Aldose reductase (AR) is implicated in the pathogenesis of the diabetic complications and osmotic cataract. AR has been identified as an osmoregulatory protein, at least in the renal medulla. An outstanding question relates to the response of AR gene expression to diet-induced galactosemia in extrarenal tissues. This paper shows that AR gene expression in different tissues is regulated by a complex multifactorial mechanism. Galactose feeding in the rat is associated with a complex and, on occasions, multiphasic pattern of changes in AR mRNA levels in kidney, testis, skeletal muscle, and brain. These changes are not in synchrony with the temporal sequence of changes in tissue galactitol, galactose, and myoinositol concentrations. Moreover, galactose feeding results in changes in tissue AR activities that are not related, temporally or quantitatively, to the alterations in tissue AR mRNA or galactitol levels. It is concluded that AR gene expression and tissue AR activities are regulated by mechanisms that are not purely dependent on nonspecific alterations in intracellular metabolite concentrations. This conclusion is supported by the finding that chronic xylose feeding, despite being associated with intracellular xylitol accumulation, does not result in alterations in AR mRNA levels, at least in the kidney. (J. Clin. Invest. 1993. 92:155-159.)
The redistribution of platelet membrane glycoprotein IV (GPIV) and the release of intracellular alpha-granule thrombospondin (TSP) were examined and the inhibition of beta-thromboglobulin (beta-TG) and platelet factor 4 (PF4) in patients with chronic myelogenous leukemia (CML) was observed and quantitation of beta-TG and PF4 in sera was conducted. GPIV in inactive platelet from CML was 36080 +/- 17010 molecules/platelet as compared with 13190 +/- 4810 from the controls (P < 0.01). No abnormality was found in the distribution of platelet membrane GPIb and GPIIb/IIIa (P > 0.05). The GPIV redistribution on active platelet membrane induced thrombin (IU/ml) from CML and healthy donors was 44320 +/- 32310 and 22800 +/- 12700 molecules/platelet respectively (P < 0.01). The difference in the release of intracellular alpha-granule TSP between CML and the control group was not found (P > 0.05). There was no direct correlation between GPIV expression and TSP binding after platelet activation. The high levels of beta-TG and PF4 in sera inhibited release of intracellular alpha-granule TSP in vitro. These results indicate that the abnormality of platelet membrane GPIV is a common marker in CML, therefore the specific increase of platelet GPIV in patients with CML may be a useful tool for the diagnosis and monitoring of the platelet dysfunction. The release of internal TSP pools is hindered by either beta-TG or PF4 in sera.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.