Role of proton dissociation in the transport of cystine and glutamate in human diploid fibroblasts in culture.

Incorporation of tritiated thymidine into acid-precipitable material was used to measure the rate of DNA synthesis in secondary cultures of human diploid fibroblasts. Confluent cultures of human diploid fibroblasts, which are synchronized in the G1 phase due to contact inhibition, were released from growth inhibition either by the addition of fresh medium to the cultures or by trypsinization and replating at nonconfluent densities. Either treatment resulted in a synchronous wave of DNA synthesis beginning 10–15 h after treatment and peaking at 20–25 h. In confluent cultures stimulated by fresh medium, either the addition of 0.25 mM N6, O2-dibutyryl-adenosine 3',5'-cyclic monophosphate (db-cAMP) to the medium in the interval 4–8 h after stimulation or the replacement of the fresh medium in that same 4 h interval with the depleted medium present on the cells for the 2 day period before stimulation delayed the synchronous onset of DNA synthesis in the cultures by about 4 h. In nonconfluent cultures freshly seeded from trypsinized confluent cultures, this same depleted medium obtained after a 2 day incubation of fresh medium on confluent cultures is shown to support the progress of the cells into S phase; however, the addition of 0.25 mM db-cAMP to the medium 3½ h after replating still partially prevented the initiation of DNA synthesis in the cultures. The results are discussed in terms of the role of serum and cAMP in the control of cell growth in fibroblast cultures.

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Role of protein kinase C-dependent A-kinase anchoring proteins in lysophosphatidic acid-induced cAMP signaling in human diploid fibroblasts

Aging Cell ◽

10.1111/j.1474-9726.2006.00239.x ◽

2006 ◽

Vol 5 (6) ◽

pp. 451-461 ◽

Cited By ~ 9

Author(s):

Ji-Heon Rhim ◽

Ik-Soon Jang ◽

Eui-Ju Yeo ◽

Kye-Yong Song ◽

Sang Chul Park

Keyword(s):

Protein Kinase C ◽

Protein Kinase ◽

Lysophosphatidic Acid ◽

Camp Signaling ◽

Diploid Fibroblasts ◽

Human Diploid Fibroblasts ◽

Kinase C ◽

Anchoring Proteins

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Screening of senescence-associated genes with specific DNA array reveals the role of IGFBP-3 in premature senescence of human diploid fibroblasts

Free Radical Biology and Medicine ◽

10.1016/j.freeradbiomed.2008.02.001 ◽

2008 ◽

Vol 44 (10) ◽

pp. 1817-1832 ◽

Cited By ~ 36

Author(s):

Florence Debacq-Chainiaux ◽

Thierry Pascal ◽

Emmanuelle Boilan ◽

Coralie Bastin ◽

Emilie Bauwens ◽

...

Keyword(s):

Premature Senescence ◽

Dna Array ◽

Diploid Fibroblasts ◽

Human Diploid Fibroblasts ◽

Senescence Associated Genes ◽

Igfbp 3

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Role of active oxygen species in metal-induced DNA strand breakage in human diploid fibroblasts

Mutation Research/DNA Repair Reports ◽

10.1016/0167-8817(88)90034-x ◽

1988 ◽

Vol 193 (3) ◽

pp. 237-246 ◽

Cited By ~ 32

Author(s):

Ronald D. Snyder

Keyword(s):

Active Oxygen Species ◽

Active Oxygen ◽

Oxygen Species ◽

Diploid Fibroblasts ◽

Human Diploid Fibroblasts ◽

Strand Breakage ◽

Dna Strand ◽

Dna Strand Breakage

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Expression of Senescence-Associated microRNAs and Target Genes in Cellular Aging and Modulation by Tocotrienol-Rich Fraction

Oxidative Medicine and Cellular Longevity ◽

10.1155/2014/725929 ◽

2014 ◽

Vol 2014 ◽

pp. 1-12 ◽

Cited By ~ 7

Author(s):

Sharon Gwee Sian Khee ◽

Yasmin Anum Mohd Yusof ◽

Suzana Makpol

Keyword(s):

Cellular Senescence ◽

Target Genes ◽

Replicative Senescence ◽

Primary Cultures ◽

Ectopic Expression ◽

Cellular Aging ◽

Diploid Fibroblasts ◽

Human Diploid Fibroblasts ◽

Tocotrienol Rich Fraction

Emerging evidences highlight the implication of microRNAs as a posttranscriptional regulator in aging. Several senescence-associated microRNAs (SA-miRNAs) are found to be differentially expressed during cellular senescence. However, the role of dietary compounds on SA-miRNAs remains elusive. This study aimed to elucidate the modulatory role of tocotrienol-rich fraction (TRF) on SA-miRNAs (miR-20a, miR-24, miR-34a, miR-106a, and miR-449a) and established target genes of miR-34a (CCND1, CDK4, and SIRT1) during replicative senescence of human diploid fibroblasts (HDFs). Primary cultures of HDFs at young and senescent were incubated with TRF at 0.5 mg/mL. Taqman microRNA assay showed significant upregulation of miR-24 and miR-34a and downregulation of miR-20a and miR-449a in senescent HDFs (P<0.05). TRF reduced miR-34a expression in senescent HDFs and increased miR-20a expression in young HDFs and increased miR-449a expression in both young and senescent HDFs. Our results also demonstrated that ectopic expression of miR-34a reduced the expression of CDK4 significantly (P<0.05). TRF inhibited miR-34a expression thus relieved its inhibition on CDK4 gene expression. No significant change was observed on the expression of CCND1, SIRT1, and miR-34a upstream transcriptional regulator, TP53. In conclusion tocotrienol-rich fraction prevented cellular senescence of human diploid fibroblasts via modulation of SA-miRNAs and target genes expression.

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Role of fibronectin in the migration of fibroblasts into plasma clots.

The Journal of Cell Biology ◽

10.1083/jcb.102.6.2318 ◽

1986 ◽

Vol 102 (6) ◽

pp. 2318-2323 ◽

Cited By ~ 81

Author(s):

P Knox ◽

S Crooks ◽

C S Rimmer

Keyword(s):

Cell Adhesion ◽

Plasma Fibronectin ◽

Diploid Fibroblasts ◽

Human Diploid Fibroblasts ◽

Absolute Requirement ◽

And Migration ◽

Migration Of Cells

The adhesion and migration of human diploid fibroblasts on plasma clots were measured. The role of plasma fibronectin was examined by depleting plasma of fibronectin before clotting. Fibronectin was not essential for cell adhesion and spreading, although rates were slightly slower on depleted clots. Rates of migration on the surface of clots were unaffected by fibronectin depletion. In contrast, fibronectin was an absolute requirement for migration of cells into plasma clots. Cells migrated rapidly into control clots but completely failed to penetrate the surface of fibronectin-depleted clots. The effect of depletion could only be reversed by adding fibronectin to depleted plasma before clotting. Adsorption of fibronectin after clotting failed to reverse the effect of depletion, suggesting that fibronectin had to be cross-linked by transglutaminase during the clotting process.

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