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Global gene expression analysis reveals a role for the alpha 1 integrin in renal pathogenesis. 总被引:7,自引:0,他引:7
N S Sampson S T Ryan D A Enke D Cosgrove V Koteliansky P Gotwals 《The Journal of biological chemistry》2001,276(36):34182-34188
Kidney fibrosis is the hallmark of most types of progressive kidney disease, including the genetic disorder Alport's syndrome. We undertook gene expression analysis in Alport's syndrome mouse kidneys using microchip arrays to characterize the development of fibrosis. In addition to matrix and matrix-remodeling genes, consistent with interstitial fibrosis, macrophage-related genes show elevated expression levels in Alport's syndrome kidneys. Immunohistochemical analysis of kidney sections illustrated that macrophages as well as myofibroblasts accumulate in the tubular interstitium. Deletion of alpha(1) integrin results in decreased accumulation of both myofibroblasts and macrophages in the tubular interstitium in Alport's syndrome mice and delays disease progression. Transforming growth factor beta antagonism, although reducing interstitial fibrosis, does not limit macrophage accumulation in the tubular interstitium and disease progression. In this study, we identified previously overlooked inflammatory events that occur in the tubulointerstitial region. We propose that in addition to the previously suggested role for the alpha(1)beta(1) integrin in mesangial expansion and abnormal laminin deposition, this integrin may be critical for monocyte accumulation that, in turn, may lead directly to renal failure. Our gene expression and immunohistochemical data indicate that macrophage accumulation is dependent on alpha(1) integrin expression on the macrophage cell surface and that anti-alpha(1) integrin strategies may be employed as therapeutics in the treatment of chronic inflammatory and fibrotic diseases. 相似文献
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Background
MicroRNAs are non-coding small RNAs of ~22 nucleotides that regulate the gene expression by base-paring with target mRNAs, leading to mRNA cleavage or translational repression. It is currently estimated that microRNAs account for ~ 1% of predicted genes in higher eukaryotic genomes and that up to 30% of genes might be regulated by microRNAs. However, only very few microRNAs have been functionally characterized and the general functions of microRNAs are not globally studied. 相似文献13.
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Ryo A Suzuki Y Ichiyama K Wakatsuki T Kondoh N Hada A Yamamoto M Yamamoto N 《FEBS letters》1999,462(1-2):182-186
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It is well recognized that diet-induced dysfunctions in skeletal muscle are closely related with many metabolic diseases,
such as obesity and diabetes. In the present study, we identified global changes in gender-dependent gene expressions in the
soleus muscle of lean and obese rats fed a high fat diet (HFD), using DNA microarray analysis. Prior to microarray analysis,
the body weight gains were found to be higher in male HFD rats than the female HFD rats. To better understand the detailed
phenotypic differences in response to HFD feeding, we identified differential gene expression in soleus muscle between the
genders. To this end, we extracted and summarized the genes that were up- or down-regulated more than 1.5-fold between the
genders in the microarray data. As expected, a greater number of genes encoding myofibrillar proteins and glycolytic proteins
were expressed higher in males than females when exposed to HFD, reflecting greater muscular activity and higher capacity
for utilizing glucose as an energy fuel. However, a series of genes involved in oxidative metabolism and cellular defenses
were more up-regulated in females than males. These results allowed us to conclude that compared to males, females have greater
fat clearing capacity in skeletal muscle through the activation of genes encoding enzymes for fat oxidation. In conclusion,
our microarray data provide a better understanding of the molecular events underlying gender dimorphism in soleus muscle,
and will provide valuable information in improving gender awareness in the health care system. 相似文献
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CMS-D8 and its restorer were developed by introducing the cytoplasm and nuclear gene Rf
2
from the wild diploid Gossypium trilobum (D8) into the cultivated tetraploid Upland cotton (Gossypium hirsutum). No information is available on how the Rf
2
gene interacts with CMS-associated genes and how CMS-D8 cytoplasm affects nuclear gene expression. The objective of this
study was to identify differentially expressed genes in anther tissues between the non-restoring fertile maintainer ARK8518
(rf
2
rf
2) and its isogenic heterozygous D8 restorer line, ARK8518R (Rf
2
rf
2) with D8 cytoplasm, by mRNA differential display (DD). Out of more than 3,000 DDRT-PCR bands amplified by 31 primer combinations
from 12 anchor primers and 8 arbitrary decamer primers, approximately 100 bands were identified as being qualitatively differentially
displayed. A total of 38 cDNA fragments including 12 preferentially expressed cDNA bands in anther were isolated, cloned and
sequenced. Reverse northern blot analysis showed that only 4 genes, including genes encoding a Cys-3-His zinc finger protein
and aminopeptidase, were up-regulated, while 22 genes, including genes for phosphoribosylanthranilate transferase (PAT), starch
synthase (SS), 4-coumarate-CoA ligase, electron transporter, calnexin, arginine decarboxylase, and polyubiquitin, were down-regulated
in the heterozygous restorer ARK8518R. The down-regulation of SS explains the lack of starch accumulation in sterile rf
2 pollen grains in the heterozygous restored plants. The molecular mechanism of CMS and its restoration, specifically the possible
roles of SS and PAT genes in relation to restoration of Rf
2 to CMS-D8, are discussed. This investigation represents the first account of such an analysis in cotton. 相似文献
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Serial analysis of gene expression in Plasmodium falciparum reveals the global expression profile of erythrocytic stages and the presence of anti-sense transcripts in the malarial parasite 总被引:9,自引:0,他引:9 下载免费PDF全文
Patankar S Munasinghe A Shoaibi A Cummings LM Wirth DF 《Molecular biology of the cell》2001,12(10):3114-3125