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S Sanfilippo

Publications and source records attributed to S Sanfilippo.

At least 19 recordsLinked to original sources
PubMed2005

Action of prolactin, IFN-gamma, TNF-alpha and LPS on heme oxygenase-1 expression and VEGF release in human monocytes/macrophages.

The pituitary hormone prolactin (PRL) has recently been regarded as a local regulator of macrophage responses. Our goal in this study was to investigate the regulatory interaction between PRL, interferon-gamma (IFN-gamma), tumor necrosis factor-alpha (TNF-alpha) and lipopolysaccharide (LPS) in the heme oxygenase-1 (HO-1) expression and the vascular endothelial growth factor (VEGF) production in human monocytes/macrophages (HMMs). In vitro treatment of HMMs with PRL, IFN-gamma, TNF-alpha and LPS was found to increase both HO-1 expression and protein synthesis in a time-dependent manner. HMMs treated with PRL, IFN-gamma, TNF-alpha and LPS also showed an enhanced release of VEGF. Moreover, co-stimulation of PRL with LPS caused activation of HMMs functions, enhancement of HO-1 expression and induction of VEGF release, whereas addition of PRL inhibited up-regulation of HO-1 or VEGF induced by IFN-gamma or TNF-alpha. Our results demonstrate that PRL, IFN-gamma, TNF-alpha and LPS modulate the expression of angiogenic factors providing additional information about the regulatory mechanism, which controls the angiogenic function of macrophages.

Heme Oxygenase (Decyclizing)↗
PubMed2004

Prolactin increases HO-1 expression and induces VEGF production in human macrophages.

The pituitary hormone prolactin (PRL) is a multifunctional polypeptide which exerts a role on cell proliferation and may also contribute to cell differentiation. PRL is also produced by immune cells and is regarded as a key component of the neuroendocrine-immune loop and as a local regulator of macrophage response. The involvement of PRL in regulating monocyte/macrophage functions is suggested by the presence of PRL receptors in these cells. It has been shown that PRL possess both angiogenic and antiangiogenic effects. Recently, we revealed that augmentation of HO-1 activity enhances PRL-mediated angiogenesis in human endothelial cells. Since macrophages are key participants in angiogenesis our objective was to investigate the effect of PRL also in human macrophages. In vitro treatment of macrophages with PRL was found to increase both heme oxygenase-1 (HO-1) expression and protein synthesis in a time and dose dependent manner as quantified respectively by reverse-transcriptase real-time polymerase chain reaction and Western blot analysis. PRL-treated macrophages also showed an enhanced release of vascular endothelial growth factor (VEGF) as demonstrated by ELISA assay. Furthermore, to determine whether PRL-induced HO-1 activity was required for VEGF production by macrophages, the effect of PRL on the induction of VEGF was studied in the presence of an inducer stannic chloride (SnCl(2)) and of an inhibitor stannic mesoporphyrin (SnMP) of HO activity. Our observations suggest that PRL may regulate monocyte activation and influences not only immune function but also angiogenesis.

Blotting, Western↗
PubMed2001

Early events of secretory granule formation in the rat parotid acinar cell under the influence of isoproterenol. An ultrastructural and lectin cytochemical study.

The events involved in the maturation process of acinar secretory granules of rat parotid gland were investigated ultrastructurally and cytochemically by using a battery of four lectins [Triticum vulgaris agglutinin (WGA), Ulex europaeus agglutinin I (UEA-I), Glycine max agglutinin (SBA), Arachys hypogaea agglutinin (PNA)]. In order to facilitate the study, parotid glands were chronically stimulated with isoproterenol to induce secretion. Specimens were embedded in the Lowicryl K4M resin. The trans-Golgi network (TGN) derived secretory granules, which we refer to as immature secretory granules, were found to be intermediate structures in the biogenesis process of the secretory granules in the rat parotid acinar cell. These early structures do not seem to be the immediate precursor of the mature secretory granules: in fact, a subsequent interaction process between these early immature granule forms and TGN elements seems to occur, leading, finally, to the mature granules. These findings could explain the origin of the polymorphic subpopulations of the secretory granules in the normal acinar cells of the rat parotid gland. The lectin staining patterns were characteristic of each lectin. Immature and mature secretory granules were labelled with WGA, SBA, PNA, and lightly with UEA-I. Cis and intermediate cisternae of the Golgi apparatus were labelled with WGA, and trans cisternae with WGA and SBA.

Acetylgalactosamine↗
PubMed1999

Lectin binding sites in parotid acinar secretory granules of normal and isoproterenol treated rat.

Lectin staining patterns in secretory granules of rat parotid gland acinar cell of untreated and isoproterenol-injected animals were examined by electron microscopy. We used four lectin-gold complexes: Ulex europaeus agglutinin I (UEA-I), Helix pomatia agglutinin (HPA), wheat germ agglutinin (WGA), Glycine max agglutinin (SBA). Specimens were low temperature embedded in the hydrophilic Lowicryl K4M resin. The normal acinar cells produced glycoconjugates which were positive for all of the lectins used and with a characteristic topographic distribution in relation to the morphological type of granule. The cells of isoproterenol-treated rat showed marked ultrastructural changes in the size and structure of granules; significant changes in lectin binding sites in the granules were also observed.

Animals↗
PubMed1996

Effects of corticotropin-releasing hormone on ovarian estrogen production in vitro.

It is a common clinical observation that stress is accompanied by dysfunction of the hypothalamic-pituitary-ovarian axis, and there is mounting experimental evidence that CRH, the principal regulator of ACTH release and the central coordinator of the stress response, is able to suppress gonadal function by inhibiting hypothalamic GnRH release. Recently, it has been shown that immunoreactive CRH, CRH messenger RNA, and CRH receptors are also present in the ovary. This prompted us to examine the role of CRH on ovarian function. To accomplish this, we studied the effects of this neuropeptide on estrogen production and cAMP intracellular content from rat granulosa and human granulosa-luteal cells. We also evaluated the activity of the enzyme aromatase by measuring the production of tritiated water from homogenates of cultured rat granulosa cells. CRH inhibited FSH-stimulated estrogen production from rat granulosa cells in a dose-dependent fashion. The maximal effect was achieved at a concentration of 10(-8) M, which suppressed estrogen production by about 30%. Low concentrations of CRH (10(-10) M), incapable of modulating maximal estrogen production in response to FSH, provoked a right-ward shift of the estrogen dose-response curve to FSH. CRH (10(-8) M) suppressed the production of tritiated water (equivalent to estrogen production) from homogenates of rat granulosa cells incubated with a half-maximal concentration of FSH. Basal estrogen production by human granulosa-luteal cells was also inhibited by CRH at a concentration of 10(-10) M. The maximal effect was achieved with a concentration of 10(-8) M, which lowered estrogen production by 25%. The CRH receptor antagonist alpha-helical CRH-(9-41) antagonized the inhibitory effect of CRH on estrogen production from rat granulosa and human granulosa-luteal cells, whereas alone it had no effect. CRH did not have any effect on the intracellular cAMP content of rat granulosa and human granulosa-luteal cells. In conclusion, these results suggest that CRH is able to suppress estrogen production from rat and human granulosa cells in vitro. This effect seems to be linked to inhibition of aromatase activity in the rat and is independent of cAMP generation. We speculate that CRH may also interfere with hypothalamic-pituitary-gonadal axis function by acting directly at the ovarian level.

Animals↗
PubMed1995

Effects of a tryptophan deficient diet on the morphology of skeletal muscle fibers of the rat. Preliminary observations at neuroendocrinological and submicroscopical levels.

It is proposed an animal model consisting of young male, L-tryptophan-deprived, namely 5-HT-free rats since their ontogenesis. This was obtained by feeding their mothers with a L-tryptophan-free (tf) diet since the day 1 of pregnancy. They were studied and compared with control rats of the same ages fed with a complete diet. Already at birth tf-litters were significantly underdeveloped as compared to the control newborn rats. Postnatal growth was in the tf-rats so poor that it worsened into a stricking dwarfism characterized by physical immaturity, muscular hypotrophy with alterations of motor activity and impairment of the hypothalamo-pituitary-axis. A radioimmunological study of growth hormone (GH) showed in tf-rats dramatic low plasma levels of the hormone, thus confirming the existence of serotonergic hypothalamo-pituitary pathways for GH in normal animals. By histological and ultrastructural examinations, hypotrophy and degenerative alterations of the muscle fibers could be observed. The possible causes for this finding are extensively considered and discussed.

Animals↗
PubMed1988

Facial midline defect in the fetal alcohol syndrome: embryogenetic considerations in two clinical cases.

We report on two unrelated patients with fetal alcohol syndrome with hypoplasia of the periocular region, resulting in a low and narrow forehead and hypotelorism. Other typical manifestations of the syndrome involving the facial midline are also present. These observations can be added to clinical and experimental evidence from other authors, supporting the concept that the facial anomalies of the fetal alcohol syndrome are the expression of a midline defect originating from the disruption of the ordered development of midline mesoderm cells during early embryogenesis.

Child↗
PubMed1988

IVIC syndrome: report of a second family.

The IVIC syndrome derives its name from the Instituto Venezolano de Investigaciones Cientìficas, where it was described by Arias et al. [Am J Med Genet 6:25-59, 1980]. We report on several individuals in a family with the IVIC syndrome, the second described in the literature. In this family there are 3 affected individuals in 2 generations. This observation shows that the IVIC syndrome is not a private syndrome, and confirms that it is due to an autosomal dominant mutation.

Abnormalities, Multiple↗
PubMed1980

Visual acuity and binocularity in unilateral high myopia.

Thirty-eight patients with unilateral high myopia ranging from 5 to 19 diopters were followed up for a median of two years. All were treated with full-spectacle correction and most had occlusion. When initially examined one patient (3%) had visual acuity of 6/12 (20/40) or better, four patients (12%) had central fusion, and 24 patients (63%) were phoric. At the conclusion of the study 12 patients (32%) had visual acuities of 6/12 (20/40) or better, 17 patients (45%) had central fusion, and 29 patients (76%) were phoric. Age at the start of treatment was not a factor in the versely affect the response to amblyopia was inversely related to both final fusion and final visual acuity.

Adolescent↗
PubMed1976

Cyclic esotropia developing after sttstrabismus surgery.

Cyclic or alternate-day esotropia developed in a patient following strabismus surgery for intermittent exotropia, which resulted in a small overresponse or overcorrection. Surgery, aimed at the deviation on the esotropic days, resulted in binocularity and loss of the cyclic pattern.

Age Factors↗