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Direct intercellular communication via gap junctions has an important role in the development of the nervous system, ranging from cell migration and neuronal differentiation to the formation of neuronal activity patterns. This study characterized and compared the specific spatio-temporal expression patterns of connexins (Cxs) 37, 43 and 45 during early human developmental stages (since the 5th until the 10th developmental week) in the spinal cord (SC) and dorsal root ganglia (DRG) using double immunofluorescence and transmission electron microscopy. We found the expression of all three investigated Cxs during early human development in all the areas of interest, in the SC, DRG, developing paravertebral ganglia of the sympathetic trunk, notochord and all three meningeal layers, with predominant expression of Cx37. Comparing the expression of different Cxs between distinct developmental periods, we did not find significant differences. Specific spatio-temporal pattern of Cxs expression might reflect their relevance in the development of all areas of interest via cellular interconnectivity and synchronization during the late embryonic and early fetal period of human development.

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Many clinical and experimental studies have revealed VEGF as an important factor in the pathophysiology of renal damage during diabetes mellitus (DM). Anti-VEGF therapy is in clinical use for treatment of DM and other diabetes-related (and unrelated) diseases. Nevertheless, little is known about the metabolism of VEGF in the kidneys. In order to determine the ultrastructural localization of VEGF in the kidney, we study the distribution of VEGF in the kidney of rats by using immunogold immunohistochemistry. Our light-microscopic data showed remarkable re-distribution of VEGF in proximal tubular cells (PTCs) during prolonged hyperglycemia, a DM type 2 model (DM2), which was confirmed by transmission electron microscopy (TEM) findings. TEM findings revealed an initial presence of VEGF in the vesicular transport apparatus of PTCs in healthy rats and its gradual translocation to the apical membrane of PTCs after renal damage caused by high sucrose treatment. The presented data add to our understanding of kidney VEGF trafficking, providing novel insight into the renal metabolism and pharmacodynamics of the cytokine. This could have a high impact on the use of VEGF and anti-VEGF therapy in different renal diseases.