Delayed Re-epithelialization in Ppm1a Gene-deficient Mice Is Mediated by Enhanced Activation of Smad2

Yang, Xue; Teng, Yan; Hou, Ning; Fan, Xiongwei; Chen, Xuan; Li, Jun; Wang, Limin; Wang, Youliang; Wu, Xiushan; Yang, Xiao

doi:10.1074/jbc.m111.292284

Cited by 22 publications

(26 citation statements)

References 37 publications

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“…The luciferase reporter gene assay was performed using a dual luciferase reporter assay system (Promega, Madison, WI) as described previously [32]. Briefly, targeted cells were transiently cotransfected with specific vectors and an IFNβ-dependent firefly luciferase reporter construct as well as a Renilla luciferase control construct.…”

Section: Methodsmentioning

confidence: 99%

PPM1B negatively regulates antiviral response via dephosphorylating TBK1

Zhao

Liang

Fan

et al. 2012

Cellular Signalling

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The production of type I interferon must be tightly regulated and aberrant production of type I interferon is harmful or even fatal to the host. TBK1 phosphorylation at Ser172 plays an essential role in TBK1-mediated antiviral response. However, how TBK1 activity is negatively regulated remains poorly understood. Using a functional genomics approach, we have identified PPM1B as a TBK1 phosphatase. PPM1B dephosphorylates TBK1 in vivo and in vitro. PPM1B wild-type but not its phosphatase-deficient R179G mutant inhibits TBK1-mediated antiviral response and facilitates VSV replication in the cells. Viral infection induces association of PPM1B with TBK1 in a transient fashion in the cells. Conversely, suppression of PPM1B expression enhances virus-induced IRF3 phosphorylation and IFNβ production. Our study identifies a previously unrecognized role for PPM1B in the negative regulation of antiviral response by acting as a TBK1 phosphatase.

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Section: Methodsmentioning

confidence: 99%

PPM1B negatively regulates antiviral response via dephosphorylating TBK1

Zhao

Liang

Fan

et al. 2012

Cellular Signalling

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“…The migration/proliferation of keratinocytes is the key step in accelerating wound healing (7,8). Cell migration/proliferation is precisely regulated by various cell cycle regulatory proteins (9,10).…”

Section: Introductionmentioning

confidence: 99%

Application of platelet-rich plasma accelerates the wound healing process in acute and chronic ulcers through rapid migration and upregulation of cyclin A and CDK4 in HaCaT cells

Kim

Ryu

Lee

et al. 2012

Molecular Medicine Reports

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Abstract. Application of autologous platelet-rich plasma (PRP) has been used for chronic wound healing. The aim of this study was to evaluate the effect of PRP on the wound healing processes of both acute and chronic ulcers and the underlying molecular mechanisms involved. We treated 16 patients affected by various acute and chronic ulcers with PRP. We performed molecular studies of cell proliferation, migration assays, immunoblotting and chloramphenicol acetyltransferase (CAT) assays in PRP-treated HaCaT keratinocyte cells. PRP treatment induced increased rates of cell proliferation and cell migration of HaCaT cells. In addition, the expression of cyclin A and cyclin dependent kinase (CDK) 4 proteins was markedly increased with a low concentration (0.5%) of PRP treatment in HaCaT cells. In 11 patients with chronic ulcers, including stasis ulcers, diabetic ulcers, venous leg ulcers, livedoid vasculitis, claw foot and traumatic ulcers, 9 patients showed 90-100% epithelization after 15.18 days. In 5 patients with acute ulcers, such as dehiscence, open wound and burn wound, 80-100% epithelization was achieved between 4 to 20 days. Topical application of PRP to acute and chronic skin ulcers significantly accelerated the epithelization process, likely through upregulation of the cell cycle regulatory proteins cyclin A and CDK4.

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“…82 These results are corroborated in a recent study showing that keratinocyte-specific Smad2 KO mice display the opposite effect-accelerated reepithelialization with enhanced keratinocyte migration. 83 Taken together, these studies suggest that epidermal Smad2 plays an important role in wound re-epithelialization.…”

Section: Smad2mentioning

confidence: 84%