Semaphorin-Plexin Signaling Guides Patterning of the Developing Vasculature

Torres-Vázquez, Jesús; Gitler, Aaron D.; Fraser, Sherri D.; Berk, Jason D.; Pham, Van N.; Fishman, Mark C.; Childs, Sarah J.; Epstein, Jonathan A.; Weinstein, Brant M.

doi:10.1016/j.devcel.2004.06.008

Cited by 352 publications

(345 citation statements)

References 31 publications

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“…Interestingly, the expression of plexin-D1 is dynamically regulated and increased in tip cells, which extend numerous filopodia and respond to attractive and repulsive guidance cues at the leading edge of the new branching blood vessels [50]. Sema3E controls vascular patterning during development by inhibiting the expansion of intersomitic vessels into the somites [15,51], and causes endothelial-tip cell filopodial retraction in growing blood vessels [52]. These data suggest that Sema3E is a potent chemorepellent for plexin-D1-expressing endothelial cells.…”

Section: Sema3ementioning

confidence: 99%

Semaphorin signaling in angiogenesis, lymphangiogenesis and cancer

2011

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Angiogenesis, the formation of new blood vessels from preexisting vasculature, is essential for many physiological processes, and aberrant angiogenesis contributes to some of the most prevalent human diseases, including cancer. Angiogenesis is controlled by delicate balance between pro-and anti-angiogenic signals. While pro-angiogenic signaling has been extensively investigated, how developmentally regulated, naturally occurring anti-angiogenic molecules prevent the excessive growth of vascular and lymphatic vessels is still poorly understood. In this review, we summarize the current knowledge on how semaphorins and their receptors, plexins and neuropilins, control normal and pathological angiogenesis, with an emphasis on semaphorin-regulated anti-angiogenic signaling circuitries in vascular and lymphatic endothelial cells. This emerging body of information may afford the opportunity to develop novel anti-angiogenic therapeutic strategies.

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Section: Sema3ementioning

confidence: 99%

Semaphorin signaling in angiogenesis, lymphangiogenesis and cancer

2011

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“…On dissociated neurons, Sema3E has either a repulsive action or a growth promoting one that is dosedependent. 31,32 As mentioned before, this protein and its receptor plexin-D1 were recently shown to control angiogenesis during development 23,33,34 and both could exert a similar function in tumors.…”

Section: Classmentioning

confidence: 85%

The brain within the tumor: new roles for axon guidance molecules in cancers

2005

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Slits, semaphorins and netrins are three families of proteins that can attract or repel growing axons and migrating neurons in the developing nervous system of vertebrates and invertebrates. Recent studies have shown that they are widely expressed outside the nervous system and that they may play important roles in cancers. Several of the genes encoding these proteins are localized on chromosomal region associated with frequent loss-of-heterozygosity in tumors and cancer cell lines and there is also significant hypermethylation of their promoter suggesting that they may act as tumor suppressors. In addition, proteins in all these families and their receptors appear to control the vascularization of the tumors. Last, many axon guidance molecules also regulate cell migration and apoptosis in normal and tumorigenic tissues. Overall, this suggests that molecules that could mimick or block the activity of axon guidance molecules may be used as therapeutic agents for the treatment of malignancy.

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“…47). In particular, Sema3E and PlexinD1 have been reported to play an active role in vascular system development 29,48,49 , but they also control the migration of mouse thymocytes 50 and tumour cells 51 . Indeed, mice lacking Plxnd1 showed impaired thymocyte trafficking 50 and a poorly developed vascular system 29 .…”

Section: Discussionmentioning

confidence: 99%

Sema3E/PlexinD1 regulates the migration of hem-derived Cajal-Retzius cells in developing cerebral cortex

et al. 2014

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During the development of the cerebral cortex, Cajal-Retzius (CR) cells settle in the preplate and coordinate the precise growth of the neocortex. Indeed, CR cells migrate tangentially from specific proliferative regions of the telencephalon (for example, the cortical hem (CH)) to populate the entire cortical surface. This is a very finely tuned process regulated by an emerging number of factors that has been sequentially revealed in recent years. However, the putative participation of one of the major families of axon guidance molecules in this process, the Semaphorins, was not explored. Here we show that Semaphorin-3E (Sema3E) is a natural negative regulator of the migration of PlexinD1-positive CR cells originating in the CH. Our results also indicate that Sema3E/PlexinD1 signalling controls the motogenic potential of CR cells in vitro and in vivo. Indeed, absence of Sema3E/PlexinD1 signalling increased the migratory properties of CR cells. This modulation implies negative effects on CXCL12/CXCR4 signalling and increased ADF/Cofilin activity.

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Semaphorin-Plexin Signaling Guides Patterning of the Developing Vasculature

Cited by 352 publications

References 31 publications

Semaphorin signaling in angiogenesis, lymphangiogenesis and cancer

Semaphorin signaling in angiogenesis, lymphangiogenesis and cancer

The brain within the tumor: new roles for axon guidance molecules in cancers

Sema3E/PlexinD1 regulates the migration of hem-derived Cajal-Retzius cells in developing cerebral cortex

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