Postnatal Schwann cell proliferation but not myelination is strictly and uniquely dependent on cyclin-dependent kinase 4 (cdk4)

Atanasoski, Suzana; Boentert, Matthias; Ventura, Lukas De; Pohl, Hartmut B.F.; Baranek, Constanze; Beier, Konstantin; Young, Peter; Barbacid, Mariano; Suter, Ueli

doi:10.1016/j.mcn.2007.11.005

Cited by 26 publications

(26 citation statements)

References 37 publications

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“…In addition, Cdk4 is dispensable for liver regeneration following partial hepatectomy [64], an assay considered to be one of the most stringent to evaluate the proliferative capacity of an adult tissue [65]. Altogether, these data support that Cdk4 is, with the exception of certain cell types [9,19,66,67], overall dispensable for adult tissue homeostasis.…”

Section: Discussionmentioning

confidence: 70%

Cdk6-Dependent Regulation of G1 Length Controls Adult Neurogenesis

et al. 2011

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The presence of neurogenic precursors in the adult mammalian brain is now widely accepted, but the mechanisms coupling their proliferation with the onset of neuronal differentiation remain unknown. Here, we unravel the major contribution of the G 1 regulator cyclin-dependent kinase 6 (Cdk6) to adult neurogenesis. We found that Cdk6 was essential for cell proliferation within the dentate gyrus of the hippocampus and the subventricular zone of the lateral ventricles. Specifically, Cdk6 deficiency prevents the expansion of neuronally committed precursors by lengthening G 1 phase duration, reducing concomitantly the production of newborn neurons. Altogether, our data support G 1 length as an essential regulator of the switch between proliferation and neuronal differentiation in the adult brain and Cdk6 as one intrinsic key molecular regulator of this process. STEM CELLS 2011;29:713-724 Disclosure of potential conflicts of interest is found at the end of this article.

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Section: Discussionmentioning

confidence: 70%

Cdk6-Dependent Regulation of G1 Length Controls Adult Neurogenesis

et al. 2011

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“…FGF2 has also been found to benefit motor neuron regeneration following sciatic nerve injury and can induce Schwann cell proliferation via transforming growth factor (TGF)-β signaling (34). LOC100504703 was paired with cyclin-dependent kinase 4 (Cdk4), which has been reported to be involved in the differentiation and proliferation of Schwann cells after sciatic nerve injury (35). NONMMUG036611, NONMMUG036609 and NONMMUG036610 were paired with CD9.…”

Section: Discussionmentioning

confidence: 99%

Time-dependent differential expression of long non-coding RNAs following peripheral nerve injury

Pan

Zhou

Liu

et al. 2017

International Journal of Molecular Medicine

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Abstract. Long non-coding RNAs (lncRNAs) are widely accepted as key players in various biological processes. However, the roles of lncRNA in peripheral nerve regeneration remain completely unknown. Thus, in this study, we performed microarray analysis to measure lncRNA expression in the distal segment of the sciatic nerve at 0, 3, 7 and 14 days following injury. We identified 5,354 lncRNAs that were differentially expressed: 3,788 lncRNAs were differentially expressed between days 0 and 3; 3,314 lncRNAs were differentially expressed between days 0 and 7; and 2,400 lncRNAs were differentially expressed between days 0 and 14. The results of RT-qPCR of two dysregulated lncRNAs were consistent with those of microarray analysis. Bioinformatics approaches, including lncRNA classification, gene ontology (GO) analysis and target prediction, were utilized to investigate the functions of these dysregulated lncRNAs in peripheral nerve damage. Importantly, we predicted that several lncRNA-mRNA pairs may participate in biological processes related to peripheral nerve injury. RT-qPCR was performed for the preliminary verification of three lncRNA-mRNA pairs. The overexpression of NONMMUG014387 promoted the proliferation of mouse Schwann cells. Thus, the findings of our study may enhance our knowledge of the role of lncRNAs in nerve injury.

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“…We showed CDK4 and E2F5 are highly expressed in the central lesion areas where astrocytes are absent but p75 + Schwann cells have infiltrated [24,38]. Postnatal Schwann cell proliferation has been known to be strictly and uniquely dependent on CDK4 [56]. However, further investigation is required to elucidate the mechanisms by which cell cycle inhibition modulates myelination after SCI.…”

Section: Discussionmentioning

confidence: 99%

Delayed expression of cell cycle proteins contributes to astroglial scar formation and chronic inflammation after rat spinal cord contusion

Pajoohesh‐Ganji

Stoica

et al. 2012

J Neuroinflammation

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BackgroundTraumatic spinal cord injury (SCI) induces secondary tissue damage that is associated with astrogliosis and inflammation. We previously reported that acute upregulation of a cluster of cell-cycle-related genes contributes to post-mitotic cell death and secondary damage after SCI. However, it remains unclear whether cell cycle activation continues more chronically and contributes to more delayed glial change. Here we examined expression of cell cycle-related proteins up to 4 months following SCI, as well as the effects of the selective cyclin-dependent kinase (CDKs) inhibitor CR8, on astrogliosis and microglial activation in a rat SCI contusion model.MethodsAdult male rats were subjected to moderate spinal cord contusion injury at T8 using a well-characterized weight-drop model. Tissue from the lesion epicenter was obtained 4 weeks or 4 months post-injury, and processed for protein expression and lesion volume. Functional recovery was assessed over the 4 months after injury.ResultsImmunoblot analysis demonstrated a marked continued upregulation of cell cycle-related proteins − including cyclin D1 and E, CDK4, E2F5 and PCNA − for 4 months post-injury that were highly expressed by GFAP+ astrocytes and microglia, and co-localized with inflammatory-related proteins. CR8 administrated systemically 3 h post-injury and continued for 7 days limited the sustained elevation of cell cycle proteins and immunoreactivity of GFAP, Iba-1 and p22PHOX − a key component of NADPH oxidase − up to 4 months after SCI. CR8 treatment significantly reduced lesion volume, which typically progressed in untreated animals between 1 and 4 months after trauma. Functional recovery was also significantly improved by CR8 treatment after SCI from week 2 through week 16.ConclusionsThese data demonstrate that cell cycle-related proteins are chronically upregulated after SCI and may contribute to astroglial scar formation, chronic inflammation and further tissue loss.

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Postnatal Schwann cell proliferation but not myelination is strictly and uniquely dependent on cyclin-dependent kinase 4 (cdk4)

Cited by 26 publications

References 37 publications

Cdk6-Dependent Regulation of G1 Length Controls Adult Neurogenesis

Cdk6-Dependent Regulation of G1 Length Controls Adult Neurogenesis

Time-dependent differential expression of long non-coding RNAs following peripheral nerve injury

Delayed expression of cell cycle proteins contributes to astroglial scar formation and chronic inflammation after rat spinal cord contusion

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