INT282599
From wiki-pain
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Sentences Mentioned In
Key: | Protein | Mutation | Event | Anatomy | Negation | Speculation | Pain term | Disease term |
Thus, other yet unknown factors influencing the expression of OCT-4 may be present in human endometrium. | |||||||||||||||
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To clarify the role of the POU domain transcription factor Oct4 in Adipose Tissue Stromal Cells (ATSCs), we investigated the regulation of Oct4 expression and other embryonic genes in fully differentiated cells, in addition to identifying expression at the gene and protein levels. | |||||||||||||||
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When Oct4 expression was recovered by exogenic Oct4 gene overexpression in damaged cells, ATSCs recovered to normal and viable cell with cell survival related signal pathway molecule such as Akt/PI3K, Bcl2, and ERK1/2. | |||||||||||||||
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We studied the effect of Oct4 overexpression on mesodermal lineage differentiation into fat, bone, and chondrocyte of ATSCs. | |||||||||||||||
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Our results show that ATSC can undergo an increase in developmental potential following reprogramming via the overexpression of the embryonic transcription factor, Rex1, Oct4, and Oct4-dependent Nanog and Sox2. | |||||||||||||||
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Our results show that ATSC can undergo an increase in developmental potential following reprogramming via the overexpression of the embryonic transcription factor, Rex1, Oct4, and Oct4-dependent Nanog and Sox2. | |||||||||||||||
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In a univariate regression model, the day of the menstrual cycle, using 3-day intervals, did not influence OCT-4 protein expression, when comparing an IRS <6 vs. ? | |||||||||||||||
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Thus, we can only rule out a profound influence of menstrual cycle-dependent changes of the human endometrium on OCT-4 expression. | |||||||||||||||
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Also, differential regulation of OCT-4 expression in women with endometriosis may be a worthwile target of investigation. | |||||||||||||||
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Menstrual cycle-dependency of OCT-4 expression has not been investigated to date.
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To clarify the role of Oct4 in adult cells, we investigated the regulation of Oct4 expression and other embryonic genes in fully differentiated cells, while identifying that it was also expressed at the gene and protein levels in ATSCs. | |||||||||||||||
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Furthermore, we demonstrated that blocking IL-6 abolished IL-17-induced up-regulation of hTERT and Oct-4 expression; however, blocking IL-17 failed to attenuate IL-6-induced up-regulation of hTERT and Oct-4 expression in KPCs. | |||||||||||||||
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However, IL-6-induced up-regulation of hTERT and Oct-4 expression was only negated by pre-treatment with IL-6 neutralizing antibody, not by IL-17 neutralizing antibody (Figure 5E). | |||||||||||||||
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To further delineate the relationship of IL-6 and IL-17 in the regulation of hTERT and Oct-4 expression in SKPs and KPCs, we pretreated cells with neutralizing antibody for either IL-17, or IL-6, or both followed by IL-17 exposure. | |||||||||||||||
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Furthermore, we demonstrated that blocking IL-6 abolished IL-17-induced up-regulation of hTERT and Oct-4 expression; however, blocking IL-17 failed to attenuate IL-6-induced up-regulation of hTERT and Oct-4 expression in KPCs. | |||||||||||||||
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All together, our results suggest that the IL-17/IL-6 axis may function to maintain the highly elevated IL-6 level in the distinct keloid niche with abilities to regulate key stem cell functions such as hTERT and Oct-4 expression, thus contributing to the formation of the benign keloid growth.
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