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Biomedical subjects

C Esposito

Publications and source records attributed to C Esposito.

At least 181 records · Page 10Linked to original sources
PubMed1976

Arginase from human full-term placenta.

Arginase was purified about 1800-fold from extracts of human full-term placenta; the enzyme appeared to be homogenous by disc electrophoresis and molecular-sieve chromatography. The mol. wt. determination by gel filtration and sodium dodecyl sulphate/polyacrylamide-gel electrophoresis yielded a value of 70000 for the most pure and the partially purified enzyme. The human placenta arginase is a metalloenzyme with an optimum pH of 9.1. The Km for L-arginine is 27 mM. L-Ornithine and L-lysine show competitive inhibition with Ki values of 6.3 and 14 mM respectively.

Arginase↗
PubMedDate not supplied

B-lipotropin 61-76 and 61-91 fragments act as transglutaminase substrates in vitro.

Both alpha- and beta-endorphin were shown to incorporate radioactive polyamines during incubation in the presence of purified transglutaminase and Ca2+, spermine acting as the best acyl acceptor substrate. The endorphin labelling is dependent on the time of exposure to the enzyme and on the substrate concentration. In the absence of acyl acceptor polyamines, isotopically labelled beta-endorphin gives rise to high molecular weight radioactive polymer(s). Moreover, when different proteins acting as transglutaminase substrates are added, beta-endorphin produces heterologous structures. These data indicate that the glutamine-71 of the beta-lipotropin chain, contained in both alpha- and beta-endorphin, functions as acyl donor substrate for the enzyme and that at least one beta-endorphin lysyl residue can serve as acyl acceptor.

Endorphins↗
PubMedDate not supplied

Biological activities of a major protein secreted from the rat seminal vesicles after structural modification catalyzed by transglutaminase in vitro.

The immunosuppressive, anti-inflammatory and anti-thrombotic properties of SV-IV, a major protein secreted from the epithelium of rat seminal vesicles, were investigated after transglutaminase-catalyzed covalent incorporation of two molecules of spermidine (Spd) into the protein at the level of Gln-9 and Gln-86. The modified molecular form of the protein (Spd2-SV-IV) showed a more marked inhibitory activity on Con A-induced lymphocyte blastogenesis in comparison with the native protein, whereas no differences in the ability to inhibit the mixed lymphocyte reaction and to decrease the rat epididymal sperm immunogenicity were found between modified and native SV-IV. Spd2-SV-IV was also less effective than native SV-IV to inhibit platelet aggregation induced in vivo by different thrombogenic agents. In contrast, superimposable inhibitory tracings were observed in the in vitro platelet aggregation experiments performed with the two different molecular forms on the protein. Finally, Spd2-SV-IV was shown to retain unchanged the anti-inflammatory activity of native SV-IV.

Animals↗
PubMedDate not supplied

Substance P inactivation by transglutaminase in vitro.

Gamma(glutamyl5)spermine derivative of substance P (Spm-SP) was synthesized in vitro in the presence of purified guinea pig liver transglutaminase and Ca2+. The spermine adduct of the neuropeptide was purified by HPLC on a reversed-phase column and characterized by fast atom bombardment mass spectrometry. The biological activities of Spm-SP were tested by assaying, in comparison with substance P, its ability to induce both the contractions of smooth muscle in vitro and the edema formation in vivo. Spm-SP was shown not to elicit contractile responses in the isolated rat stomach strip and duodenum and not to antagonize the spasmogenic effect evoked by the native neuropeptide. Furthermore, Spm-SP was unable, when administered into rats by plantar injection, either to provoke an acute inflammatory response in the hind limb or to antagonize the edema formation induced by a concurrent administration of substance P. These results indicate that the introduction of a large size hydrophilic moiety at the glutamine5 level negatively affects the ability of the neuropeptide to bind to its receptor(s), thus supporting the view that the hydrophobic middle portion of substance P plays a key role in receptor recognition.

Amino Acid Sequence↗
PubMedDate not supplied

Henoch-Schönlein purpura in a chronic hemodialysis patient.

We describe a patient on maintenance hemodialysis who developed purpura, abdominal pain with bloody stool, and gross hematuria. A skin biopsy revealed leukocytoclastic vasculitis with IgA deposits. This is the first report of Henoch-Schönlein purpura in a hemodialysis patient.

Aged↗
PubMedDate not supplied

[Hepatocyte growth factor (HGF) reduces the expression of profibrotic factors in human isolated glomeruli].

BACKGROUND: The imbalance between the synthesis and degradation of the mesangial matrix causes glomerulosclerosis and ultimately leads to chronic renal failure. HGF is a pleiotropic cytokine involved in angiogenesis, morphogenesis, organogenesis, and bone remodeling. Recently, we and other investigators have shown that HGF has a central role in the recovery of acute renal failure. Furthermore, HGF treatment halts the progression of kidney disease in a murine model of chronic renal failure. The aim of the present study was to evaluate the effect of HGF on the mRNA levels of molecules involved in the extracellular matrix turnover and of the c-met receptor in isolated human glomeruli. METHODS: Human glomeruli were isolated by microdissection from donor kidney biopsies just before transplantation. Glomeruli were extensively washed and incubated with culture media containing HGF (50 ng/mL) for 24 h at 37 C. Glomeruli incubated without HGF were used as controls. After 24 h, glomeruli were washed and freezed and thawed three times. The expression of c-met, (alpha2) IV collagen, TGF-beta, metalloproteases 9 (MMP9), and of the inhibitor of metalloproteases-1, TIMP-1 was evaluated by in situ reverse transcription (RT) and polymerase chain reaction (PCR). beta-actin was used as a housekeeping gene. RESULTS: The (alpha2)IV collagen mRNA level was decreased by HGF in human glomeruli. TGF-beta and TIMP-1 gene expression was markedly reduced by HGF treatment, whereas the expression of MMP-9 and c-met did not change. Under light-microscopic examination, kidney biopsies showed neither glomerular hypercellularity nor mesangial expansion. CONCLUSIONS: HGF treatment reduces the expression of extracellular matrix components and of profibrotic factors in human glomeruli. Our results confirm a protective role of HGF in glomerulosclerosis.

Hepatocyte Growth Factor↗
PubMedDate not supplied

[Diffusive and convective treatments in the clinical practice: observation study of the Pavia district nephrology group].

UNLABELLED: PURPOSE. Although convective treatments are widely used, there is no evidence that they can improve patient survival or hospitalizations nor clinical criteria indicating which patients could benefit from them. This study was carried out to evaluate the dialysis modality distribution and the clinical criteria used in choosing the dialysis therapy by the four dialysis Centers in the district of Pavia, a district characterized by a quite homogeneous population. METHODS: We evaluated age, gender, body mass index (BMI), time on dialysis, number of sessions per week, dialysis duration, dialysis modality, criteria used in choosing dialysis therapy, vascular access (VA), Kt/V, and the number of hypotensive episodes. RESULTS: Two hundred and seventy-two patients were enrolled in the study. Mean age was 67.3 +/- 12 yrs, BMI was 26.3 +/- 6.1, dialytic age was 5.49 +/- 5.5 yrs, Kt/V was 1.4 +/- 0.3, mean session time was 238 min. Fifty-two patients (19.2%) were on a convective treatment. Age, BMI, time on dialysis, dialysis duration and number of sessions per week were no different between convective treatment patients and diffusive treatment patients. Kt/V was significantly different between convective and diffusive methods (1.55 +/- 0.37 vs 1.4 +/- 0.28, p<0.05). Convective treatments were prescribed for cardiovascular (CV) instability by the nephrologists from the Pavia district in the majority of patients (90.9%). There was no difference in hypotensive episodes between convective and diffusive methods. CONCLUSIONS: Our study demonstrated that lacking clinical evidence indicating an improvement in the long-term outcome with convective techniques, nephrologists in the Pavia district choose this type of dialysis treatment to ameliorate CV stability in uremic patients.

Aged↗
PubMedDate not supplied

[Hepatocyte growth factor and kidney].

HGF is a multifunctional polypeptide with mitogenic, motogenic and morphogenic effects. These effects are mediated by c-met, a specific receptor of HGF and a member of the receptor tyrosine kinase superfamily, virtually expressed in every type of kidney cell. HGF has a central role during embryogenesis since it stimulates epithelial differentiation of metanephric mesenchymal cells and induces branching tubules, as experiments in epithelial cells cultures demonstrated. Several studies have shown also that HGF accelerates the recovery from toxic-ischemic acute renal failure. This effect seems to be mediated by the inhibition of programmed cell death and an increased cell survival. HGF inhibits apoptosis by upregulating the protooncogene Bcl-2 and downregulating Bax. Since HGF can modulate extracellular matrix turnover, authors suggest its beneficial role in tissue remodelling and particularly in chronic renal diseases. Several studies reported a key role for HGF in reducing interstitial fibrosis and glomerular sclerosis, both in in vivo and in vitro models. This protective effect is secondary to HGF antagonizing the profibrotic action of TGF-beta. HGF modulates the balance between synthesis and degradation of extracellular matrix, increasing the expression of metalloproteases and reducing the production of their specific inhibitors TIMPs. Furthermore HGF suppresses the effect of TGF-beta by blocking the axis TGF-beta/Smad. Last, the antifibrotic effect of HGF might be modulated by the proliferative status of target cells. To sum up, the supplementation of exogenous HGF or the induction of endogenous HGF expression may provide an effective therapeutic strategy for combating chronic renal diseases.

Hepatocyte Growth Factor↗