Cell Proliferation Rates in Common Cancer Target Tissues of B6C3F1 Mice and F344 Rats: Effects of Age, Gender, and Choice of Marker

Eldridge, Sandra R.; Goldsworthy, Susan M.

doi:10.1006/faat.1996.0119

Cited by 39 publications

(17 citation statements)

References 12 publications

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“…Modelling was based on proliferation rates determined by Ki67 + hepatocytes at 2 months of age revealing that Mcl-1 Δhep mice have about 10- to 25-fold higher Ki67 rates (see Figure 2). Calculation is based on the following assumptions: A wild type mouse liver weighting 2 g consists of ∼2x10 8 hepatocytes, and assuming a proliferation index of 0.2 (Eldridge and Goldsworthy, 1996), 4x10 5 proliferating hepatocytes. Further, assuming an replication error rate of 10 -8 per cell per generation (Tago et al., 2005), and 24 h cycle duration (Alexiades and Cepko, 1996), taking Poisson distribution as basis, the expected number of replications errors after 1 year of is 1.46 for wild type mice, 14.6 for Mcl-1 Δhep mice with low hepatocyte proliferative activity, and 36.8 for Mcl-1 Δhep mice with high hepatocyte proliferative activity.…”

Section: Methodsmentioning

confidence: 99%

A Dual Role of Caspase-8 in Triggering and Sensing Proliferation-Associated DNA Damage, a Key Determinant of Liver Cancer Development

et al. 2017

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SummaryConcomitant hepatocyte apoptosis and regeneration is a hallmark of chronic liver diseases (CLDs) predisposing to hepatocellular carcinoma (HCC). Here, we mechanistically link caspase-8-dependent apoptosis to HCC development via proliferation- and replication-associated DNA damage. Proliferation-associated replication stress, DNA damage, and genetic instability are detectable in CLDs before any neoplastic changes occur. Accumulated levels of hepatocyte apoptosis determine and predict subsequent hepatocarcinogenesis. Proliferation-associated DNA damage is sensed by a complex comprising caspase-8, FADD, c-FLIP, and a kinase-dependent function of RIPK1. This platform requires a non-apoptotic function of caspase-8, but no caspase-3 or caspase-8 cleavage. It may represent a DNA damage-sensing mechanism in hepatocytes that can act via JNK and subsequent phosphorylation of the histone variant H2AX.

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Section: Methodsmentioning

confidence: 99%

A Dual Role of Caspase-8 in Triggering and Sensing Proliferation-Associated DNA Damage, a Key Determinant of Liver Cancer Development

et al. 2017

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“…Demonstration of proliferating cell nuclear antigen (PCNA) immunoreactivity in renal sections of normal and treated rats was performed according to the method described by Eldridge and Goldsworthy [ 34 ]. Tissue sections were deparaffinized and incubated with a monoclonal antibody to PCNA (Dako Corp, Carpenteria, CA).…”

Section: Methodsmentioning

confidence: 99%

Renoprotective Effect of Lactoferrin against Chromium-Induced Acute Kidney Injury in Rats: Involvement of IL-18 and IGF-1 Inhibition

et al. 2016

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Hexavalent chromium (CrVI) is a heavy metal widely used in more than 50 industries. Nephrotoxicity is a major adverse effect of chromium poisoning. The present study investigated the potential renoprotective effect of lactoferrin (Lf) against potassium dichromate (PDC)-induced acute kidney injury (AKI) in rats. Beside, because previous studies suggest that interlukin-18 (IL-18) and insulin-like growth factor-1 (IGF-1) play important roles in promoting kidney damage, the present work aimed to evaluate the involvement of these two cytokines in PDC model of AKI and in the potential renoprotective effect of lactoferrin. Adult male albino Wistar rats were pretreated with Lf (200mg/kg/day, p.o.) or (300mg/kg/day, p.o.); the doses that are usually used in the experiment studies, for 14 days followed by a single dose of PDC (15mg/kg, s.c.). PDC caused significant increase in serum urea, creatinine, and total protein levels. This was accompanied with decreased renal glutathione content, and increased renal malondialdehyde, IL-18, IL-4, nuclear factor kappa B (NFκB), IGF-1, and the phosphorylated form of forkhead box protein O1 (FoxO1) levels. Moreover, normal expression IFN-γ mRNA and enhanced expression of TNF-α mRNA was demonstrated in renal tissues. Histopathological investigations provoked deleterious changes in the renal tissues. Tubular epithelial hyperplasia and apoptosis were demonstrated immunohistochemically by positive proliferating cell nuclear antigen (PCNA), Bax, and Caspase-3 expression, respectively. Pretreatment of rats with Lf in both doses significantly corrected all previously mentioned PDC-induced changes with no significant difference between both doses. In conclusion, the findings of the present study demonstrated the involvement of oxidative stress, inflammatory reactions, tubular hyperplasia and apoptosis in PDC-induced AKI. It suggested a role of IL-18 through stimulation of IL-4-induced inflammatory pathway, and IGF-1 through triggering FoxO1-induced cell proliferation. Moreover, the study revealed that Lf protected the kidney against Cr-induced AKI in rats and significantly showed antioxidant, anti-inflammatory, and anti-proliferative properties with down-regulation of IL-18 and IGF-1.

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“…Detection of proliferating cell nuclear antigen (PCNA) expression on kidney’s paraffin sections of selected control and treated rats using avidin-biotin Peroxidase (DAB, Sigma Chemical Co.) was done according to method described by [ 23 ]. Tissue sections were incubated with a monoclonal antibody to PCNA (Dako Corp, Carpenteria, CA) and reagents required for the avidin-biotin peroxidase (Vactastain ABC peroxidase kit, Vector Laboratories) method for the detection of the antigen—antibody complex.…”

Section: Methodsmentioning

confidence: 99%

The Remedial Efficacy of Spirulina platensis versus Chromium-Induced Nephrotoxicity in Male Sprague-Dawley Rats

et al. 2015

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This study was conducted to investigate the possible protective effect of Spirulina platensis against chromium-induced nephrotoxicity. A total of 36 adult male Sprague-Dawley rats were divided into 4 equal groups (Gps). Gp1 served as control, rats of Gps 2, 3, and 4 were exposed to Spirulina platensis (300 mg/kg b.wt per os) and sodium dichromate dihydrate (SDD) via drinking water at concentration of 520 mg /l respectively. Chromium administration caused alterations in the renal function markers as evidenced by significant increase of blood urea and creatinine levels accompanied with significant increase in kidney’s chromium residues and MDA level as well as decreased catalase activity and glutathion content in kidney tissue. Histologically, Cr provoked deleterious changes including: vascular congestion, wide spread tubular epithelium necrobiotic changes, atrophy of glomerular tuft and proliferative hyperplasia. The latter was accompanied with positive PCNA expression in kidney tissues as well as DNA ploidy interpretation of major cellular population of degenerated cells, appearance of tetraploid cells, high proliferation index and high DNA index. Morphometrical measurements revealed marked glomerular and tubular lumen alterations. On contrary, spirulina co-treatment with Cr significantly restored the histopathological changes, antioxidants and renal function markers and all the previously mentioned changes as well.

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Cell Proliferation Rates in Common Cancer Target Tissues of B6C3F1 Mice and F344 Rats: Effects of Age, Gender, and Choice of Marker

Cited by 39 publications

References 12 publications

A Dual Role of Caspase-8 in Triggering and Sensing Proliferation-Associated DNA Damage, a Key Determinant of Liver Cancer Development

A Dual Role of Caspase-8 in Triggering and Sensing Proliferation-Associated DNA Damage, a Key Determinant of Liver Cancer Development

Renoprotective Effect of Lactoferrin against Chromium-Induced Acute Kidney Injury in Rats: Involvement of IL-18 and IGF-1 Inhibition

The Remedial Efficacy of Spirulina platensis versus Chromium-Induced Nephrotoxicity in Male Sprague-Dawley Rats

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