Artemin Is a Vascular-Derived Neurotropic Factor for Developing Sympathetic Neurons

Honma, Yutaka; Araki, Toshiyuki; Gianino, Scott M.; Bruce, Allen T.; Heuckeroth, Robert O.; Johnson, Eugene M.; Milbrandt, Jeffrey

doi:10.1016/s0896-6273(02)00774-2

Cited by 287 publications

(278 citation statements)

References 62 publications

(10 reference statements)

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“…In fact, sympathetic nerves follow arteries into the periphery 68 and their development is stunted when endothelial development is blocked. 69 Massive acidosis offers an explanation for or may contribute to many of the observed pathologies. The lung seems to be affected in early stages of disease in SMA animals.…”

Section: Discussionmentioning

confidence: 99%

Severe SMA mice show organ impairment that cannot be rescued by therapy with the HDACi JNJ-26481585

et al. 2012

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Spinal muscular atrophy (SMA) is the leading genetic cause of early childhood death worldwide and no therapy is available today. Many drugs, especially histone deacetylase inhibitors (HDACi), increase SMN levels. As all HDACi tested so far only mildly ameliorate the SMA phenotype or are unsuitable for use in humans, there is still need to identify more potent drugs. Here, we assessed the therapeutic power of the pan-HDACi JNJ-26481585 for SMA, which is currently used in various clinical cancer trials. When administered for 64 h at 100 nM, JNJ-26481585 upregulated SMN levels in SMA fibroblast cell lines, including those from non-responders to valproic acid. Oral treatment of Taiwanese SMA mice and control littermates starting at P0 showed no overt extension of lifespan, despite mild improvements in motor abilities and weight progression. Many treated and untreated animals showed a very rapid decline or unexpected sudden death. We performed exploratory autopsy and histological assessment at different disease stages and found consistent abnormalities in the intestine, heart and lung and skeletal muscle vasculature of SMA animals, which were not prevented by JNJ-26481585 treatment. Interestingly, some of these features may be only indirectly caused by a-motoneuron function loss but may be major life-limiting factors in the course of disease. A better understanding of -primary or secondary -non-neuromuscular organ involvement in SMA patients may improve standard of care and may lead to reassessment of how to investigate SMA patients clinically.

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Section: Discussionmentioning

confidence: 99%

Severe SMA mice show organ impairment that cannot be rescued by therapy with the HDACi JNJ-26481585

et al. 2012

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“…The autonomic nerve element showed a strong tendency to accompany arteries, especially the branches of the CT and SMA, possibly because of vascular-derived neurotrophic factors (Honma et al, 2002). Actually, Isogai et al (2010) recently demonstrated, using rat embryos, the tyrosine hydroxylase-positive paraaortic ridge contributes much to the development of retroperitoneal visceral arteries.…”

Section: Discussionmentioning

confidence: 99%

Fetal Topographical Anatomy of the Upper Abdominal Lymphatics: Its Specific Features in Comparison With Other Abdominopelvic Regions

Kim¹,

Han²,

Jin³

et al. 2011

The Anatomical Record

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Using semiserial sections from 19 human fetuses of 8-30 weeks gestation, we examined the topohistology of the upper abdominal lymphatics and compared it with that of the lower abdominal and pelvic lymphatics. The upper abdominal lymphatics were characterized by an intimate relationship with the peritoneal lining, a common mesentery for the celiac trunk and superior mesenteric artery (SMA). Lymphatic connections from the upper abdominal viscera to the paraaortic and paracaval areas followed two routes: (1) from the intestinal mesentery, along the peritoneum on the left aspect of the proximal SMA, via the chain of lymph follicles (LFs) lying along the retropancreatic fusion fascia, to drain into the LFs around the left renal vein; (2) from sites along the peritoneum on the posterior wall of the omental bursa, via the root of the hepatoduodenal ligament, to drain into LFs around the vena cava. The development of these two posterior drainage routes seemed to be promoted by the peritoneum or a peritoneal remnant (i.e., fusion fascia) attaching to the great vessels, and inhibited or impeded by the developing nerves and diaphragm. No paraaortic, paracaval, or pelvic LFs lay along the peritoneum. The pelvic Abbreviations used: AO ¼ aorta; CHA ¼ common hepatic artery; crus ¼ crus of the diaphragm; CT ¼ celiac trunk; D1, D2, D3, and D4 ¼ the first, second, third, or fourth portion of the duodenum, respectively; GL ¼ autonomic ganglion; IVC ¼ inferior vena cava; JA ¼ upper jejunal artery; LGA ¼ left gastric artery; LF ¼ lymph follicle; LRV ¼ left renal vein; panc ¼ pancreas; PC ¼ peritoneal cavity; PV ¼ portal vein; RGEA ¼ right gastroepiploic artery; SMA ¼ superior mesenteric artery; SMV ¼ superior mesenteric vein; SPA ¼ splenic artery; t.colon ¼ transverse colon; TD ¼ thoracic duct; VP ¼ Vater's papilla.

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“…Thus, BDNF and NT-3 -sensitive trigeminal neurons extend toward their target fields in the periphery and are sensitive to both TrkB and TrkC deletion (O'Connor and Tessier-Lavigne 1999). GDNF family members may have a role in early phases of extension of sympathetic ganglion cell axons, but whether this generalizes to other PNS neurons is not yet certain (Honma et al 2002;Kuruvilla et al 2004;Luo et al 2007). Later stages of axon growth along vessels appear to require NT-3 acting locally (Kuruvilla et al 2004).…”

Section: Control Of Axon Elongation By Neuronal Growth Factorsmentioning

confidence: 99%

Initiating and Growing an Axon

Polleux¹,

Snider²

2010

Cold Spring Harbor Perspectives in Biology

160

127

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The ability of neurons to form a single axon and multiple dendrites underlies the directional flow of information transfer in the central nervous system. Dendrites and axons are molecularly and functionally distinct domains. Dendrites integrate synaptic inputs, triggering the generation of action potentials at the level of the soma. Action potentials then propagate along the axon, which makes presynaptic contacts onto target cells. This article reviews what is known about the cellular and molecular mechanisms underlying the ability of neurons to initiate and extend a single axon during development. Remarkably, neurons can polarize to form a single axon, multiple dendrites, and later establish functional synaptic contacts in reductionist in vitro conditions. This approach became, and remains, the dominant model to study axon initiation and growth and has yielded the identification of many molecules that regulate axon formation in vitro (Dotti et al. 1988). At present, only a few of the genes identified using in vitro approaches have been shown to be required for axon initiation and outgrowth in vivo. In vitro, axon initiation and elongation are largely intrinsic properties of neurons that are established in the absence of relevant extracellular cues. However, the importance of extracellular cues to axon initiation and outgrowth in vivo is emerging as a major theme in neural development (Barnes and Polleux 2009). In this article, we focus our attention on the extracellular cues and signaling pathways required in vivo for axon initiation and axon extension.

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Artemin Is a Vascular-Derived Neurotropic Factor for Developing Sympathetic Neurons

Cited by 287 publications

References 62 publications

Severe SMA mice show organ impairment that cannot be rescued by therapy with the HDACi JNJ-26481585

Severe SMA mice show organ impairment that cannot be rescued by therapy with the HDACi JNJ-26481585

Fetal Topographical Anatomy of the Upper Abdominal Lymphatics: Its Specific Features in Comparison With Other Abdominopelvic Regions

Initiating and Growing an Axon

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