Zyxin is upregulated in the nucleus by thymosin β4 in SiHa cells

Moon, Hye Sung; Even-Ram, Sharona; Kleinman, Hynda K.; Jae, Hee

doi:10.1016/j.yexcr.2006.07.021

Cited by 27 publications

(40 citation statements)

References 49 publications

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“…Indeed, T4 has been detected in the nucleus of cells, where it might alter the expression of different genes directly involved in the determination of neuronal fate (Huff et al, 2004;Moon et al, 2006). In this respect, our study also shows that a reduction in T4 facilitates neuronal differentiation of NPCs without increasing the proliferation of neural progenitors, probably by enhancing exit from the cell cycle and having an instructive differentiating effect.…”

Section: Discussionsupporting

confidence: 60%

Downregulation of thymosin β4 in neural progenitor grafts promotes spinal cord regeneration

Mollinari

Ricci–Vitiani

Pieri

et al. 2009

Journal of Cell Science

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Thymosin β4 (Tβ4) is an actin-binding peptide whose expression in developing brain correlates with migration and neurite extension of neurons. Here, we studied the effects of the downregulation of Tβ4 expression on growth and differentiation of murine neural progenitor cells (NPCs), using an antisense lentiviral vector. In differentiation-promoting medium, we found twice the number of neurons derived from the Tβ4-antisense-transduced NPCs, which showed enhanced neurite outgrowth accompanied by increased expression of the adhesion complex N-cadherin–β-catenin and increased ERK activation. Importantly, when the Tβ4-antisense-transduced NPCs were transplanted in vivo into a mouse model of spinal cord injury, they promoted a significantly greater functional recovery. Locomotory recovery correlated with increased expression of the regeneration-promoting cell adhesion molecule L1 by the grafted Tβ4-antisense-transduced NPCs. This resulted in an increased number of regenerating axons and in sprouting of serotonergic fibers surrounding and contacting the Tβ4-antisense-transduced NPCs grafted into the lesion site. In conclusion, our data identify a new role for Tβ4 in neuronal differentiation of NPCs by regulating fate determination and process outgrowth. Moreover, NPCs with reduced Tβ4 levels generate an L1-enriched environment in the lesioned spinal cord that favors growth and sprouting of spared host axons and enhances the endogenous tissue-repair processes.

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Section: Discussionsupporting

confidence: 60%

Downregulation of thymosin β4 in neural progenitor grafts promotes spinal cord regeneration

Mollinari

Ricci–Vitiani

Pieri

et al. 2009

Journal of Cell Science

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“…Images are representative. Scale bars ϭ 20 m. a pronounced nuclear staining of T␤ 4 in the human cervical cancer cell line SiHa and the mammary carcinoma cell line MCF-7 (57,59). Interestingly, we also discovered that T␤ 4 and RelA/p65 colocalized in the cytoplasm, especially in the perinuclear areas.…”

Section: T␤ 4 Colocalizes With the Nf-b Subunit Rela/p65 In Both The mentioning

confidence: 54%

Thymosin β₄inhibits TNF‐α‐induced NF‐κB activation, IL‐8 expression, and the sensitizing effects by its partners PINCH‐1 and ILK

Qiu¹,

Wheater²,

Qiu³

et al. 2011

FASEB j.

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The mechanisms by which thymosin β 4 (Tβ(4)) regulates the inflammatory response to injury are poorly understood. Previously, we demonstrated that ectopic Tβ(4) treatment inhibits injury-induced proinflammatory cytokine and chemokine production. We have also shown that Tβ(4) suppresses TNF-α-mediated NF-κB activation. Herein, we present novel evidence that Tβ(4) directly targets the NF-κB RelA/p65 subunit. We find that enforced expression of Tβ(4) interferes with TNF-α-mediated NF-κB activation, as well as downstream IL-8 gene transcription. These activities are independent of the G-actin-binding properties of Tβ(4). Tβ(4) blocks RelA/p65 nuclear translocation and targeting to the cognate κB site in the proximal region of the IL-8 gene promoter. Tβ(4) also inhibits the sensitizing effects of its intracellular binding partners, PINCH-1 and ILK, on NF-κB activity after TNF-α stimulation. The identification of a functional regulatory role by Tβ(4) and the focal adhesion proteins PINCH-1 and ILK on NF-κB activity in this study opens a new window for scientific exploration of how Tβ(4) modulates inflammation. In addition, the results of this study serve as a foundation for developing Tβ(4) as a new anti-inflammatory therapy.

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“…Among the other genes up-regulated by Tb4 are cytoskeletal-related proteins, including myosin IIA, a-actinin, tropomyosin, talin, a 5 -integrin, vinculin [84] and zyxin [85], extracellular matrix (ECM) components such as laminin-5 [86] and matrix metalloproteinases, which degrade components of ECM [41,87] consistent with a role for Tb4 in co-ordinating the necessary changes to the cytoskeleton and ECM which are required to effect cell migration.…”

Section: Does Endogenous Tb4 Stimulate Angiogenesis?mentioning

confidence: 82%

Thymosin β4 and angiogenesis: modes of action and therapeutic potential

Smart¹,

Rossdeutsch²,

Riley³

2007

Angiogenesis

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Zyxin is upregulated in the nucleus by thymosin β4 in SiHa cells

Cited by 27 publications

References 49 publications

Downregulation of thymosin β4 in neural progenitor grafts promotes spinal cord regeneration

Downregulation of thymosin β4 in neural progenitor grafts promotes spinal cord regeneration

Thymosin β₄inhibits TNF‐α‐induced NF‐κB activation, IL‐8 expression, and the sensitizing effects by its partners PINCH‐1 and ILK

Thymosin β4 and angiogenesis: modes of action and therapeutic potential

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Zyxin is upregulated in the nucleus by thymosin β4 in SiHa cells

Cited by 27 publications

References 49 publications

Downregulation of thymosin β4 in neural progenitor grafts promotes spinal cord regeneration

Downregulation of thymosin β4 in neural progenitor grafts promotes spinal cord regeneration

Thymosin β4inhibits TNF‐α‐induced NF‐κB activation, IL‐8 expression, and the sensitizing effects by its partners PINCH‐1 and ILK

Thymosin β4 and angiogenesis: modes of action and therapeutic potential

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Thymosin β₄inhibits TNF‐α‐induced NF‐κB activation, IL‐8 expression, and the sensitizing effects by its partners PINCH‐1 and ILK