Expression of nerve growth factor carried by pseudotyped lentivirus improves neuron survival and cognitive functional recovery of post‐ischemia in rats

Abstract

This study demonstrates a potential β-NGF gene therapy by utilization of pseudolentivirus in ischemia and indicates future applications of NGF gene treatment in ischemic patients.

Determination of a Tumor-Promoting Microenvironment in Recurrent Medulloblastoma: A Multi-Omics Study of Cerebrospinal Fluid

“…In contrast, the detectable potential pro-inflammatory proteins MX2, SPP1 and PIBF1 were found to be down-regulated ( Figure 3 B, red), whereas the rather anti-inflammatory proteins ANXA1, LTBP1, SERPINA4 and TXN were found to be up-regulated in MB samples ( Figure 3 B, orange). Remarkable was the detection of a distinct molecular signature indicative for hypoxia, represented by the up-regulated proteins ADAMTS1 [ 38 ], GAP43 [ 39 ] and GPR37 [ 40 ] ( Figure 3 B, blue). The detailed classification of proteins is documented in Table S6 .…”

Kir4.1 channels in NG2-glia play a role in development, potassium signaling, and ischemia-related myelin loss

“…As illustrated in Fig. 2a 29 , the MCA of mouse was occluded for 30 min and then reperfused for 24 h before carrying out electrophysiological and immunohistochemical examinations. Hippocampal NG2-glia in ipsilateral SR showed depolarized RMPs and increased membrane resistances, as compared with that in the contralateral region (RMPs: contralateral, −84.5 ± 0.5 mV, n  = 43 vs. ipsilateral, −79.7 ± 1.1 mV, n  = 42, P  < 0.0001, two-tailed unpaired t -test; membrane resistances: contralateral, 78 ± 4.2 MΩ, n  = 43 vs. ipsilateral, 269.1 ± 29.4 MΩ, n  = 42, P  < 0.0001, two-tailed unpaired t -test, Fig.…”

A Nerve Growth Factor Dipeptide Mimetic Stimulates Neurogenesis and Synaptogenesis in the Hippocampus and Striatum of Adult Rats with Focal Cerebral Ischemia

“…3). During middle cerebral artery occlusion, NGF is known to stimulate the proliferative activity and increase the survival of neuroblasts in the subventricular zone and striatum of rats [6, 10]. In the same brain ischemia model, by using the BrdU proliferation marker, intranasal administration of NGF was shown to increase the survival rate of progenitor cells in the striatum about 1.5-fold after 4 weeks [6].…”

“…In the same brain ischemia model, by using the BrdU proliferation marker, intranasal administration of NGF was shown to increase the survival rate of progenitor cells in the striatum about 1.5-fold after 4 weeks [6]. By using another proliferation marker, Ki67, NGF expressed in the rat brain using a lentiviral vector was found [10] to stimulate neurogenesis in the injured striatum, increasing the number of neuroblasts about 2-fold compared to that in untreated animals 3 weeks after a simulated stroke.…”

“…The efficacy of intracerebral and intranasal administration of NGF has been proven in various cerebral ischemia models in rodents. It is extremely important that the neurotrophin remains active upon delayed administration – 24 h after a simulated stroke [6, 10]. Applications of NGF in clinical practice are limited not only due to its unsatisfactory pharmacokinetic properties, but also due to serious pleiotropic side effects, such as hyperalgesia, catastrophic weight loss, excessive neuritogenesis, and angiogenesis [11].…”