Carotid artery transplantation of brain endothelial cells enhances neuroprotection and neurorepair in ischaemic stroke rats.

Brain microvascular endothelial cells (BMECs), an important component of the neurovascular unit, can promote angiogenesis and synaptic formation in ischaemic mice after brain parenchyma transplantation. Since the therapeutic efficacy of cell-based therapies depends on the extent of transplanted cell residence in the target tissue and cell migration ability, the delivery route has become a hot research topic. In this study, we investigated the effects of carotid artery transplantation of BMECs on neuronal injury, neurorepair, and neurological dysfunction in rats after cerebral ischaemic attack.

BMECs Ameliorate High Glucose-Induced Morphological Aberrations and Synaptic Dysfunction via VEGF-Mediated Modulation of Glucose Uptake in Cortical Neurons.

It has been demonstrated that diabetes cause neurite degeneration in the brain and cognitive impairment and neurovascular interactions are crucial for maintaining brain function. However, the role of vascular endothelial cells in neurite outgrowth and synaptic formation in diabetic brain is still unclear. Therefore, present study investigated effects of brain microvascular endothelial cells (BMECs) on high glucose (HG)-induced neuritic dystrophy using a coculture model of BMECs with neurons.

Neuroprotective Effect of Angiopoietin2 Is Associated with Angiogenesis in Mouse Brain Following Ischemic Stroke.

Angiogenic factors play an important role in protecting, repairing, and reconstructing vessels after ischemic stroke. In the brains of transient focal cerebral ischemic mice, we observed a reduction in infarct volume after the administration of Angiopoietin 2 (Angpt2), but whether this process is promoted by Angpt2-induced angiogenesis has not been fully elaborated. Therefore, this study explored the angiogenic activities, in reference to CD34 which is a marker of activated ECs and blood vessels, of cultured ECs in vitro and in ischemic damaged cerebral area in mice following Angpt2 administration.

[Replication of a model of injury to human renal proximal tubular cells induced by hypoxia/reoxygenation].

Objective: To replicate a new model of injury to human renal proximal tubular cells (HK-2) induced by hypoxia/reoxygenation.

Methods: Human renal proximal tubular cell line HK-2 cell was used as the target cell. Tubular cells were divided into six groups: 4 hours of hypoxia, 12 hours of hypoxia, 24 hours of hypoxia, and 24 hours of hypoxia followed by reoxygenation 4, 12 or 24 hours later groups.

[The relationship between TNF-alpha and the injury of renal tubular cells caused by anoxia/reoxygenation].

Aim: To investigate the relationship between TNF-alpha and renal tubular cell injury caused by anoxia/reoxygenation.

Methods: Human renal proximal tubular cell line HK-2 was used as model. Anoxia/reoxygenation were produced by covering/de-covering the cell culture with liquid paraffin wax.