly affected pathway by the de novo and rare transmitted mutations was the Ephrin receptor signaling pathway. .
Genetics of congenital cataract, its diagnosis and therapeutics
Published in Egyptian Journal of Basic and Applied Sciences, 2018
Luqman Khan, Nargis Shaheen, Qaisar Hanif, Shah Fahad, Muhammad Usman
The EPHA2 (ephrin receptor A2) gene encodes a transmembrane tyrosine kinase receptor (epithelial cell) which comprises an extracellular ligand-binding domain and is expressed in the human lens [32]. Inhibition of EPHA2 induces apoptosis and repeals tumorigenic development of tumour cells [33]. Actually, the downstream signalling of stimulated EPHA2 encourages the ant oxidative capability of lens epithelial cells to eliminate the overproduction of ROS [34]. It is possible that the loss of EPHA2 role could affect the structural stability of the cell, cell-to-cell crosstalk, protein folding and transcriptional activation [35]. Thus, the cytoprotective and ant apoptotic functions of EPHA2 in the lens specify the promising role of EPHA2 in evading lens opacity.