RhoE is spatiotemporally regulated in the postnatal mouse CNS

Ballester-Lurbe, Begoña; Poch, Enric; Mocholí, Enric; Guasch, Rosa M.; Pérez‐Roger, Ignacio; Terrado, José

doi:10.1016/j.neuroscience.2009.06.062

Cited by 10 publications

(20 citation statements)

References 31 publications

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“…The expression profiles of Rnd3 in the CNS were examined in mouse postnatal development (7), and showed that Rnd3 protein expression is detected in all regions of the adult brain and spinal cord, with the highest levels in the olfactory bulb and cortex. Rnd3 protein expressions were significantly higher in all of the regions of the CNS during the first 2–3 weeks of postnatal development, and gradually decreased to lower levels as development approached adulthood.…”

Section: Pathological Functions Of Rnd3mentioning

confidence: 99%

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Pathophysiological Functions of Rnd 3/ RhoE

Jie

Andrade

Lin

et al. 2015

Comprehensive Physiology

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Rnd3, also known as RhoE, belongs to the Rnd subclass of the Rho family of small GTP-binding proteins. Rnd proteins are unique due to their inability to switch from a GTP-bound to GDP-bound conformation. Even though studies of the biological function of Rnd3 are far from being concluded, information is available regarding its expression pattern, cellular localization, and its activity, which can be altered depending on the conditions. The compiled data from these studies implies that Rnd3 may not be a traditional small GTPase. The basic role of Rnd3 is to report as an endogenous antagonist of RhoA signaling-mediated actin cytoskeleton dynamics, which specifically contributes to cell migration and neuron polarity. In addition, Rnd3 also plays a critical role in arresting cell cycle distribution, inhibiting cell growth, and inducing apoptosis and differentiation. Increasing data have shown that aberrant Rnd3 expression may be the leading cause of some systemic diseases; particularly highlighted in apoptotic cardiomyopathy, developmental arrhythmogenesis and heart failure, hydrocephalus, as well as tumor metastasis and chemotherapy resistance. Therefore, a better understanding of the function of Rnd3 under different physiological and pathological conditions, through the use of suitable models, would provide a novel insight into the origin and treatment of multiple human diseases.

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Section: Pathological Functions Of Rnd3mentioning

confidence: 99%

“…Recent studies have been released in which Rnd3 was shown to be involved in cell differentiation. However, more studies should be extended using various types of stem cells, because Rnd3 defects lead to disorders in cortex neuron development (7, 103) and myoblast cell differentiation (37). …”

Section: Conclusion and Prospectivementioning

confidence: 99%

Pathophysiological Functions of Rnd 3/ RhoE

Jie

Andrade

Lin

et al. 2015

Comprehensive Physiology

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“…For example, Rnd1 and Rnd3 show overlapping patterns of expression during somitogenesis in Xenopus, and are regulated during this process by Notch [28]. Rnd2 and Rnd3 genes also show specific expression patterns in the developing brain, and in the case of Rnd2 its expression is induced by the developmentally regulated transcription factor neurogenin [29,30]. Rnd proteins might also play a role in neuronal remodelling in the adult brain (see below), since expression of Rnd2 and Rnd3 is induced in regions of the adult brain by the drugs MDMA and cocaine [31].…”

Section: Rnd Expression Is Regulated By Diverse Stimuli Transcriptionmentioning

confidence: 99%

Rnd proteins: Multifunctional regulators of the cytoskeleton and cell cycle progression

2010

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Rnd3/RhoE has two distinct functions, regulating the actin cytoskeleton and cell proliferation. This might explain why its expression is often altered in cancer and by multiple stimuli during development and disease. Rnd3 together with its relatives Rnd1 and Rnd2 are atypical members of the Rho GTPase family in that they do not hydrolyse GTP. Rnd3 and Rnd1 both antagonise RhoA/ROCK-mediated actomyosin contractility, thereby regulating cell migration, smooth muscle contractility and neurite extension. In addition, Rnd3 has been shown to have a separate role in inhibiting cell cycle progression by reducing translation of cell cycle regulators, including cyclin D1 and Myc. We propose that Rnd3 could act as a tumour suppressor to limit proliferation, but when mutations bypass this activity of Rnd3, it can promote cancer invasion through its effects in the actin cytoskeleton.

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“…SVZ neuroblasts proliferate and migrate through the RMS to the OB where they differentiate into several cell types. In the previous work, we showed high levels of RhoE expression in the SVZ-RMS-OB in the early postnatal life (Ballester-Lurbe et al 2009). Here, we show that RhoE has an important role for the correct development of this system since it affects cell proliferation, migration and differentiation.…”

Section: Discussionmentioning

confidence: 81%

“…In addition, their hippocampal neurons exhibit decreased number and length of the neurites, reduction in axon outgrowth and delay in the process of neuronal polarization (Peris et al 2012). By using these mice, we analyze here the role of RhoE in the postnatal SVZ-RMS-OB cells, a system that shows high levels of RhoE expression (Ballester-Lurbe et al 2009). Our results indicate that RhoE is essential for the correct development of SVZ cells and calbindinexpressing cells in the olfactory bulb.…”

Section: Introductionmentioning

confidence: 99%

RhoE deficiency alters postnatal subventricular zone development and the number of calbindin-expressing neurons in the olfactory bulb of mouse

et al. 2014

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The subventricular zone represents an important reservoir of progenitor cells in the adult brain. Cells from the subventricular zone migrate along the rostral migratory stream and reach the olfactory bulb, where they originate different types of interneurons. In this work, we have analyzed the role of the small GTPase RhoE/Rnd3 in subventricular zone cell development using mice-lacking RhoE expression. Our results show that RhoE null mice display a remarkable postnatal broadening of the subventricular zone and caudal rostral migratory stream. This broadening was caused by an increase in progenitor proliferation, observed in the second postnatal week but not before, and by an altered migration of the cells, which appeared in disorganized cell arrangements that impaired the appropriate contact between cells in the rostral migratory stream. In addition, the thickness of the granule cell layer in the olfactory bulb was reduced, although the density of granule cells did not differ between wild-type and RhoE null mice. Finally, the lack of RhoE expression affected the olfactory glomeruli inducing a severe reduction of calbindin-expressing interneurons in the periglomerular layer. This was already evident in the newborns and even more pronounced 15 days later when RhoE null mice displayed 89% less cells than control mice. Our results indicate that RhoE has pleiotropic functions on subventricular cells because of its role in proliferation and tangential migration, affecting mainly the development of calbindin-expressing cells in the olfactory bulb.

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RhoE is spatiotemporally regulated in the postnatal mouse CNS

Cited by 10 publications

References 31 publications

Pathophysiological Functions of Rnd 3/ RhoE

Pathophysiological Functions of Rnd 3/ RhoE

Rnd proteins: Multifunctional regulators of the cytoskeleton and cell cycle progression

RhoE deficiency alters postnatal subventricular zone development and the number of calbindin-expressing neurons in the olfactory bulb of mouse

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