The division cycle and RNA-synthesis in diploid human cells at different passage levels in vitro

Macieira‐Coelho, A.; Pontén, Jan; Philipson, Lennart

doi:10.1016/0014-4827(66)90280-1

Cited by 268 publications

(47 citation statements)

References 9 publications

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“…Blocks in G0/G1 and G2 have been associated with aging in vitro (2)(3)(4)(5). Studies demonstrating that entry into S phase in immortal cell lines is inhibited by fusion to senescent cells (40,41) suggest that an inhibitor of DNA synthesis accumulates in senescent cells.…”

Section: Discussionmentioning

confidence: 99%

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Effects of beta interferon on human fibroblasts at different population doubling levels. Proliferation, cell volume, thymidine uptake, and DNA synthesis.

Jasny¹,

Pfeffer²,

Tamm³

1984

The Journal of Experimental Medicine

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Cellular aging had no effect on the ability of beta interferon to increase cell volume and population doubling time in 76-109 cells, a line of human skin fibroblasts. However, DNA synthesis in cells at high population doubling levels (PDL 55-70) was inhibited after 72 h of beta interferon treatment (1,000 U/ml) while no inhibition of DNA synthesis was observed in cells at middle population doubling levels (PDL 30-40).

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Section: Discussionmentioning

confidence: 99%

“…Cultures of senescent populations exhibit a marked decrease in the percentage of S phase cells. Most of the cells are blocked in G0/G2 although some appear to be blocked in G2 (2)(3)(4)(5). In vitro aging is associated with increases in cell volume and nuclear area (6) and with a decrease in cell locomotion (7,8).…”

mentioning

confidence: 99%

Effects of beta interferon on human fibroblasts at different population doubling levels. Proliferation, cell volume, thymidine uptake, and DNA synthesis.

Jasny¹,

Pfeffer²,

Tamm³

1984

The Journal of Experimental Medicine

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“…To determine whether or not differences in the rates of mitosis in young and old BPAECs accounted for gap closure after MCF-7 breast cancer cells were added to the BPAECs, we first sought to verify that the younger cells did indeed have a higher proliferation rate as has been reported for other cell types (Macieira-Coelho et al, 1966a, 1966b. As shown in Figure 1A, the number of young BPAECs doubled, in contrast to the old BPAECs in which the number of cells at 48 hours after plating did not differ from the number plated.…”

Section: Mitosis Studiesmentioning

confidence: 99%

“…The first mechanism involves age-related differences in mitotic indexes. It has been well documented that lower passage cultured cells have higher proliferation rates (Macieira-Coelho et al, 1966a, 1966b. Perhaps, the gap closure is due to mitotic division after gap formation induced by the addition of the cancer cells.…”

mentioning

confidence: 99%

Studies on Breast Cancer Cell Interactions with Aged Endothelial Cells in Culture and Rat Models

Merkle¹

2006

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Public reporting burden for this collection of information is estimated to average 1 hour per response, including the time for reviewing instructions, searching existing data sources, gathering and maintaining the data needed, and completing and reviewing this collection of information. Send comments regarding this burden estimate or any other aspect of this collection of information, including suggestions for reducing this burden to Department of Defense, Washington Headquarters Services, Directorate for Information Operations and Reports (0704-0188), 1215 Jefferson Davis Highway, Suite 1204, Arlington, VA 22202-4302. Respondents should be aware that notwithstanding any other provision of law, no person shall be subject to any penalty for failing to comply with a collection of information if it does not display a currently valid OMB control number. PLEASE DO NOT RETURN YOUR FORM TO THE ABOVE ADDRESS. (From -To) REPORT DATE (DD-MM-YYYY) 01-05-2006 REPORT TYPE Final DATES COVERED PERFORMING ORGANIZATION NAME(S) AND ADDRESS(ES) 8. PERFORMING ORGANIZATION REPORT NUMBERUniversity of Arizona Tucson, Arizona 85722-3308 SPONSORING / MONITORING AGENCY NAME(S) AND ADDRESS(ES) 10. SPONSOR/MONITOR'S ACRONYM(S) U.S. Army Medical Research and Materiel Command Fort Detrick, Maryland 21702-5012 SPONSOR/MONITOR'S REPORT NUMBER(S) DISTRIBUTION / AVAILABILITY STATEMENTApproved for Public Release; Distribution Unlimited SUPPLEMENTARY NOTES ABSTRACTThe specific aim is to determine if breast cancer cells induce persistent gaps between aged endothelial cells, as compared to "young" endothelial cells, to cause increased cancer cell extravasation and metastasis. The objectives are: 1. To further elucidate the interactions of breast cancer cells with aged endothelial cells using co-cultures, 2. To investigate possible mechanisms of breast cancer cell-induced persistent gap formation in in-vitro aged endothelial monolayers, and 3. To begin examining the relevance of the in-vitro age-related differences in endothelial cell responses to breast cancer cell addition using rat in-vivo aging and metastasis models. In this final report, we find that: 1. Addition of rat breast cancer cells to microvascular endothelial cells harvested from young rats causes transient gaps between endothelial cells, whereas cancer addition to endothelial cells from old rats causes persistent gaps; 2. Early analysis shows that more breast cancer cells transmigrate endothelial cells harvested from young rats; and 3. Though metastases are larger in old rats, compared to young rats, after tail vein injection of cancer cells, differences in immune function may be a confounding factor as cancer cell injection the mammary fat pads causes larger "tumors" in the old rats. SUBJECT TERMS IntroductionThe risks for developing and dying from breast cancer increase with age. Death from breast cancer is usually due to metastatic disease. Key events in the metastatic cascade process involve breast cancer cell passage through endothelial cells. In cell culture experiments, w...

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“…Hayflick's original description of the growth kinetics of primary fibroblast cultures suggested that the population was composed of cells with essentially identical proliferative capacities and that the final failure to expand was the direct result of cell death. The idea that senescence was cell death was disproved very rapidly (Macieira-Coelho et al 1966). However, determining whether the proliferative capacities of the members of a population were the same or different was a considerably more complicated task and required greater time to complete.…”

Section: How Do Cells Become Senescent?mentioning

confidence: 99%

Bridging the gap: ageing, pharmacokinetics and pharmacodynamics

Burton

Allen

Bird

et al. 2005

Journal of Pharmacy and Pharmacology

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Changes in pharmacokinetics and pharmacodynamics in elderly patients generally result in an increase in the incidence of drug toxicity and adverse drug reactions. Molecular alterations associated with ageing could bring about biological changes, a consequence of which is an altered response to pharmacological agents. Unfortunately, research in this area has yet to progress beyond the cataloguing of the pharmacokinetic and pharmacodynamic changes observed in the elderly. Therefore, real progress in our understanding of pharmacogerontology could be achieved if it were possible to merge pharmacokinetic and pharmacodynamic studies with recent advances in our understanding of the causal processes bringing about ageing changes at the cellular level. Therefore, this review will focus on the mechanisms of ageing in the hope that the information will be of value to those planning independent studies.

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The division cycle and RNA-synthesis in diploid human cells at different passage levels in vitro

Cited by 268 publications

References 9 publications

Effects of beta interferon on human fibroblasts at different population doubling levels. Proliferation, cell volume, thymidine uptake, and DNA synthesis.

Effects of beta interferon on human fibroblasts at different population doubling levels. Proliferation, cell volume, thymidine uptake, and DNA synthesis.

Studies on Breast Cancer Cell Interactions with Aged Endothelial Cells in Culture and Rat Models

Bridging the gap: ageing, pharmacokinetics and pharmacodynamics

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