PubMed Health⌕ Search

Biomedical subjects

A Maggi

Publications and source records attributed to A Maggi.

137 records · Page 8Linked to original sources
PubMedDate not supplied

5-Lipoxygenase gene expression in HL60 cells during differentiation with DMSO.

The model of promyelocytic leukemia cells HL60 was utilized to study the accumulation of 5-lipoxygenase mRNA during the cellular differentiation induced by DMSO. In the present study a strict correlation between the increase in state of differentiation of HL60 and accumulation of 5-lipoxygenase mRNA is demonstrated, indicating that HL60 cells are an interesting model for the study of drugs which could interfere with the synthesis of the enzyme.

Arachidonate 5-Lipoxygenase↗
PubMedDate not supplied

Growth hormone regulation of growth hormone-releasing hormone gene expression.

Slot-blot hybridization technique was used to evaluate growth hormone-releasing hormone (GHRH) mRNA levels in the hypothalamus of long-term (14 days) hypophysectomized (HPX) rats treated or not with 125 micrograms hGH/rat, twice daily IP, since the first day postsurgery. In addition, mRNA levels were determined in the hypothalamus of short-term (4 days) GH-treated (250 micrograms hGH/rat, twice daily IP) intact rats. GHRH mRNA levels were increased in HPX rats, and GH treatment partially counteracted this rise. Short-term administration of GH decreased GHRH mRNA levels in intact rats. These results, evaluated together with previous findings showing decreased hypothalamic GHRH-like immunoreactivity in both HPX rats and intact rats given GH (6, 7, 9), indicate that GH exerts a negative feedback action on the synthesis and release of GHRH.

Animals↗
PubMedDate not supplied

Reduced growth hormone releasing factor (GHRF)-like immunoreactivity and GHRF gene expression in the hypothalamus of aged rats.

Growth hormone releasing factor-like immunoreactivity (GHRF-LI) and GHRF mRNA levels were evaluated in the hypothalamus of aged (24 months) and young (3 months) rats by semiquantitative immunocytochemistry and slot blot hybridization technique, respectively. Simultaneous detection of reduced GHRF-LI and GHRF mRNA levels in aged rats as compared to young counterparts demonstrates the existence in aged rats of an impaired function of GHRF-producing neurons.

Aging↗
PubMedDate not supplied

Testosterone and GHRH gene expression in adult and old rats.

The effect of castration and testosterone replacement on GHRH gene expression was evaluated in adult male rats. Castration for 21 days did not affect GHRH mRNA levels, and also ineffective in this context was acute or chronic administration of testosterone to castrated rats. Hypothalamic GHRH mRNA was significantly reduced in aged male rats, but restoration of plasma testosterone concentrations via implanted capsules did not modify the low levels of GHRH mRNA. All in all, these findings support the notion that in adult and aged male rats GHRH-producing structures are insensitive to androgens.

Aging↗
PubMedDate not supplied

Brain cytochromes P-450 are responsive to phenobarbital and tricyclic amines.

Cytochrome P-450 form b has been detected for the first time in rat brain by cross-hybridization of poly(A+) RNA with a radiolabelled cDNA probe. The cross-hybridizable material was easily detectable in rats after treatment with phenobarbital but not in untreated rats. Moreover, treatment of rats with amitriptyline or imipramine, tricyclic antidepressants in wide therapeutic use for depression, markedly increases the amount of RNA species hybridizing with P-450b cDNA probe in comparison to untreated controls. These observations raise the issue of a possible role for brain cytochromes P-450 in the metabolism of drugs such as the tricyclic antidepressants.

Animals↗
PubMedDate not supplied

Expression of the estrogen-regulated gene Nip2 during rat brain maturation.

The present study stems from previous observations demonstrating that in the neuroblastoma cell line SK-ER3 the mRNA content of the pro-apoptotic gene Nip2 is decreased following treatment with estradiol. We investigate the content of Nip2 mRNA during the maturation of rat embryo brain and we show that Nip2 mRNA is very low at embryo day 15 and steadily increases up to day 20. At day 21 Nip2 mRNA is decreased almost to the low levels observed in the mature brain. Studies in neurons from rat embryo at day 18 show that Nip2 mRNA content is significantly decreased by exposure to estradiol at 1 nM concentration demonstrating that the observations previously done in the SK-ER3 neuroblastoma cell line can be reproduced in neurons in culture. The finding that estrogens may modulate the activity of Nip2 gene activity may be of relevance not only with regard to the effects of estradiol on brain maturation, but also for the understanding of the neuroprotective effects recently described for this hormone.

Animals↗
PubMedDate not supplied

Estrogens, apoptosis and cells of neural origin.

In mammals, estrogens have a multiplicity of effects in all known neural cells. We review here some of the mechanisms enabling estrogens to differentiate their influence on neural targets. In view of the potential interest in the use of estrogens in the therapy of several pathologies of the nervous system, we have proposed the use of a reductionist approach for the systematic understanding of estrogen activities in each specific type of target cell. We have therefore generated a model system in which to study the activation of one of the known estrogen receptors: estrogen receptor alpha. This system allowed us to identify a number of novel genes, the expression of which may be influenced following the activation of this receptor subtype by estradiol. We here report on preliminary data obtained by the study of one of these target genes, nip2, which encodes a proapoptotic protein product. We hypothesize that Nip2 might be an important molecular determinant for estrogen anti-apoptotic activity in cells of neural origin.

Apoptosis↗