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The molecular circuitries controlling the process of skin wound healing have gained new significant insights in recent years. This knowledge is built on landmark studies on skin embryogenesis, maturation, and differentiation. Furthermore, the identification, characterization, and elucidation of the biological roles of adult skin epithelial stem cells and their influence in tissue homeostasis have provided the foundation for the overall understanding of the process of skin wound healing and tissue repair. Among numerous signaling pathways associated with epithelial functions, the PI3K/Akt/mTOR signaling route has gained substantial attention with the generation of animal models capable of dissecting individual components of the pathway, thereby providing a novel insight into the molecular framework underlying skin homeostasis and tissue regeneration. In this review, we focus on recent findings regarding the mechanisms involved in wound healing associated with the upregulation of the activity of the PI3K/Akt/mTOR circuitry. This review highlights critical findings on the molecular mechanisms controlling the activation of mTOR, a downstream component of the PI3K–PTEN pathway, which is directly involved in epithelial migration and proliferation. We discuss how this emerging information can be exploited for the development of novel pharmacological intervention strategies to accelerate the healing of critical size wounds. 相似文献
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Here we have tested the inhibitory activity of the late untranslated region (UTR) of nine different human papillomavirus (HPV) types representing three different genera and six different species. These HPVs include both low-risk and high-risk types. We found that the late UTR of the various HPVs all displayed inhibitory activity, although they inhibited gene expression to various extent. The late UTR from the two distantly related HPV types 1 and 16, which are two different species that belong to different genera, each interacted with a 55 kDa protein. This protein cross-linked specifically to both HPV-1 and HPV-16 late UTR, although it bound more strongly to HPV-16 than to HPV-1, which correlated with the higher inhibitory activity of the HPV-16 late UTR. Mutagenesis experiments revealed that inactivation of two UGUUUGU motifs in the HPV-16 late UTR or two UAUUUAU motifs in the HPV-1 late UTR resulted in loss of binding of p55. In summary, these results demonstrate that the presence inhibitory elements encoding PuU(3-5)Pu-motifs in the HPV late UTR is a conserved property of different HPV types, species and genera, and suggest that these elements play an important role in the viral life cycle. 相似文献
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Arthur J. Matas Erika S. Helgeson Robert Gaston Fernando Cosio Roslyn Mannon Bertram L. Kasiske Lawrence Hunsicker Sita Gourishankar David Rush J Michael Cecka John Connett Joseph P. Grande 《American journal of transplantation》2020,20(9):2509-2521
Inflammation in areas of fibrosis (i‐IFTA) in posttransplant biopsy specimens has been associated with decreased death‐censored graft survival (DC‐GS). Additionally, an i‐IFTA score ≥ 2 is part of the diagnostic criteria for chronic active TCMR (CA TCMR). We examined the impact of i‐IFTA and t‐IFTA (tubulitis in areas of atrophy) in the first biopsy for cause after 90 days posttransplant (n = 598); mean (SD) 1.7 ± 1.4 years posttransplant. I‐IFTA, present in 196 biopsy specimens, was strongly correlated with t‐IFTA, and Banff i. Of the 196, 37 (18.9%) had a previous acute rejection episode; 96 (49%) had concurrent i score = 0. Unlike previous studies, i‐IFTA = 1 (vs 0) was associated with worse 3‐year DC‐GS: (i‐IFTA = 0, 81.7%, [95% CI 77.7 to 85.9%]); i‐IFTA = 1, 68.1%, [95% CI 59.7 to 77.6%]; i‐IFTA = 2, 56.1%, [95% CI 43.2 to 72.8%], i‐IFTA = 3, 48.5%, [95% CI 31.8 to 74.0%]). The association of i‐IFTA with decreased DC‐GS remained significant when adjusted for serum creatinine at the time of the biopsy, Banff i, ci and ct, C4d and DSA. T‐IFTA was similarly associated with decreased DC‐GS. Of these indication biopsies, those with i‐IFTA ≥ 2, without meeting other criteria for CA TCMR had similar postbiopsy DC‐GS as those with CA TCMR. Those with i‐IFTA = 1 and t ≥ 2, ti ≥ 2 had postbiopsy DC‐GS similar to CA TCMR. Biopsies with i‐IFTA = 1 had similar survival as CA TCMR when biopsy specimens also met Banff criteria for TCMR and/or AMR. Studies of i‐IFTA and t‐IFTA in additional cohorts, integrating analyses of Banff scores meeting criteria for other Banff diagnoses, are needed. 相似文献
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Rachelle Ashcroft Jose Silveira Brian Rush Kwame McKenzie 《Revue canadienne de psychiatrie》2014,59(7):385-392