PubMed · 7752773
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J A Rowan, R A North. 1995-05-27. Abnormal liver function tests after pre-eclampsia.. https://doi.org/10.1016/s0140-6736(95)92565-1
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Marine picocyanobacteria of the genera Prochlorococcus and Synechococcus, the two most abundant phototrophs on Earth, thrive in oligotrophic oceanic regions. While it is well known that specific lineages are exquisitely adapted to prevailing in situ light and temperature regimes, much less is known of the molecular machinery required to facilitate occupancy of these low-nutrient environments. Here, we describe a hitherto unknown alkaline phosphatase, Psip1, that has a substantially higher affinity for phosphomonoesters than other well-known phosphatases like PhoA, PhoX, or PhoD and is restricted to clade III Synechococcus and a subset of high light I-adapted Prochlorococcus strains, suggesting niche specificity. We demonstrate that Psip1 has undergone convergent evolution with PhoX, requiring both iron and calcium for activity and likely possessing identical key residues around the active site, despite generally very low sequence homology. Interrogation of metagenomes and transcriptomes from TARA oceans and an Atlantic Meridional transect shows that psip1 is abundant and highly expressed in picocyanobacterial populations from the Mediterranean Sea and north Atlantic gyre, regions well recognized to be phosphorus (P)-deplete. Together, this identifies psip1 as an important oligotrophy-specific gene for P recycling in these organisms. Furthermore, psip1 is not restricted to picocyanobacteria and is abundant and highly transcribed in some α-proteobacteria and eukaryotic algae, suggesting that such a high-affinity phosphatase is important across the microbial taxonomic world to occupy low-P environments.
The specific effects of interferon alpha (IFNalpha), on the differentiation pathways of human osteogenic cells are not known. The aim of this study was to investigate possible effects of IFNalpha on osteogenic development by investigating cell differentiation, colony formation (colony forming unit-fibroblastic, CFU-F), cell proliferation, and gene expression, in particular bone morphogenetic protein (BMP) expression, of human bone marrow osteoprogenitor cells. Human bone marrow fibroblasts were cultured with or without the addition of IFNalpha (5-1,000 IU/ml) in the presence and absence of dexamethasone (10 nM) and ascorbate (100 microM), which are agents known to affect osteogenic differentiation. IFNalpha produced a significant dose-dependent inhibition of cell proliferation and alkaline phosphatase specific activity at concentrations as low as 50 IU/ml. IFNalpha (50-1,000 IU/ml) inhibited the stimulation of alkaline phosphatase specific activity induced by ascorbate and dexamethasone. Examination of CFU-F showed dose- and time-dependent inhibitions of colony formation and reductions in both colony size and alkaline phosphatase-positive CFU-F colonies particularly at earlier times. Reactivity with an antibody specific for osteoprogenitors (HOP-26), was reduced in IFNalpha-treated cultures. Northern blot analysis showed a significant dose-dependent up-regulation of BMP-2 mRNA, estrogen receptor alpha mRNA and osteocalcin mRNA expression in ascorbate/dexamethasone cultures. In contrast, IFNalpha significantly inhibited BMP-2 mRNA expression in the absence of ascorbate and dexamethasone. In conclusion, IFNalpha inhibits human osteoprogenitor cell proliferation, CFU- F formation, HOP-26 expression, and alkaline phosphatase specific activity and modulates BMP-2 gene expression. These results suggest a role for IFNalpha in local bone turnover through the specific and direct modulation of osteoprogenitor proliferation and differentiation.
We evaluated the expression and activity of rat 12-lipoxygenase (LO) in rat intestinal epithelial (RIE) cells during apoptosis and cell differentiation. Sodium butyrate (NaBT) treatment induced wild-type RIE (W-RIE) cells to undergo differentiation and apoptosis. Alkaline phosphatase (ALP) activity, a marker of cell differentiation, and DNA fragmentation, an index of apoptosis, were increased by NaBT treatment. Arachidonic acid was metabolized primarily to 12-hydroxyeicosatetraenoic acid (HETE) suggesting induction of 12-LO activity. In contrast, sense-RIE (S-RIE) cells engineered to overexpress COX-2 were resistant to apoptosis by treatment with 5 mM NaBT and NaBT did not induce 12-LO activity. The upregulation of 12-LO expression by NaBT in W-RIE cells was confirmed at both the transcriptional and translational level but 12-LO was undetectable in S-RIE cells following NaBT treatment. The expression of 12-LO mRNA in W-RIE cells occurs as early as 6 h after treatment and reaches maximum expression at 24 h following treatment. This inducible 12-LO was isolated by RT-PCR and identified as rat "leukocyte-type" 12-LO. The level of 12-LO expression in W-RIE cells was dependent on the concentration of NaBT and appears to reflect the extent of cell differentiation. NDGA, a lipoxygenase inhibitor, attenuated induction of ALP activity by NaBT treatment of W-RIE cells. These observations suggested that 12-LO is regulated by treatment with NaBT and is associated with cell differentiation in rat intestinal epithelial cells.