A cell kinetic analysis of human umbilical vein endothelial cells

Kalashnik, Lena; Bridgeman, Collette J; King, Andrea R; Francis, Sheila E.; Mikhalovsky, Sergey V.; Wallis, Corrin; Denyer, Stephen Paul; Crossman, David C.; Faragher, R. G. A.

doi:10.1016/s0047-6374(00)00179-2

Cited by 29 publications

(18 citation statements)

References 15 publications

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“…3, if the frequency of Ki67-positive ␤-cells were 1%, we would predict the corresponding rate of ␤-cell mitosis to be 0.025%events/h. These data imply that an average ␤-cell undergoing cell replication is Ki67 positive for ϳ40 h, comparable to the duration observed for other cell types (16,17,19,32,34,39,41). ␤-Cell apoptosis.…”

Section: ␤-Cell Replicationsupporting

confidence: 73%

Development of factors to convert frequency to rate for β-cell replication and apoptosis quantified by time-lapse video microscopy and immunohistochemistry

Saisho

Manesso

Gurlo

et al. 2009

American Journal of Physiology-Endocrinology and Metabolism

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Saisho Y, Manesso E, Gurlo T, Huang CJ, Toffolo GM, Cobelli C, Butler PC. Development of factors to convert frequency to rate for ␤-cell replication and apoptosis quantified by time-lapse video microscopy and immunohistochemistry. Am J Physiol Endocrinol Metab 296: E89 -E96, 2009. First published October 21, 2008 doi:10.1152/ajpendo.90697.2008.-An obstacle to development of methods to quantify ␤-cell turnover from pancreas tissue is the lack of conversion factors for the frequency of ␤-cell replication or apoptosis detected by immunohistochemistry to rates of replication or apoptosis. We addressed this obstacle in islets from 1-mo-old rats by quantifying the relationship between the rate of ␤-cell replication observed directly by time-lapse video microscopy (TLVM) and the frequency of ␤-cell replication in the same islets detected by immunohistochemistry using antibodies against Ki67 and insulin in the same islets fixed immediately after TLVM. Similarly, we quantified the rate of ␤-cell apoptosis by TLVM and then the frequency of apoptosis in the same islets using TdT-mediated dUTP nick-end labeling and insulin. Conversion factors were developed by regression analysis. The conversion factor from Ki67 labeling frequency (%) to actual replication rate (%events/h) is 0.025 Ϯ 0.003 h Ϫ1 . The conversion factor from TdT-mediated dUTP nick-end labeling frequency (%) to actual apoptosis rate (%events/h) is 0.41 Ϯ 0.05 h Ϫ1 . These conversion factors will permit development of models to evaluate ␤-cell turnover in fixed pancreas tissue.Ki67; TdT-mediated dUTP nick-end labeling; insulin; conversion factor BOTH TYPE 1 AND TYPE 2 DIABETES are characterized by a deficiency of ␤-cells (5,6,22,30). Pancreas transplantation restores glycemic control in type 1 and type 2 diabetes (10, 26). However, given the insufficient number of pancreases available for transplantation and the risks of prolonged immunosuppression, restoration of ␤-cells by transplantation is not a viable option for most people with diabetes.A potential alternative strategy is restoration of ␤-cells through endogenous regeneration. Induction of diabetes in young rodents by ␤-cell toxins or partial surgical pancreas resection has been followed by regeneration of ␤-cell mass and reversal of diabetes (4, 40). The origin of these ␤-cells has been actively debated: some have proposed duplication of existing ␤-cells, and others have suggested formation of new ␤-cells from a variety of sources (7). Although ongoing lineage studies will provide insights into the origins of ␤-cells in mice (3,11,12,27,37), this approach is not available in humans and does not provide guidance as to the rate of ␤-cell formation that might be anticipated in humans. Thus, although there is indirect evidence that there might be ongoing ␤-cell formation in adult humans with type 1 diabetes (22), there is no information as to rate of ␤-cell turnover in human pancreas. Although methods do exist for detection of ␤-cell replication and ␤-cell apoptosis, these methods cannot yet be used to comp...

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Section: ␤-Cell Replicationsupporting

confidence: 73%

Development of factors to convert frequency to rate for β-cell replication and apoptosis quantified by time-lapse video microscopy and immunohistochemistry

Saisho

Manesso

Gurlo

et al. 2009

American Journal of Physiology-Endocrinology and Metabolism

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“…However, a number of in-vitro studies have suggested that senescent cells may be resistant to apoptosis (and thus more likely to persist in tissues), at least in fibroblasts where most of the research has been conducted (Wang et al 1994;Marcotte et al 2004;Hampel et al 2005). No difference between the apoptotic potential of senescent human vascular endothelial cells compared with their mitotic counterparts has also been observed (Kalashnik et al 2000).…”

Section: Apoptosis and Stem Cellsmentioning

confidence: 99%

Cellular senescence, ageing and disease

Burton

2008

AGE

118

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Cellular senescence is the irreversible growth arrest of individual mitotic cells, which as a consequence display a radically altered phenotype that is thought to impair tissue function and predispose tissues to disease development and/or progression as they gradually accumulate. However, in the past, research into mechanisms of ageing has commonly been researched and treated separately from disease development. This may partly be due to the lack of understanding concerning mechanisms of ageing and the difficulty in implementing what was known into models of disease development. Only in the last 10 years, with increasing knowledge of the senescent phenotype and the ability to detect senescent cells in human tissues, have biologists been able to investigate the relationship between cellular senescence and disease. This review therefore brings together and discusses recent findings which suggest that cellular senescence does contribute to ageing and the development/ progression of disease.

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“…To test this hypothesis, we assessed proliferation in LacZ-positive MPMEC by quantifying nuclear expression of Ki67, a marker of proliferation for several cell types, including endothelial cells (Fig. 8A) (Kalashnik et al, 2000) in plugs collected 4 and 10 days post-transplantation. The numbers of LacZ-positive/Ki67-positive nuclei were comparable in EphA2 +/-versus EphA2 -/-MPMEC at each time point (Fig.…”

Section: Epha2 Deficiency Impairs Vascular Assembly and Endothelial Cmentioning

confidence: 99%

EphA2 receptor tyrosine kinase regulates endothelial cell migration and vascular assembly through phosphoinositide 3-kinase-mediated Rac1 GTPase activation

Brantley-Sieders

Caughron

Hicks

et al. 2004

Journal of Cell Science

180

221

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A cell kinetic analysis of human umbilical vein endothelial cells

Cited by 29 publications

References 15 publications

Development of factors to convert frequency to rate for β-cell replication and apoptosis quantified by time-lapse video microscopy and immunohistochemistry

Development of factors to convert frequency to rate for β-cell replication and apoptosis quantified by time-lapse video microscopy and immunohistochemistry

Cellular senescence, ageing and disease

EphA2 receptor tyrosine kinase regulates endothelial cell migration and vascular assembly through phosphoinositide 3-kinase-mediated Rac1 GTPase activation

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