INT245172
From wiki-pain
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Sentences Mentioned In
Key: | Protein | Mutation | Event | Anatomy | Negation | Speculation | Pain term | Disease term |
According to present data, among the factors identified in the antler, only Midkine is significantly overexpressed in the antler velvet with respect to normal skin, suggesting a possible role promoting fast axonal growth. | |||||||||||||||
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The only exception is Midkine, which was significantly overexpressed in the velvet respect to frontal skin samples, though not respect to pedicle skin. | |||||||||||||||
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Only Midkine expression appeared significantly upregulated in velvet compared to frontal samples, although it remained unchanged compared to pedicle. | |||||||||||||||
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Midkine expression was increased in pancreatic cancer cell lines and pancreatic cancer tissues. | |||||||||||||||
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In contrast, Ad5MK had no effect on AsPC-1 cells as far as the designated conditions, although these cells showed strong midkine expression. | |||||||||||||||
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MK expression increased 10-fold during cell culture without hormones or serum. | |||||||||||||||
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Midkine mRNA expression was strong in AsPC-1 and CFPAC-1 cells, but it was weak in MIAPaCa-2 cells. | |||||||||||||||
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While these observations provided a potential mechanism for the integration of GC and retinoid effects in late gestation fetal lung development, whether GC and RA also influence MK gene expression during postnatal lung development remained unknown. | |||||||||||||||
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Midkine expression is increased in various human tumors, including gastrointestinal cancers [19-22]. | |||||||||||||||
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Both midkine mRNA expression and midkine protein expression were strong in AsPC-1 and CFPAC-1 cell liens, moderate in BxPC-3, HPAC, and Suit-2 cell lines, and weak in PANC-1 and MIAPaCa-2 cell lines. | |||||||||||||||
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Midkine expression is increased in a number of malignant tumors, including esophageal, stomach, colon, hepatocellular, breast and pancreatic carcinoma, when compared with the level of expression in adjacent non-cancerous tissues [19-22]. | |||||||||||||||
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Both midkine mRNA expression and midkine protein expression were strong in AsPC-1 and CFPAC-1 cell liens, moderate in BxPC-3, HPAC, and Suit-2 cell lines, and weak in PANC-1 and MIAPaCa-2 cell lines. | |||||||||||||||
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High levels of MK expression are observed at embryonic day (E)13-16.5 and then again at postnatal days 5-12, primarily in respiratory epithelium early in lung development and increasingly localized to lung stroma and pulmonary blood vessels postnatally [21]. | |||||||||||||||
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We hypothesized that MK expression in both lungs and in isolated AT2 cells would be decreased by corticosteroids and increased by RA.
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DEX treatment of rat pups decreased, and RA treatment increased lung MK expression, whereas concurrent DEX+RA treatment prevented the DEX-induced decrease in MK expression. | |||||||||||||||
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Further, in the normal developing lung, MK expression increases from PN2, peaks at PN4, and decreases thereafter [8]. | |||||||||||||||
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This finding is in concordance with Matsuura et al. who showed a transient increase in MK expression in normal lungs between two to seven days postnatally [8]. | |||||||||||||||
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Using human alveolar type 2 (AT2)-like cells differentiated in culture, we confirmed that DEX and cAMP decreased, and RA increased MK expression.
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Midkine mRNA expression was strong in AsPC-1 and CFPAC-1 cells, but it was weak in MIAPaCa-2 cells. | |||||||||||||||
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Both midkine mRNA expression and midkine protein expression were strong in AsPC-1 and CFPAC-1 cell liens, moderate in BxPC-3, HPAC, and Suit-2 cell lines, and weak in PANC-1 and MIAPaCa-2 cell lines. | |||||||||||||||
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