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11.
Identification of key tissue type for antler regeneration through pedicle periosteum deletion 总被引:5,自引:0,他引:5
Epimorphic regeneration is the “holy grail” of regenerative medicine. Research aimed at investigating the various models of
epimorphic regeneration is essential if a fundamental understanding of the factors underpinning this process are to be established.
Deer antlers are the only mammalian appendages that are subject to an annual cycle of epimorphic regeneration. In our previous
studies, we have reported that histogenesis of antler regeneration relies on cells resident within the pedicle periosteum
(PP). The present study elaborates this finding by means of functional studies involving the deletion of PP. Four yearling
and four 2-year-old stags were selected for total PP deletion or partial PP deletion experiments. Of the animals in the total
PP deletion group, one showed no signs of antler regeneration throughout the antler growth season. Two showed substantial
and one showed marginal delays in antler regeneration (at 34, 20 and 7 days, respectively) compared with the corresponding
sham-operated sides. Histological investigation revealed that the delayed antlers were derived from regenerated PP. Unexpectedly,
the regenerative capacity of the antler from the total periosteum-deleted pedicles depended on antler length at surgery. Of
the four deer that had partial PP deletion, two regenerated antlers exclusively from the left-over PP on the pedicle shafts
in the absence of participation from the pedicle bone proper. The combined results from the PP deletion experiments convincingly
demonstrate that the cells of the PP are responsible for antler regeneration.
The authors thank the New Zealand Foundation of Research, Science and Technology and Deer Industry New Zealand for funding
their research. 相似文献
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J. S. Mackintosh 《BMJ (Clinical research ed.)》1912,2(2692):279-280
17.
SUMMARY Anthelmintics are the cornerstone of parasitic helminth control. Surprisingly, understanding of the biochemical pathways used by parasitic helminths to detoxify anthelmintics is fragmented, despite the increasing global threat of anthelmintic resistance within the ruminant and equine industries. Reductionist biochemistry has likely over-estimated the enzymatic role of glutathione transferases in anthelmintic metabolism and neglected the potential role of the cytochrome P-450 superfamily (CYPs). Proteomic technologies offers the opportunity to support genomics, reverse genetics and pharmacokinetics, and provide an integrated insight into both the cellular mechanisms underpinning response to anthelmintics and also the identification of biomarker panels for monitoring the development of anthelmintic resistance. To date, there have been limited attempts to include proteomics in anthelmintic metabolism studies. Optimisations of membrane, post-translational modification and interaction proteomic technologies in helminths are needed to especially study Phase I CYPs and Phase III ABC transporter pumps for anthelmintics and their metabolites. 相似文献
18.
14-3-3 proteins regulate cellular responses to stimuli by docking onto pairs of phosphorylated residues on target proteins. The present study shows that the human 14-3-3-binding phosphoproteome is highly enriched in 2R-ohnologues, which are proteins in families of two to four members that were generated by two rounds of whole genome duplication at the origin of the vertebrates. We identify 2R-ohnologue families whose members share a 'lynchpin', defined as a 14-3-3-binding phosphosite that is conserved across members of a given family, and aligns with a Ser/Thr residue in pro-orthologues from the invertebrate chordates. For example, the human receptor expression enhancing protein (REEP) 1-4 family has the commonest type of lynchpin motif in current datasets, with a phosphorylatable serine in the -2 position relative to the 14-3-3-binding phosphosite. In contrast, the second 14-3-3-binding sites of REEPs 1-4 differ and are phosphorylated by different kinases, and hence the REEPs display different affinities for 14-3-3 dimers. We suggest a conceptual model for intracellular regulation involving protein families whose evolution into signal multiplexing systems was facilitated by 14-3-3 dimer binding to lynchpins, which gave freedom for other regulatory sites to evolve. While increased signalling complexity was needed for vertebrate life, these systems also generate vulnerability to genetic disorders. 相似文献
19.
M González-González L Muñoz-Bellvis C Mackintosh C Fontanillo ML Gutiérrez MM Abad O Bengoechea C Teodosio E Fonseca M Fuentes J De Las Rivas A Orfao J María Sayagués 《PloS one》2012,7(8):e42683
Background
Most sporadic colorectal cancer (sCRC) deaths are caused by metastatic dissemination of the primary tumor. New advances in genetic profiling of sCRC suggest that the primary tumor may contain a cell population with metastatic potential. Here we compare the cytogenetic profile of primary tumors from liver metastatic versus non-metastatic sCRC.Methodology/Principal Findings
We prospectively analyzed the frequency of numerical/structural abnormalities of chromosomes 1, 7, 8, 13, 14, 17, 18, 20, and 22 by iFISH in 58 sCRC patients: thirty-one non-metastatic (54%) vs. 27 metastatic (46%) disease. From a total of 18 probes, significant differences emerged only for the 17p11.2 and 22q11.2 chromosomal regions. Patients with liver metastatic sCRC showed an increased frequency of del(17p11.2) (10% vs. 67%;p<.001) and del(22q11.2) (0% vs. 22%;p = .02) versusnon-metastatic cases. Multivariate analysis of prognostic factors for overall survival (OS) showed that the only clinical and cytogenetic parameters that had an independent adverse impact on patient outcome were the presence of del(17p) with a 17p11.2 breakpoint and del(22q11.2). Based on these two cytogenetic variables, patients were classified into three groups: low- (no adverse features), intermediate- (one adverse feature) and high-risk (two adverse features)- with significantly different OS rates at 5-years (p<.001): 92%, 53% and 0%, respectively.Conclusions/Significance
Our results unravel the potential implication of del(17p11.2) in sCRC patients with liver metastasis as this cytogenetic alteration appears to be intrinsically related to an increased metastatic potential and a poor outcome, providing additional prognostic information to that associated with other cytogenetic alterations such as del(22q11.2). Additional prospective studies in larger series of patients would be required to confirm the clinical utility of the new prognostic markers identified. 相似文献20.