Accumulation and spatial location of aldose reductase mRNA in a lens tumor of an alpha A-crystallin/SV40 T antigen transgenic mouse line.
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Aldehyde Reductase↗
Biomedical subjects
C Bondy
Publications and source records attributed to C Bondy.
Cellular pattern of insulin-like growth factor-I (IGF-I) and IGF-I receptor gene expression in the developing and mature ovarian follicle.
We have employed in situ hybridization histochemistry to map the cellular pattern of insulin-like growth factor-I (IGF-I) and IGF-I receptor gene expression in developing rat ovaries from the time of birth through adulthood, and in response to hypophysectomy and gonadotropin replacement. From the early postnatal period, both IGF-I and IGF-I receptor messenger RNAs (mRNAs) were highly abundant and evenly distributed in granulosa cells of small, growing follicles. In large follicles, however, IGF-I gene expression was heterogeneous. IGF-I mRNA was most abundant in granulosa cells lining the antrum and surrounding the oocyte, but was low or undetectable in mural granulosa cells of Graafian follicles, and was also undetectable in luteinized granulosa cells of corpora lutea. IGF-I receptor mRNA was evenly distributed in developing and mature follicles and was highly abundant in the luteinized granulosa cells of corpora lutea. IGF-I receptor but not IGF-I mRNA was detected in growing oocytes. Hypophysectomy resulted in a decrease and treatment with PMSG resulted in an increase in follicular IGF-I receptor mRNA levels, whereas there was no change in IGF-I mRNA levels in the same protocol. In summary, high levels of both IGF-I and IGF-I receptor gene expression occur in the granulosa cells of actively growing follicles, suggesting that granulosa cell IGF-I may have a role in follicular or oocyte growth. IGF-I gene expression is lost concomitant with follicular enlargement and granulosa cell differentiation, whereas IGF-I receptor gene expression continues at high levels in luteinized granulosa cells, suggesting that IGF effects on differentiated granulosa cell function are due to circulating, not local, hormone. Finally, granulosa cell IGF-I receptor gene expression appears to be regulated by the gonadotropin present in pregnant mare serum.
Animals↗
Prevalence of thyroid abnormalities in patients with dermatitis herpetiformis and in control subjects with HLA-B8/-DR3.
PURPOSE: The prevalence of thyroid dysfunction as measured by the presence of overt thyroid disease, abnormal results of thyroid function tests, or antithyroid antibodies was compared in patients with dermatitis herpetiformis (DH) and a normal control group who had the HLA-B8/-DR3 haplotype. PATIENTS AND METHODS: The study population consisted of 56 patients with DH and 26 control subjects with the HLA-B8/-DR3 haplotype. All were examined for thyroid function abnormalities and thyroid autoantibodies. RESULTS: Patients with DH had a statistically significant increase in the prevalence of abnormal thyroid function test results and autoantibodies: 32% versus 4% for controls (Z = 2.01, p less than 0.02). In patients with DH, hypothyroidism was the most common thyroid abnormality (12 of 56) followed by hyperthyroidism (four of 56). Two patients had normal thyroid function test results with thyroid autoantibodies. Risk factors for thyroid abnormalities in patients with DH were increasing age (chi 2 = 6.55, p less than 0.02, significant) and the presence of thyroid microsomal antibodies. The HLA-B8/-DR3 haplotype was not a risk factor for thyroid abnormalities. CONCLUSION: The findings suggest that thyroid disease is independently associated with DH. Examination of patients with DH should include thyroid function tests along with assays for antithyroid antibodies.
Adult↗
Aldose reductase messenger RNA in the lens epithelium in vivo: effects of diabetes mellitus and galactosaemia.
1. Quantitative in situ hybridization histochemistry was used to examine the regulation of aldose reductase messenger RNA in the rat lens after the induction of diabetes mellitus or after feeding a 50% (w/w) galactose diet. 2. Although increased staining for aldose reductase in the lens epithelium has previously been observed by immunohistochemistry after 3 weeks of diabetes or after 7 days of galactose feeding, we have not been able to detect any increase in the amount of aldose reductase messenger RNA in these cells as compared with controls (113 +/- 7%, 105 +/- 9%, 100 +/- 7%, respectively) at these time points (P greater than 0.05). 3. After 15 days of galactose feeding, however, there was a significant increase of 140% (+/- 12%) in the amount of aldose reductase messenger RNA in the lens epithelial cells as compared with controls (P = less than 0.001). 4. These results demonstrate that increased availability of galactose, a high-affinity substrate for the enzyme, leads to increased aldose reductase messenger RNA, which suggests a role for aldose reductase in sugar metabolism in the lens.
Aldehyde Reductase↗
Feedback inhibition of aldose reductase gene expression in rat renal medulla. Galactitol accumulation reduces enzyme mRNA levels and depletes cellular inositol content.
Aldose reductase (AR) is an enzyme responsible for converting glucose into sorbitol and galactose into galactitol. In the renal inner medulla, where sorbitol production plays a role in cellular osmoregulation, AR gene expression has been shown to be osmotically regulated. The present study examined the effects of the accumulation of the AR end product, galactitol, induced by galactose feeding, on AR gene expression and on the balance of other cellular osmolytes, including inositol, in the renal medulla. To differentiate between the effects of excess substrate, product, and intervening osmotic factors, rats were fed either control, galactose, galactose and sorbinil (an AR inhibitor), or control plus sorbinil diets. Renal papillae were assayed for AR mRNA, sodium, urea, galactose, galactitol, sorbitol, inositol, and other organic osmolytes. Galactose feeding resulted in a great accumulation of galactitol and reduction in AR mRNA levels in renal papillae. Associated with these changes was a significant depletion of renal papillary sorbitol, inositol, and glycerolphosphocholine. These effects were largely attenuated by sorbinil. The present findings suggest that renal cellular accumulation of the enzyme's polyol product causes downregulation of AR gene expression. Furthermore, our findings suggest that the inositol depletion associated with sorbitol or galactitol accumulation in various cell types during hyperglycemia may be a function of cellular osmoregulation.
Aldehyde Reductase↗