Biomedical subjects

Z G Ren

Publications and source records attributed to Z G Ren.

3 recordsLinked to original sources

PubMed2004

Pacinian corpuscle development involves multiple Trk signaling pathways.

The development of crural Pacinian corpuscles was explored in neonatal mutant mice lacking nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF), neurotrophin-3 (NT3) or neurotrophin-4 (NT4), or their cognate Trk receptors. Deficits of the corpuscles and their afferents were greatest in NT3, less in BDNF, and least in NT4 null mice. Deletion of NGF or p75(NTR) genes had little or no impact. No Pacinian corpuscles were present in NT3;BDNF and NT3;NT4 double or NT3;BDNF;NT4 triple null mice. Deficits were larger in NT3 than TrkC mutants and were comparable to deficits observed in TrkB or TrkA mutants. Afferents of all corpuscles coexpressed TrkA and TrkB receptors, and some afferents coexpressed all three Trk receptors. Our results suggest that multiple neurotrophins, in particular NT3, regulate the density of crural Pacinian corpuscles, most likely by regulating the survival of sensory neurons. In addition, NT3/TrkB and/or NT3/TrkA signaling plays a greater role than NT3/TrkC signaling in afferents to developing Pacinian corpuscles.

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PubMed2001

Autocrine regulation of norepinephrine transporter expression.

The norepinephrine transporter (NET) is a neurotransmitter scavenger and site of drug action in noradrenergic neurons. The aim of this study was to identify mechanisms that regulate NET expression during the development of quail (q) sympathetic neuroblasts, which develop from neural crest stem cells. Neurotrophin-3 (NT-3) and transforming growth factor beta1 (TGF-beta1) cause an increase of qNET mRNA levels in neural crest cells. When combined, the growth factors are additive in increasing qNET mRNA levels. Both NT-3 and TGF-beta1 are synthesized by neural crest cells. Onset of NET expression precedes the onset of neural crest stem cell emigration from the neural tube. In older embryos, qNET is expressed by several crest-derived and noncrest tissues. The data show that qNET expression in presumptive sympathetic neurons is initiated early in embryonic development by growth factors that are produced by neural crest cells themselves. Moreover, the results support our previous observations that norepinephrine transport contributes to the regulation of the differentiation of neural crest stem cells into sympathetic neurons.

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PubMedDate not supplied

Ubiquitous embryonic expression of the norepinephrine transporter.

We report that the norepinephrine transporter (NET) is expressed in avian and mouse embryos by numerous tissues that are derived from all three germ layers. In the nervous system, NET is expressed in the neuroepithelium of the brain and the spinal cord (ventral horn and floor plate), forming mesencephalic nuclei, neural crest, dorsal root ganglion, sympathetic ganglion and spinal nerve. Nonneuronal embryonic NET-expressing structures include the olfactory epithelium, the notochord, the somitic dermamyotome and mesenchymal cells in the limb bud. NET is expressed prominently in the cardiovascular system, including endothelial cells of forming blood vessels, the walls of the aorta and veins, the epicardium, myocardium and a subset of blood cells. The gut, lung buds, and in particular the kidneys, are intensely NET immunoreactive. Since neurotransmitters are known to affect proliferation, survival and differentiation of many mesenchymal cell types, NET function may be a physiologically relevant regulatory element in embryonic development. A working model is proposed for neurotransmitter transporter function in the embryo as a system for the concentration and targeted delivery of neurotransmitter.

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