Involvement of nitric oxide in the head regeneration of Hydra vulgaris

Colasanti, Marco; Mazzone, Valeria; Mancinelli, Livia; Leone, Stefano; Venturini, Giorgio

doi:10.1016/j.niox.2009.07.003

Cited by 16 publications

(11 citation statements)

References 42 publications

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“…After tail transection in zebrafish larvae, iNOS gene expression increases significantly in the regenerative site and in skin cells (Lepiller et al 2009) and the use of NOS or specific guanilate cyclase inhibitors reduces head regeneration in Hydra, whereas an NO donor has the opposite effect (Colasanti et al 2009). Fig.…”

Section: Discussionmentioning

confidence: 99%

Tail regenerative capacity and iNOS immunolocalization in Xenopus laevis tadpoles

Franchini

Bertolotti

2011

Cell Tissue Res

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The morphology and the immuno-distribution of the inducible isoform of nitric oxide synthase (iNOS) have been examined in regenerating tails from differently aged Xenopus laevis larvae. By comparing stage-50 and stage-55/56 tadpoles, various morphological aspects and immunoreactivity to anti-iNOS antibody in terms of the number and duration of positive cells have been demonstrated in the regenerating buds. Unlike in stage-50 larvae, the extent of responses to tail amputation in older larvae is more dependent on the individual tadpole and a high percentage (70%-80%) of malformed tails has been seen. The findings indicate that the decline in the efficiency of Xenopus tail regeneration is driven by differences in the inflammatory responses and in the involvement of nitric oxide. This molecule is induced and required for normal tail regeneration, whereas in excess, it is probably associated with progressive loss in the regeneration capability.

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Section: Discussionmentioning

confidence: 99%

Tail regenerative capacity and iNOS immunolocalization in Xenopus laevis tadpoles

Franchini

Bertolotti

2011

Cell Tissue Res

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“…Injury can also activate the transcription of the enzyme nitric oxide synthase (NOS), resulting in an elevation of nitric oxide (NO) at the wound site and the consequent activation of cGMP signaling. The use of the NO donor NOC-18 or of NOS inhibitors (L-NAME) has shown that pathways activated by NO can promote proliferation via the release of cytokines or growth factors (Buono et al, 2012;Colasanti, Mazzone, Mancinelli, Leone, & Venturini, 2009;Filippin et al, 2011;Ronco FIGURE 2 Signaling pathways for regulation of injury-induced hyper-proliferation (IIHP) in distantly related animal species. Schematics show the known molecular regulators of IIHP in three distantly related model systems (mouse, planarians, and Hydra, which diverged from their last common ancestor~650 million years ago).…”

Section: Small Diffusible Mitogenic Moleculesmentioning

confidence: 99%

“…HGF, hepatocyte growth factor; HGF-A, HGH-activator; HGFR, HGF receptor; CREB, cAMP responsive element binding protein; mTORC1, mechanistic target of rapamycin complex 1; CBP, CREB binding protein; SMG-1, suppressor with morphogenetic effect on genitalia; Akt, RAC-alpha serine/threonine-protein kinase; RSK, ribosomal S6 kinase; MAPK, mitogen-activated protein kinase; NO, nitric oxide; Msx, muscle segment homeobox; h/dpa, hours/days post-amputation Spallotta et al, 2013;Ten Broek, Grefte, & Von Den Hoff, 2010). This mitogenic role for NO has been demonstrated in distantly related species ranging from mammals to cnidarians, which diverged~650 million years ago (Colasanti et al, 2009;Filippin et al, 2011;Figures 2 and 4).…”

Section: Small Diffusible Mitogenic Moleculesmentioning

confidence: 99%

Wound‐induced cell proliferation during animal regeneration

Ricci

Srivastava

2018

WIREs Developmental Biology

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Many animal species are capable of replacing missing tissues that are lost upon injury or amputation through the process of regeneration. Although the extent of regeneration is variable across animals, that is, some animals can regenerate any missing cell type whereas some can only regenerate certain organs or tissues, regulated cell proliferation underlies the formation of new tissues in most systems. Notably, many species display an increase in proliferation within hours or days upon wounding. While different cell types proliferate in response to wounding in various animal taxa, comparative molecular data are beginning to point to shared wound-induced mechanisms that regulate cell division during regeneration. Here, we synthesize current insights about early molecular pathways of regeneration from diverse model and emerging systems by considering these species in their evolutionary contexts. Despite the great diversity of mechanisms underlying injury-induced cell proliferation across animals, and sometimes even in the same species, similar pathways for proliferation have been implicated in distantly related species (e.g., small diffusible molecules, signaling from apoptotic cells, growth factor signaling, mTOR and Hippo signaling, and Wnt and Bmp pathways). Studies that explicitly interrogate molecular and cellular regenerative mechanisms in understudied animal phyla will reveal the extent to which early pathways in the process of regeneration are conserved or independently evolved. This article is categorized under: Comparative Development and Evolution > Body Plan Evolution Adult Stem Cells, Tissue Renewal, and Regeneration > Regeneration Comparative Development and Evolution > Model Systems.

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“…Apart from molluscs, only the relatively simpler nervous system of the medicinal leech (59, 60) and the salamander retina (335, 336) has been shown to posses large and individually identified classes of nitrergic cells. Today, the data about the distribution and function of NO in invertebrates is growing and covers a relatively large spectrum of organisms from jellyfish (61) and hydra (337-339) to fly (64) and parasitic worms (340, 341). However, the diversity of proposed functions of NO in invertebrates (reviewed by (63, 82, 342)) contrasts dramatically with the limited information available about the molecular biology and enzymology of NOS from different animal groups (343).…”

Section: Nos In Invertebrates and Their Nervous Systemsmentioning

confidence: 99%

Parallel evolution of Nitric Oxide signaling: Diversity of synthesis and memory pathways

Moroz

Kohn²

2011

Front Biosci

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The origin of NO signaling can be traceable back to the origin of life with the large scale of parallel evolution of NO synthases (NOSs). Inducible-like NOSs may be the most basal prototype of all NOSs and that neuronal-like NOS might have evolved several times from this prototype. Other enzymatic and non-enzymatic pathways for NO synthesis have been discovered using reduction of nitrites, an alternative source of NO. Diverse synthetic mechanisms can co-exist within the same cell providing a complex NO-oxygen microenvironment tightly coupled with cellular energetics. The dissection of multiple sources of NO formation is crucial in analysis of complex biological processes such as neuronal integration and learning mechanisms when NO can act as a volume transmitter within memory-forming circuits. In particular, the molecular analysis of learning mechanisms (most notably in insects and gastropod molluscs) opens conceptually different perspectives to understand the logic of recruiting evolutionarily conserved pathways for novel functions. Giant uniquely identified cells from Aplysia and related species precent unuque opportunities for integrative analysis of NO signaling at the single cell level.

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Involvement of nitric oxide in the head regeneration of Hydra vulgaris

Cited by 16 publications

References 42 publications

Tail regenerative capacity and iNOS immunolocalization in Xenopus laevis tadpoles

Tail regenerative capacity and iNOS immunolocalization in Xenopus laevis tadpoles

Wound‐induced cell proliferation during animal regeneration

Parallel evolution of Nitric Oxide signaling: Diversity of synthesis and memory pathways

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