PC10 monoclonal antibody to proliferating cell nuclear antigen as probe for cycling cell detection in developing tissues

Casasco, Andrea; Giordano, Monica; Danova, Marco; Casasco, Marco; Cornaglia, Antonia Icaro; Calligaro, Alberto

doi:10.1007/bf00269137

Cited by 49 publications

(29 citation statements)

References 21 publications

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“…This distribution may reflect the synthesis or degradation of the protein. Cytoplasmic PCNA staining has also been described in lymphoma cells (Sabattini et al, 1993) as well as in normal tissues (Nakane et al, 1989;Hall et al, 1990;Casasco et al, 1993).…”

Section: Discussionmentioning

confidence: 92%

“…Placentas were obtained from 24 animals between 22 and 153 days of pregnancy (gestation is 168 days). Our specimens were fixed for 4-5 hr, thus eliminating variations in staining due to extended exposure to paraformaldehyde (Hall et al, 1990;Casasco et al, 1993). Paraffin sections were prepared and mounted on poly-L-lysine coated slides, dewaxed in xylene, and rehydrated to water in decreasing concentrations of ethanol.…”

Section: Methodsmentioning

confidence: 99%

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Developmental expression of Ki‐67 antigen and proliferating cell nuclear antigen in macaque placentas

Blankenship

King

1994

Developmental Dynamics

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Placental growth is largely determined by the proliferation of cytotrophoblast cells. However, the distribution of cytotrophoblast cells engaged in the cell cycle during placental development is poorly understood. Recently, antibodies have been developed that identify two proteins directly involved with DNA synthesis: Ki-67 protein and proliferating cell nuclear antigen (PCNA). Immunolocalization of Ki-67 and PCNA provides a measure of the proliferating cells in tissues. We examined, in macaque placentas, the spatiotemporal pattern of expression of these proteins during gestation. Tissues from 24 macaque placentas collected from 22-153 days of pregnancy were prepared for paraffin sections. Standard immunoperoxidase techniques were used to identify Ki-67 and PCNA. The proteins generally co-localized, although PCNA was usually represented in more cells than Ki-67. Early in gestation the cell columns contained many labeled cells. The cytotrophoblastic shell was occupied by numerous cells with PCNA positive nuclei, but few were reactive for Ki-67. By 45 days of pregnancy the immunolabeled cells in the cell columns were concentrated in the proximal regions, adjacent to the anchoring villus tips. The number of positive cells decreased by 100 days when the cell columns were diminished, leaving the anchoring villus tips buried in the shell. Labeled cells were rarely present in the shell at late pregnancy. The single layer of cytotrophoblast cells in the chorionic plate contained numerous reactive cells throughout early and mid-gestation. After approximately 100 days the cytotrophoblast layer of the chorionic plate was stratified over large areas. Soon thereafter few cells of the chorionic plate were labeled. The chorionic villi contained reactive cytotrophoblastic cells throughout gestation. Extravillous cytotrophoblast cells invading spiral arteries were sometimes labeled for PCNA but not Ki-67. We conclude that compartments of the placenta are distinguished by specific patterns of cytotrophoblast cell proliferation. Moreover, these patterns correspond to macroscopic growth parameters of the placenta. Evidence suggests that the macaque placenta slows its rate of diametrical growth at approximately 100 days of gestation. It is at about this time that the cell columns are absorbed into the trophoblastic shell and this pool ofproliferating cells is diminished. The growth in diameter of the chorionic plate matches that of the shell. In this compartment also the architecture changes at about 100 days as the cytotrophoblast layer stratifies. This stratification may result from continued proliferation of cytotrophoblast cells when the diametrical rate of growth is decreasing. Soon thereafter, proliferation decreases in this compartment also. By contrast, labeled cells were found in chorionic villi throughout gestation. Continued villous growth and branching probably accounts for most of the increases in placental thickness and weight that occurs during late gestation. 0 1994 Wiley-Liss, Inc.

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Section: Discussionmentioning

confidence: 92%

Section: Methodsmentioning

confidence: 99%

Developmental expression of Ki‐67 antigen and proliferating cell nuclear antigen in macaque placentas

Blankenship

King

1994

Developmental Dynamics

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“…The advent of PC 10, an MAb against PCNA that can recognize proliferating cells in fixed and paraffin-embedded tissues, appears to provide a feasible tool for retrospective evaluation of cell kinetics (6,12,40). During the cell cycle, PCNA expression increases through the GI-phase, becomes maximal at early S-phase, and declines throughout Gz-phase (7,27).…”

Section: Discussionmentioning

confidence: 99%

In vivo modulation of proliferating cell nuclear antigen in growth plate chondrocytes from normal, hypophysectomized, growth hormone-treated hypophysectomized rats: a comparative immunohistochemical study with image analysis.

Tajima¹,

Kato²,

Maruyama³

et al. 1996

J Histochem Cytochem.

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Growth hormone (GH) regulates the proliferation and maturation of chondrocytes in the epiphyseal growth plate, in which a temporal dimension is superimposed on the septal organization of the tissue. In this study we investigated the in vivo effects of hypophysectomy (Hypox) and injection of GH into Hypox animals (Hypox + GH) on the proliferative activity of the growth plate chondrocytes. We assessed the immunohistochemical expression of proliferating cell nudear antigen (PCNA) in pataffi-embedded tissues, using monoclonal antibody PC 10 against PCNA combined with immunogold-silver staining. We subjected the immunostained sections to computer-based image analysis by ACAS 570 interactive laser cytometry employing a conventional microscopic light source. Hypox was carried out on 20 rats at 8 weeks of age, half of which received a hypodermic injection of human GH at a dose of 1 IUlkg twice a day for 1 week after the operation. Another group of five rats of the same age were used as normal controls. In normal rats, a distinct PCNA immunoreaction was observed in the proliferative IntroductionThe long-bone growth plate provides an opportunity to investigate the sequence of events that occur during the lifespan of chondrocytes and in cartilage matrix production (5). The epiphyseal growth plate continues to form new cartilage with renewal of chondrocytes, and consequently participates in the longitudinal growth of long bones (20). The growth plate itself consists of several morphologi-'

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“…34,35 The final stage of myogenesis within the developing PPF involves the fusion of myoblasts to form primary myotubes which can be detected via immunolabeling for the polysialylated neural cell adhesion molecule (PSA-NCAM), the neural cell adhesion molecule (NCAM), or desmin. 26,27 Another aspect of interest is the underlying mechanisms responsible for guiding diaphragmatic muscle precursors (and phrenic axons) to the PPF.…”

Section: Future Directions Towards Studying Normal and Pathological Pmentioning

confidence: 99%

Recent advances in understanding the pathogenesis of nitrofen-induced congenital diaphragmatic hernia

et al. 2000

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In this review, we discuss recent advances in the study of the pathogenesis of congenital diaphragmatic hernia (CDH). Much of the research has involved the use of an animal model of CDH in which diaphragmatic defects are produced in fetal rats by administering the herbicide nitrofen to dams during mid‐gestation. The animal model is described and the relevance to the human condition is discussed. The data derived from the animal studies are critically assessed in the context of commonly cited hypotheses proposed for the pathogenesis of CDH. Finally, experimental strategies are proposed for systematically examining the normal and pathological formation of the pleuroperitoneal fold. We conclude that a malformation of the primordial diaphragm, the pleuroperitoneal fold, underlies the muscle defects associated with CDH. Pediatr Pulmonol. 2000; 29:394–399. © 2000 Wiley‐Liss, Inc.

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PC10 monoclonal antibody to proliferating cell nuclear antigen as probe for cycling cell detection in developing tissues

Cited by 49 publications

References 21 publications

Developmental expression of Ki‐67 antigen and proliferating cell nuclear antigen in macaque placentas

Developmental expression of Ki‐67 antigen and proliferating cell nuclear antigen in macaque placentas

In vivo modulation of proliferating cell nuclear antigen in growth plate chondrocytes from normal, hypophysectomized, growth hormone-treated hypophysectomized rats: a comparative immunohistochemical study with image analysis.

Recent advances in understanding the pathogenesis of nitrofen-induced congenital diaphragmatic hernia

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