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Biomedical subjects

P Ronco

Publications and source records attributed to P Ronco.

At least 73 records · Page 4Linked to original sources
PubMed1992

Regulation by calcitonin of Na(+)-K(+)-Cl- cotransport in a rabbit thick ascending limb cell line.

The hormonal regulation of a Na(+)-K(+)-Cl- cotransport was investigated in a renal tubule cell line (RC.SV2 cells) transformed by the simian virus 40. This cell line has the main characteristics of cells from the thick ascending limb of Henle, including the presence of Tamm-Horsfall protein and stimulation of adenosine 3',5'-cyclic monophosphate (cAMP) production by calcitonin (CT). Kinetic studies with 22Na+, 36Cl-, and 86Rb+ indicated the existence of a Na(+)-K(+)-Cl- cotransport with a stoichiometry of 1Na+:1K+: 2Cl-. All compounds stimulating cAMP production enhanced the ouabain-resistant bumetanide-sensitive (Or-Bs) Rb+ influx mediated by Na(+)-K(+)-Cl- cotransport. CT (100 ng/ml) increased the Or-Bs influx twofold by enhancing maximum velocity without changing the apparent Michaelis constant. The K(+)-channel blocker barium blunted the CT-stimulated Or-Bs influx by 64-74%, whereas the Cl(-)-channel blocker 5-nitro-2-(3-phenylpropylamino)benzoate reduced the CT-stimulated influx by 28-40%. These results suggest that CT stimulates the Na(+)-K(+)-Cl- cotransport by a cAMP-dependent mechanism and that K+ recycling through K+ membrane channels is an important modulator of cotransporter-mediated ion fluxes.

Animals↗
PubMed1992

Nephropathy associated with infection by human immunodeficiency virus: a report on 11 cases including 6 treated with zidovudine.

The human immunodeficiency virus (HIV) was recently suggested to be involved in generating kidney lesions in HIV-associated nephropathy (HIVN). The possibility that antiretroviral agents can slow down the usually explosive evolution of HIVN to end-stage renal failure (ESRF) has not been studied in many of the series of cases published. The present work is a retrospective analysis of 11 patients with histologically proven HIVN, 6 of whom were treated with zidovudine. Seven patients (group 1) either required dialysis at the outset, when HIVN was diagnosed, or progressed very fast to ESRF within 15-45 days. Two patients of this group were treated with zidovudine, but it had no effect on kidney function. In the remaining 4 patients (group 2), HIVN progressed more slowly than in group 1. All 4 patients were treated with zidovudine at an earlier stage of the disease than ESRF. Only 1 deteriorated to ESRF in 9 months. The 3 others, who did not have ESRF, were followed up for 13, 10 and 32 months, respectively. Although this is a preliminary study, its results do suggest that zidovudine can slow down the evolution of HIVN to ESRF. They highlight the need to screen HIV-positive patients regularly for proteinuria, in order to detect HIVN by renal biopsies at an early stage of renal lesion formation.

AIDS-Associated Nephropathy↗
PubMed1992

[Mechanism of action and catabolism of atrial natriuretic factor in cultured human and animal kidney cells].

Cultures of renal cells from human or animal origins have allowed the modes of action and the degradation pathways of atrial natriuretic factor (ANF) to be characterized. Human glomerular mesangial and epithelial cells possess ANF receptors of both types, only clearance receptors (C) in mesangial cells, receptors with guanylate cyclase activity (A) and C receptors in epithelial cells which are, in addition, equipped with ectoenzymes rapidly degrading extracellular ANF. Epithelial cells which have been stimulated by ANF secrete cyclic guanosine monophosphate (cGMP) at their apical side. Vascular smooth muscle cells prepared from the rabbit renal cortex also possess A receptors of high affinity and C receptors. Neutral endopeptidase (NEP), an enzyme of which ANF is a specific substrate in the kidney, is expressed at the cell surface. Its expression is inhibited by factors present in the serum and is increased by glucocorticoids. Principal cells of the collecting duct are also a target for ANF via A and C receptors. Taken together, these studies demonstrate that the kidneys are sites both for the physiological effects and the degradation of ANF. Production of cGMP results in vasodilation in the renal cortex, increase of glomerular filtration rate and decrease of sodium reabsorption in the collecting duct. Degradation of ANF occurs via two different ways, its conversion into inactive peptides by NEP and its internalization after binding to C receptors.

Animals↗
PubMed1992

Association of chronic interstitial cystitis, protein-losing enteropathy and paralytic ileus with seronegative systemic lupus erythematosus: case report and review of the literature.

We report the case of a female patient with seronegative lupus and predominant bladder and intestinal involvement in the form of interstitial cystitis and protein-losing enteropathy. This association is exceptional in the literature but may be underestimated because of frequent latency of interstitial cystitis. It may define a peculiar subgroup of lupus patients usually responsive to steroid therapy. In this case, only cyclophosphamide markedly improved the protein-losing enteropathy but did not influence the bladder disease.

Adult↗
PubMed1992

Coexpression in humans by kidney and fetal envelopes of a 280 kDa-coated pit-restricted protein. Similarity with the murine target of teratogenic antibodies.

Experimental studies performed in the rat over the last three decades have shown that antibodies raised against kidney or yolk sac, which, in the rat, surrounds the embryo and serves as a placenta during the major part of pregnancy, induced fetal resorptions or malformations. It is generally considered that the teratogenic antibodies decrease internalization and degradation of maternal proteins by yolk sac epithelial cells leading to an inadequate supply of nutriments to the embryo. These observations demonstrating the pathogenic role of antibodies to fetal envelopes are of great potential interest in clinical pathology since most cases of fetal malformations in humans are of unknown cause. The authors have recently shown that the key teratogenic antibodies in the murine system were directed against a 280 kDa-coated pit protein (gp280) specific for the brush border of epithelial cells lining the renal proximal tubule and the yolk sac. This observation allows for the unique opportunity to search for a similar system in humans. In this study, the presence in humans of a protein closely related to murine gp280 is shown, as indicated by extensive immunologic crossreactivity, close apparent molecular weights, strong homology of bidimensional peptide maps, and restricted distribution at the organ and subcellular level. In addition to kidney and yolk sac, human gp280 was also detected within the coated pits of the placental syncytiotrophoblastic cells. When introduced in an in vitro rat embryo culture system, antibodies to human gp280-induced developmental anomalies in a dose-dependent manner. These observations indicate that the antigenic component of the murine model is present in humans and can give rise to heterologous antibodies that cause developmental anomalies, suggesting that the experimental model might be of significance in human pathology.

Animals↗
PubMed1991

[Necrotizing extracapillary glomerulonephritis without immunoglobulin deposits. Renal localization of systemic vasculitis with anti-cytoplasm polynuclear antibodies].

Necrotizing and crescentic glomerulonephritis without immunoglobulin deposits (also called pauci-immune glomerulonephritis) is the cause of approximately 50 percent of acute renal failures of glomerular origin. Our study, based on 40 case-records selected on histological criteria, and on data from the literature, shows that in most cases, if not all, this type of glomerulonephritis is part of a wider systemic vasculitis which predominantly affects the glomerular capillaries. Anti-neutrophil cytoplasm antibodies are detected in three-quarters of the cases, with a specific distribution that varies according to the clinical features. In spite of the patients' age (mean: 62 years), the severity of glomerular lesions and the extra-renal diffusion of the disease, 60 percent of these patients can be cured and recover a normal, or at least acceptable renal function, provided the corticosteroid and sometimes immunosuppressive therapy is initiated at an early stage.

Adolescent↗
PubMed1991

[Contribution of experimental pathology to the understanding of human immune glomerulonephritis].

Immune glomerulonephritis (GN) progresses in three phases. Induction corresponding to the development of immune response; transduction characterized by the appearance of immunological reactants in the glomerulus, and mediation responsible for glomerular lesions and proteinuria. Studies of experimental models have resulted in significant advances in our understanding of these phases. The most striking acquisitions concern the genetic control of GN and its link with the major histocompatibility system; the identification of target antigens involved in Goodpasture's syndrome and in experimental epimembranous GN; the re-evaluation of the role played by circulating immune complexes in the in situ formation of immune complexes in the glomerular capillary wall; the identification of numerous mediatory systems (notably cytokines) which play an important part in glomerular inflammation and in the development of fibrosis. These advances may lead, in the short- or medium-term, to interesting therapeutic novelties.

Animals↗
PubMed1991

Presence of renin, angiotensinogen, angiotensin II in the lamb anterior pituitary gland: immunocytochemical study after cryoultramicrotomy.

The presence of renin, angiotensin I-converting enzyme and angiotensin II detected by immunocytochemistry in the adult male rat anterior pituitary has suggested the existence of a pituitary renin-angiotensin system. To establish another mammalian experimental model we have investigated the presence of renin, angiotensinogen, angiotensin I-converting enzyme, and angiotensin II II in five normal lamb anterior pituitaries by immunocytochemistry after cryoultramicrotomy. Renin, angiotensinogen and angiotensin II immunoreactivities were observed only in cytoplasmic granules of lactotrophs, and the three proteins were found co-localized with prolactin in the same granules by double immunolabelling. No immunoreactive angiotensin I-converting enzyme was observed. These results suggest an activation of renin in the cytoplasmic granules of lactotrophs leading to a local synthesis of angiotensin II. Thus, the lamb anterior pituitary may provide a good experimental model for investigating the possible autocrine action of a local renin-angiotensin system on prolactin release in the human pituitary.

Angiotensin II↗
PubMed1991

Immunoautoradiographic localisation of enkephalinase (EC 3.4.24.11) in rat gastrointestinal tract.

Enkephalinase (EC 3.4.24.11, membrane metalloendopeptidase) is a zinc peptidase expressed by neurons and a variety of epithelial cells, and responsible for the inactivation of enkephalins in brain. Its functions in the gastrointestinal (GI) tract are less well understood although enkephalinase inhibitors were reported to induce a constellation of antisecretory and motor responses. Its localisation in various segments of the rat GI tract was established autoradiographically using a 125I-labelled monoclonal antibody. All along the GI tract, the highest immunoreactivity was found in mucosal layers e.g., in intestinal villi, basal epithelial layers of the oesophagus or gastric cardia, muscularis mucosae of the stomach and large intestine. The immunoreactivity was also high in the stomach submucosae and moderate in the muscularis propria of the caecum. A faint patchy immunoreactivity was also observed in several other layers. This distribution suggests that the membrane peptidase is expressed by enterocytes and a variety of other cells. Its high expression in mucosal layers is consistent with its participation in protein digestion and also in the inactivation of endogenous peptides, particularly the enkephalins, acting at this level to control secretory mechanisms and hydroelectrolytic fluxes. Its presence in submucosal layers may account for some naloxone-reversible motor responses elicited by enkephalinase inhibitors.

Animals↗
PubMed1991

Establishment of permanent renal tubule cell lines by infection with the wild-type and a thermosensitive mutant of the simian virus 40.

This study summarizes the properties of rabbit renal tubule cell lines transformed by the simian virus 40 (SV40). By infection with the wild type SV40, it was possible to establish three different cell lines exhibiting the main functions of proximal (RC.SV1), thick ascending limb-distal (RC.SV2), and collecting (RC.SV3) tubules. Another cell line infected with a thermosensitive mutant of SV40 (RC.SVtsA58) was highly sensitive to arginine vasopressin when cells were cultured at the restrictive temperature of 39.5 degrees C, suggesting they derived from principal cells of the collecting tubule.

Animals↗
PubMed1991

A restriction fragment of the C2 gene is a unique marker for C2 deficiency and the uncommon C2 allele C2*B (a marker for type 1 diabetes).

There are three common C2 protein alleles in caucasians, C2*C, C2*B, and C2*Q0, with allele frequencies of 0.96, 0.03, and 0.01, as well as Sst I RFLP variants of 2.75, 2.7, 2.65, 2.55, and 2.4 kb, with frequencies of 0.017, 0.533, 0.358, 0.017, and 0.075. Thus, C2*C is informatively split by the RFLP. Of 94 nonrandomly ascertained caucasian complotypes, 77 contained C2*C, four contained C2*Q0, and 13 had C2*B. None of the C2*C-containing complotypes carried the 2.75 kb Sst I fragment and all of the complotypes with C2*B or C2*Q0 carried it. All of the C2*Q0 alleles were associated with C4A*4, C4B*2 in the complotype S042 as previously reported. C2*B was usually (9/13) in the complotype SB42, occasionally (1/13 each) in SB45, SB41, SB(4,3)0, and SB31. Thus, the association of the C2 2.75-kb fragment was with C2*B and C2*Q0, not with C4A*4, C4B*2, or even C4A*4 alone. The complotype SC42 was associated with the 2.65-kb Sst I fragment in four of five instances and in a single example with the 2.7-kb fragment. C2*B and C2*Q0 possibly had a common evolutionary ancestor complotype which carried the 2.75-kb Sst I fragment, and BF*S, C4A*4, and C4B*2. C2*B (particularly as the haplotype HLA-Bw62, SB42, DR4) is associated with type 1 diabetes but C2*Q0 is protective.

Alleles↗
PubMed1990

Polarized membrane expression of brush-border hydrolases in primary cultures of kidney proximal tubular cells depends on cell differentiation and is induced by dexamethasone.

To analyze the influence of cell differentiation and the effects of hormones on the subcellular distribution of apical antigens in polarized epithelial cells, we have compared the localization of three brush border (BB) hydrolases [neutral endopeptidase (ENDO), aminopeptidase N (APN), and dipeptidylpeptidase IV (DPPIV)] in primary cultures of renal proximal tubule cells grown in various culture media. The degree of cell differentiation modulated by medium composition was estimated by measuring proximal functions, including glucose transport, specific enzymatic activities, and PTH responsiveness. In the dedifferentiated state observed in cells grown in 1% fetal calf serum (FCS)-supplemented medium, the three hydrolases are abnormally concentrated in a cytoplasmic vesicle compartment with weak expression on both membrane domains. By contrast, in serum-free hormonally defined medium (DM: insulin, 5 microgram/ml; dexamethasone, 5 x 10(-8) M), which markedly enhances morphological and functional cell differentiation, the distribution of hydrolases parallels that observed in the normal tubule. When added to the DM devoid of hormones, insulin has little polarizing effect, whereas dexamethasone dramatically increases the apical expression of the hydrolases, which then almost disappear from the basolateral membrane and cytoplasmic vesicular compartments. This glucocorticoid hormone augments the amount of immunoreactive antigen detectable on the apical domain in paraformaldehyde-fixed cells but does not change the total enzymatic activity. This suggests the presence in tubular cells of a dexamethasone-dependent polarizing machinery that requires de novo RNA and protein synthesis, and probably acts mainly by targeting a storage cytoplasmic pool of enzyme to the apical domain.

Aminopeptidases↗