SP-40,40, a newly identified normal human serum protein found in the SC5b-9 complex of complement and in the immune deposits in glomerulonephritis.

Murphy, Brendan; Kirszbaum, L.; Walker, Ian D.; d’Apice, Anthony J.F.

doi:10.1172/jci113531

Cited by 293 publications

(194 citation statements)

References 31 publications

(24 reference statements)

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“…The specificity of E5 was demonstrated in the original publication by immunoprecipitation and Western blot analysis using human serum. 21 After PBS washes, the sections were incubated with biotinylated link antibody and then with peroxidase-labeled streptavidin. The staining was complete after a 10 minutes of incubation with a freshly prepared substrate-chromogen solution.…”

Section: Immunohistochemical Stainingmentioning

confidence: 99%

Overexpression of Clusterin in Human Breast Carcinoma

Redondo

Villar

Torres-Muñoz

et al. 2000

The American Journal of Pathology

229

181

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Clusterin has been implicated in numerous processes including active cell death, immune regulation, cell adhesion and morphological transformation. The purpose of this study was to examine clusterin expression in a large series of breast carcinomas by immunohistochemistry and in situ hybridization. The study included 40 samples of non-neoplastic glandular epithelia, 42 benign lesions, 15 atypical intraductal hyperplasias, 35 carcinomas in situ, 114 invasive carcinomas, and lymph node metastases from 40 patients. Epithelial normal cells were always negative for clusterin expression and only 19% of the benign lesions presented positive staining. In contrast to the benign lesions, however, the frequency of clusterin positive samples increased in atypical hyperplasias (47%, P ‫؍‬ 0.08), intraductal carcinomas (49%, P ‫؍‬ 0.01) and invasive carcinomas (53%, P < 0.001). Positive staining presented a cytoplasmic pattern, except in 3 cases of invasive carcinomas which had nuclear staining. Clusterin mRNA by in situ hybridization confirmed the specific cellular pattern of clusterin expression by immunohistochemistry. Clusterin expression was associated with large tumor size (P ‫؍‬ 0.04), estrogen and progesterone receptor negative status (P ‫؍‬ 0.02 and P ‫؍‬ 0.001, respectively) and with the progression from primary carcinoma to metastatic carcinoma in lymph nodes (80% metastatic nodes had positive expression) (P ‫؍‬ 0.004). Ten of 15 (67%) primary carcinomas without clusterin expression became positive in lymph node metastases, while most (

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Section: Immunohistochemical Stainingmentioning

confidence: 99%

Overexpression of Clusterin in Human Breast Carcinoma

Redondo

Villar

Torres-Muñoz

et al. 2000

The American Journal of Pathology

229

181

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“…These findings suggest that endothelium would be relatively resistant to direct attack by homologous eomplement and that vessel damage in LCV may at least in part be caused by TCC-induced proinflammatory non-lethal effects such as release of arachidonic or oxygen-active metabolites by endothelial cells [16]. In this regard, recent immunofluorescenee studies of skin and renal biopsies in human glomerulonephritis and in Henoch-Schonlein purpura showed that TCC deposits are at least partially in an inactive form which contains the inhibitory S-protcin (vitronectin)[l l]or bolh S-protein and the newly discovered SP-40,40 protein [17][18][19], also called clusterin. sulphated glycoprotein-2 (SGP-2).…”

Section: Introductionmentioning

confidence: 99%

Local and systemic activationofthe whole complement cascade in human leukocytoclastic cutaneous vasculitis; C3d,g and terminal complement complex as sensitive markers

Dauchel

Joly

Delpech

et al. 1993

Clinical and Experimental Immunology

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SUMMARY We have studied complement activation both in plasma samples and In lesional skin from palients with leukocytoclaslic cutaneous vasculitis (LCV). Enzyme immunoassay (EIA) quantification of the complement activation markers. C3d,g and fhe terminal complement complex (TCC) in plasma, showed lhal their levels were significantly increased in 66% and 55% of the patienis, respectively (n = 29) compared with healthy controls, whereas the standard measurements of C3, factor B, Clq, C4and C2 were generally within normal range. Elevations of C3d,g and TCC levels in plasma were signifieantly eorrelated. Importantly, a signifieant correlation was found between the severity of the vasculitis and both C3d,g and TCC plasma levels. Immunofluorescence studies of skin biopsy specimens demonstrated simultaneous presence of peri vascular dermal deposits of C3d,g and TCC in lesional skin from 96 Mi and 80% respectively of the patients (n= 25). There was a significant eorrelation between the intensity of the deposits of bolh markers. Clusterin, a TCC inhibitory protein, was always found at the same sites of perivascular TCC deposits, Immunofluorescence studies at the epidermal basemenl membrane zone (BMZ) revealed in each case deposits of C3d,g which were accompanied by TCC deposits in 52% of the biopsy specimens. These data demonstrate that there is a local and systemic activation of the whole complement cascade in human LCV. The presenee of both C3d,g and clusterin‐associatcd TCC perivascular deposits suggests an intervention of a regulatory mechanism oflocal complement activation in LCV. Einally, measurement of plasma C3d,g and TCC appears to be a sensitive indicator of systemic complement activation and disease severity in LCV.

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“…Clusterin is a major glycoprotein in mammalian semen. Abnormal increases and decreases in clusterin are often indicative of poor-quality semen [12,14,20,23,24]. Regardless of whether or not the semen is normal, it is generally agreed that clusterin mainly exists on the surfaces of immature, low motile, or morphologically abnormal spermatozoa [7,13,26].…”

Section: Introductionmentioning

confidence: 99%

Presence, localization, and origin of clusterin in normal human spermatozoa

Han

Wang

Cheng

et al. 2012

J Assist Reprod Genet

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Purpose Clusterin in mammalian semen is a secretory form of clusterin (sCLU) with the heterodimeric structure. It is secreted by the epididymis and seminal vesicle. It is generally agreed that clusterin mainly exists on the surface of abnormal spermatozoa and is implicated in decreased sperm motility, sperm aggregation and infertility. However, few studies observe clusterin in normal spermatozoa, which is presumed to be a novel form. Up to now, the systematical information about the presence, localization, origin and function of clusterin in normal human spermatozoa has yet not been established. The aim of our current study is to systematically research clusterin in normal human spermatozoa.Methods We detected the presence of clusterin via western blot, explored the localization of clusterin using immunofluorescence, and investigated the origin and distribution of clusterin in human testis by western blot and immunohistochemistry. Results We found native clusterin in the inner plasma membrane of normal human spermatozoa. It was derived from the testis and showed similar molecular weight and heterodimeric structure compared with sCLU in semen and on the surface of abnormal spermatozoa. Conclusion Clusterin in normal spermatozoa should be self-synthesized during the later stage of spermatogenesis. The different localization and origin suggested that the clusterin observed by us may be a novel form compared with conventional sCLU on the surface of abnormal spermatozoa.

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SP-40,40, a newly identified normal human serum protein found in the SC5b-9 complex of complement and in the immune deposits in glomerulonephritis.

Cited by 293 publications

References 31 publications

Overexpression of Clusterin in Human Breast Carcinoma

Overexpression of Clusterin in Human Breast Carcinoma

Local and systemic activationofthe whole complement cascade in human leukocytoclastic cutaneous vasculitis; C3d,g and terminal complement complex as sensitive markers

Presence, localization, and origin of clusterin in normal human spermatozoa

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