Production of axial skeletal malformations with the nitric oxide synthesis inhibitor N<sup>G</sup>‐nitro‐<scp>L</scp>‐arginine methyl ester (<scp>L</scp>‐NAME) in the mouse

Tiboni, Gian Mario; Marotta, Francesca; Barbacane, Lisa

doi:10.1002/bdrb.20100

Cited by 5 publications

(2 citation statements)

References 23 publications

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“…On day E8.5 (day 9 post coitum) mice were intraperitoneally injected with 300 mg kg −1 of L-NAME or D-NAME (Sigma) dissolved in sterile, apyrogenic saline solution using a dose volume of 10 ml kg −1 (ref. 37). The injection was repeated after 24 h. Exactly 24 h after the second injection, mice were killed with CO 2 , embryos were harvested, and a conservative dissection of the AGM was performed.…”

Section: Methodsmentioning

confidence: 99%

Biomechanical forces promote embryonic haematopoiesis

Adamo

Naveiras

Wenzel

et al. 2009

Nature

473

420

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Biomechanical forces are emerging as critical regulators of embryogenesis, particularly in the developing cardiovascular system 1,2 . After initiation of the heartbeat in vertebrates, cells lining the ventral aspect of the dorsal aorta, the placental vessels, and the umbilical and vitelline arteries initiate expression of the transcription factor Runx1 (refs 3-5), a master regulator of haematopoiesis, and give rise to haematopoietic cells 4 . It remains unknown whether the biomechanical forces imposed on the vascular wall at this developmental stage act as a determinant of haematopoietic potential 6 . Here, using mouse embryonic stem cells differentiated in vitro, we show that fluid shear stress increases the expression of Runx1 in CD41 + c-Kit + haematopoietic progenitor cells 7 ,concomitantly augmenting their haematopoietic colony-forming potential. Moreover, we find that shear stress increases haematopoietic colony-forming potential and expression of haematopoietic markers in the paraaortic splanchnopleura/aorta-gonads-mesonephros of mouse embryos and that abrogation of nitric oxide, a mediator of shear-stress-induced signalling 8 , compromises haematopoietic potential in vitro and in vivo. Collectively, these data reveal a critical role for biomechanical forces in haematopoietic development.In the mouse, the first haemogenic areas appear in the yolk sac starting at day 7.5 of development (E7.5) 9 . After the establishment of circulation and the onset of vascular flow at day 8.5, additional haemogenic sites appear between day 9 and 10.5 as Runx1 + regions within

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Section: Methodsmentioning

confidence: 99%

Biomechanical forces promote embryonic haematopoiesis

Adamo

Naveiras

Wenzel

et al. 2009

Nature

473

420

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“…These defects phenocopy the limb reduction defects detected in eNOS null mice. Recent data have shown that embryonic exposures to NOS inhibitors during organogenesis can cause skeletal malformations [326]. There is a known role for NO in bone [327].…”

Section: B the Teratology Of Nomentioning

confidence: 99%

Interactive Endogenous Small Molecule (Gaseous) Signaling: Implications for Teratogenesis

Fukuto¹,

Collins²

2007

CPD

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Dioxygen (O2) is an exogenously supplied gas with a number of properties that make it valuable as a biological source of energy and as a result much of life has become dependent on this molecule. Nitric oxide (NO), carbon dioxide (CO) and hydrogen sulfide (H2S) are small molecules that are sometimes in a gaseous state and that can be either exogenously or endogenously supplied. The chemistry of these four molecules allows them to share some common biological targets and signal transduction pathways as well as providing for unique aspects to the biochemistry of each one. Dioxygen can be teratogenic either in excess (hyperoxia) or in deficiency (hypoxia). Although there is a great deal known about the chemistry and physiology of dioxygen, the mechanisms by which it induces toxic endpoints, such as teratogenesis, are unknown. This review examines some fundamental concepts of these four signaling molecules and considers some of the molecular targets and pathways by which they interact. The information regarding the teratogenicity of either excess or deficiency of the four gases is summarized. Interaction information is generally unavailable for teratogenicity endpoints with the four gases and also a mechanistic understanding of the toxicodynamics of the compounds is lacking. Although it could be theoretically predicted that certain interactions would be additive, for example carbon monoxide and hypoxia, based on the physiological role of these molecules, the data is unavailable. Consequently, these small (gaseous) signaling molecules have been demonstrated to interact with respect to signaling pathways, but whether this indicates a similar result for teratogenesis remains unevaluated.

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Inhibition of nitric oxide synthesis enhances the teratogenic response to valproic acid

Tiboni

Marotta

Verrotti

2013

Reproductive Toxicology

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Production of axial skeletal malformations with the nitric oxide synthesis inhibitor N^G‐nitro‐L‐arginine methyl ester (L‐NAME) in the mouse

Abstract: This study provides evidence that in utero exposure to L-NAME can affect organogenesis of the axial skeleton.

Cited by 5 publications

References 23 publications

Biomechanical forces promote embryonic haematopoiesis

Biomechanical forces promote embryonic haematopoiesis

Interactive Endogenous Small Molecule (Gaseous) Signaling: Implications for Teratogenesis

Inhibition of nitric oxide synthesis enhances the teratogenic response to valproic acid

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Production of axial skeletal malformations with the nitric oxide synthesis inhibitor NG‐nitro‐L‐arginine methyl ester (L‐NAME) in the mouse

Abstract: This study provides evidence that in utero exposure to L-NAME can affect organogenesis of the axial skeleton.

Cited by 5 publications

References 23 publications

Biomechanical forces promote embryonic haematopoiesis

Biomechanical forces promote embryonic haematopoiesis

Interactive Endogenous Small Molecule (Gaseous) Signaling: Implications for Teratogenesis

Inhibition of nitric oxide synthesis enhances the teratogenic response to valproic acid

Contact Info

Product

Resources

About

Production of axial skeletal malformations with the nitric oxide synthesis inhibitor N^G‐nitro‐L‐arginine methyl ester (L‐NAME) in the mouse