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000162729 0247_ $$2doi$$a10.1016/j.neuron.2021.08.014
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000162729 041__ $$aEnglish
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000162729 1001_ $$0P:(DE-2719)2810277$$aStern, Sina$$b0$$eFirst author$$udzne
000162729 245__ $$aRhoA drives actin compaction to restrict axon regeneration and astrocyte reactivity after CNS injury.
000162729 260__ $$aNew York, NY$$bElsevier$$c2021
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000162729 520__ $$aAn inhibitory extracellular milieu and neuron-intrinsic processes prevent axons from regenerating in the adult central nervous system (CNS). Here we show how the two aspects are interwoven. Genetic loss-of-function experiments determine that the small GTPase RhoA relays extracellular inhibitory signals to the cytoskeleton by adapting mechanisms set in place during neuronal polarization. In response to extracellular inhibitors, neuronal RhoA restricts axon regeneration by activating myosin II to compact actin and, thereby, restrain microtubule protrusion. However, astrocytic RhoA restricts injury-induced astrogliosis through myosin II independent of microtubules by activating Yes-activated protein (YAP) signaling. Cell-type-specific deletion in spinal-cord-injured mice shows that neuronal RhoA activation prevents axon regeneration, whereas astrocytic RhoA is beneficial for regenerating axons. These data demonstrate how extracellular inhibitors regulate axon regeneration, shed light on the capacity of reactive astrocytes to be growth inhibitory after CNS injury, and reveal cell-specific RhoA targeting as a promising therapeutic avenue.
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000162729 650_7 $$2Other$$aF-actin density
000162729 650_7 $$2Other$$aRhoA
000162729 650_7 $$2Other$$aYAP signaling
000162729 650_7 $$2Other$$aastrocyte reactivity
000162729 650_7 $$2Other$$aaxon regeneration
000162729 650_7 $$2Other$$amicrotubule protrusion
000162729 650_7 $$2Other$$amyosin II
000162729 650_2 $$2MeSH$$aActins: metabolism
000162729 650_2 $$2MeSH$$aAnimals
000162729 650_2 $$2MeSH$$aAstrocytes: metabolism
000162729 650_2 $$2MeSH$$aAxons: metabolism
000162729 650_2 $$2MeSH$$aCentral Nervous System: metabolism
000162729 650_2 $$2MeSH$$aCentral Nervous System: pathology
000162729 650_2 $$2MeSH$$aCentral Nervous System Diseases: metabolism
000162729 650_2 $$2MeSH$$aCentral Nervous System Diseases: pathology
000162729 650_2 $$2MeSH$$aMice
000162729 650_2 $$2MeSH$$aNerve Regeneration: physiology
000162729 650_2 $$2MeSH$$arhoA GTP-Binding Protein: metabolism
000162729 7001_ $$0P:(DE-2719)2812271$$aHilton, Brett Jason$$b1$$udzne
000162729 7001_ $$0P:(DE-2719)9000509$$aBurnside, Emily$$b2$$udzne
000162729 7001_ $$0P:(DE-2719)2810386$$aDupraz, Sebastian$$b3$$udzne
000162729 7001_ $$0P:(DE-2719)9000569$$aHandley, Emily$$b4$$udzne
000162729 7001_ $$0P:(DE-2719)2811702$$aGonyer, Jessica$$b5$$udzne
000162729 7001_ $$aBrakebusch, Cord$$b6
000162729 7001_ $$0P:(DE-2719)2810270$$aBradke, Frank$$b7$$eLast author$$udzne
000162729 773__ $$0PERI:(DE-600)2001944-0$$a10.1016/j.neuron.2021.08.014$$gVol. 109, no. 21, p. 3436 - 3455.e9$$n21$$p3436 - 3455.e9$$tNeuron$$v109$$x0896-6273$$y2021
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