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101.
Mingzhi Shen Danna Bai Bei Liu Xiaozhao Lu Rongrong Hou Chao Zeng Na Li Zhenhong Fu Congye Li Ling Tao Haichang Wang Tao Yin 《生物化学与生物物理学报:疾病的分子基础》2018,1864(12):3735-3745
Hyperglycemia-induced impairment of angiogenesis contributes to the unfavorable prognosis of myocardial ischemia in long-standing diabetes mellitus. The underlying mechanism remains largely unknown and therapeutic strategies thereby limited. In the present study, we investigated the possible involvement of thioredoxin-interacting protein (TXNIP) and Wnt/β-catenin signaling in the context, and their possible relation was also explored. STZ induced diabetic mice were subjected to myocardial infarction (MI). Adenovirus expressing shTXNIP, shCtnnb1 (β-catenin) driven by VE-Cadherin promoter was administered intramyocardially immediately after MI. Cardiac function, histology, and molecular analyses were performed at predetermined time points. Increased endothelial expression of TXNIP was found in diabetic hearts, which correlated well with reduced nuclear β-catenin expression, insufficient angiogenesis, aggravated cardiac remodeling, and poor survival. Endothelial-specific knockdown of TXNIP significantly rescued β-catenin activity, together with increased angiogenesis, preserved cardiac function, and improved survival rate. Moreover, additional knockdown of β-catenin essentially reversed the beneficial effects of TXNIP downregulation. In vitro, high glucose treatment of human umbilical vein endothelial cells (HUVECs) increased TXNIP levels and ROS concentration, while it reduced β-catenin activity. Silencing TXNIP or ROS scavenger restored the high glucose induced reduction of Wnt/β-catenin activity in HUVECs. In addition, either reduction of TXNIP expression or supplementation of exogenous Wnt3a improved the HUVECs quantity and migration under high glucose conditions. Diabetes-induced increase of TXNIP expression in the endothelium contributes to impaired angiogenesis after MI, especially via the elevation of ROS and the impaired Wnt/β-catenin signaling. Targeting TXNIP-ROS-Wnt is a promising strategy in improving the prognosis. 相似文献
102.
Potato plants (Solanum tuberosum L.) were grown in water culturein a controlled environment. The growth rates of individualtubers were closely reflected by their 14C-content 20 h after14CO2 had been applied to the aerial parts of the shoot for4 h. The 14C-content of the tuber (sink strength) was significantlycorrelated to the 14C-concentration of the tuber tissue (14Cg1 fr. wt.=sink activity). The sink activity, which differedbetween individual tubers by up to a factor of 10, was alsoclosely related to the conversion rates of 14C into the starchand the remainder as well as to the 14C-content in the ethanolsoluble fraction. This indicates the simultaneous use of photosynthatefor growth and storage in the growing tubers. No preferenceof photosynthate utilization for either of these processes couldbe detected in relation to the sink activity of the tubers.Tubers with high sink activity imported 14C-labelled photosynthateat higher rates although their tissue contained higher concentrationsof reducing sugars and sucrose than the tissue of tubers withlow sink activity. Despite the close relationship between sinkactivity and the rate of starch synthesis (14C-conversion intostarch), no significant correlation was found between sink activityand the actual starch concentration of the tissue. The applicationof zeatin riboside directly onto individual tubers increasedtheir growth rates in comparison to non-treated tubers of thesame plant. The results indicate the importance of both growthand storage processes for the regulation of sink activity inyoung potato tubers. Key words: Potato tuber, 14C-photosynthate partitioning, zeatin riboside application 相似文献
103.
In the parasitic waspNasonia vitripennis, certain males carry a B chromosome, called PSR (paternal sex ratio), which causes the compaction and subsequent loss of the paternal chromosomes in fertilized eggs. BecauseNasonia are haplo-diploid, this leads to the production of all-male broods. Three families (PSR2, PSR18, PSR22) of related, tandemly repetitive DNAs were shown to be present solely on the PSR chromosome. These three families shared two conserved, palindromic ANA sequences, which may play a role in either PSR function or amplification of the tandem arrays. The tandem repeat family NV79 was determined to be present on the PSR chromosome as well as on at least one of the A chromosomes. This shared repeat as well as two repeat families (NV85, NV126) that were localized on the A chromosomes were detected in two sibling species ofN. vitripennis. NV79 and NV126 were also found in the more distantly related species,Trichomalopsis dubius.by H.F. Willard 相似文献
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105.
Kurt Randerath Pei-Fang Yang Tracy F. Danna Ranjani Reddy William P. Watson Erika Randerath 《Mutation research》1991,250(1-2):135-144
Oxygen free radicals, such as the hydroxyl radical generated by interaction of Fe2+ and H2O2 (Fenton reaction), are produced in mammalian cells as a result of aerobic metabolism and under various pathological conditions and are known to elicit mutations and potentially other adverse effects by reacting with DNA bases. Several products thus formed have recently been characterized as hydroxylated derivatives of cytosine, thymine, adenine, and guanine and imidazole-ring-opened derivatives of adenine and guanine in DNA. As shown herein by 32P-postlabeling, incubation of DNA under Fenton reaction conditions led to additional products which, by virtue of resistance to nuclease P1 catalyzed 3′-dephosphorylation and chromatographic behavior, appeared to be bulky adducts rather than small polar, hydroxylated or ring-opened nucleotide derivatives. Two major and five minor DNA derivatives were measured after 32P-postlabeling and TLC mapping of DNA oxidized in vitro under conditions known to lead to formation of reactive oxygen species. Amounts of products formed depended on Fe2+ and H2O2 concentrations and increased in the presence of
-ascorbic acid. One of the two major products was also detected in lung DNA of rats where its amount increased with animal age. Thus, at least one I-compound appeared to have its origin in the interaction of DNA with reactive oxygen species. 相似文献
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107.
Summary A novel nickel resistant, hyperaccumulatingN.crassa nir-2 mutant, isolated by us, sequestered 90% of Ni2+ from medium with 120 mg/l Ni2+. The parent wild strain showed comparable efficiency only at much lower concentrations (<10mg/l). The initial rapid rate and efficiency of Ni2+ removal could be maintained beyond 2 h by fresh addition of mycelial biomass. The results have been discussed from the stand point of the utility of metal resistant fungi in the control of environmental pollution. 相似文献
108.
Matthew D. Mazalouskas Raquel Godoy-Ruiz David J. Weber Danna B. Zimmer Richard E. Honkanen Brian E. Wadzinski 《The Journal of biological chemistry》2014,289(7):4219-4232
Serine/threonine protein phosphatase 5 (PP5, PPP5C) is known to interact with the chaperonin heat shock protein 90 (HSP90) and is involved in the regulation of multiple cellular signaling cascades that control diverse cellular processes, such as cell growth, differentiation, proliferation, motility, and apoptosis. Here, we identify PP5 in stable complexes with extracellular signal-regulated kinases (ERKs). Studies using mutant proteins reveal that the formation of PP5·ERK1 and PP5·ERK2 complexes partially depends on HSP90 binding to PP5 but does not require PP5 or ERK1/2 activity. However, PP5 and ERK activity regulates the phosphorylation state of Raf1 kinase, an upstream activator of ERK signaling. Whereas expression of constitutively active Rac1 promotes the assembly of PP5·ERK1/2 complexes, acute activation of ERK1/2 fails to influence the phosphatase-kinase interaction. Introduction of oncogenic HRas (HRasV12) has no effect on PP5-ERK1 binding but selectively decreases the interaction of PP5 with ERK2, in a manner that is independent of PP5 and MAPK/ERK kinase (MEK) activity, yet paradoxically requires ERK2 activity. Additional studies conducted with oncogenic variants of KRas4B reveal that KRasL61, but not KRasV12, also decreases the PP5-ERK2 interaction. The expression of wild type HRas or KRas proteins fails to reduce PP5-ERK2 binding, indicating that the effect is specific to HRasV12 and KRasL61 gain-of-function mutations. These findings reveal a novel, differential responsiveness of PP5-ERK1 and PP5-ERK2 interactions to select oncogenic Ras variants and also support a role for PP5·ERK complexes in regulating the feedback phosphorylation of PP5-associated Raf1. 相似文献
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110.