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Human Endothelial Cell Life Extension by Telomerase Expression

Yang, Jiwei, Chang, Edwin, Cherry, Athena M., Bangs, Charles D., Oei, Yoko, Bodnar, Andrea, Bronstein, Adrienne, Chiu, Choy-Pik, Herron, G. Scott·1999·Journal of Biological Chemistry
DOI 10.1074/jbc.274.37.26141
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FIG. 1 Telomerase activity and telomere length in human endothelial cells after hTERT expression. A, telomerase activity measured by the TRAP assay (see under 'Materials and Methods') was detected in both early (PDL 5) parental HDMECs PD5 and all hTERTECs from as little as 1000 cell equivalents, but was not detected in middle or late passage parental, sham-infected (LacZ) or heat-treated ( HT ) hTERT-HUVECs, hTERT-HAECs, and hTERTHDMECs. B, hTERT-HDMEC telomerase activity was quantified using PCR-ELISA and showed persistent activity up to PDL 100, at levels ranging between 80 and 120% of that of the embryonic kidney tumor cell line, 293. Similar results were obtained from two other human cell strains, hTERT-HCAECs and hTERTHSVECs. C, TRF length of DNA from hTERT-HDMECs at different PDLs showing loss of telomeric DNA from approximately 9 to 4 kbp spanning PDL 100. D, mean TRF length at the indicated PDLs for four representative hTERT-HUVEC clones showing stabilization of telomere length at approximately 2.5 kbp.
FIG. 1 Telomerase activity and telomere length in human endothelial cells after hTERT expression. A, telomerase activity measured by the TRAP assay (see under 'Materials and Methods') was detected in both early (PDL 5) parental HDMECs PD5 and all hTERTECs from as little as 1000 cell equivalents, but was not detected in middle or late passage parental, sham-infected (LacZ) or heat-treated ( HT ) hTERT-HUVECs, hTERT-HAECs, and hTERTHDMECs. B, hTERT-HDMEC telomerase activity was quantified using PCR-ELISA and showed persistent activity up to PDL 100, at levels ranging between 80 and 120% of that of the embryonic kidney tumor cell line, 293. Similar results were obtained from two other human cell strains, hTERT-HCAECs and hTERTHSVECs. C, TRF length of DNA from hTERT-HDMECs at different PDLs showing loss of telomeric DNA from approximately 9 to 4 kbp spanning PDL 100. D, mean TRF length at the indicated PDLs for four representative hTERT-HUVEC clones showing stabilization of telomere length at approximately 2.5 kbp.CC-BY · From the PDF
FIG. 2 Cell morphology of continuously passaged parental and hTERT-HDMECs as a function of PDL. A early passage, primary parental HDMECs at PDL 6; B, senescent parental HDMEC at PDL 30. C and D, sham-transduced (LacZ) parental HDMECs at PDL 6 ( C ) and at PDL 30 ( D ). E and F, hTERT-HDMECs at PDL 6 ( E ) and at PDL 30 ( F ). Bar, 10 m m.
FIG. 2 Cell morphology of continuously passaged parental and hTERT-HDMECs as a function of PDL. A early passage, primary parental HDMECs at PDL 6; B, senescent parental HDMEC at PDL 30. C and D, sham-transduced (LacZ) parental HDMECs at PDL 6 ( C ) and at PDL 30 ( D ). E and F, hTERT-HDMECs at PDL 6 ( E ) and at PDL 30 ( F ). Bar, 10 m m.CC-BY · From the PDF
FIG. 3 Morphogenetic responses of different EC types exposed to Matrigel and 3D collagen. A, early passage primary HUVECs (PDL 27) grown on Matigel formed angiogenic webs as efficiently as hTERT-HUVECs at PDL 127 ( B ). Similarly, early passage (PDL 5) primary HDMECs formed tubule-like structures after 3D collagen exposure ( C ), as did hTERT-HDMECs at PDL 50 ( D ). However, both senescent HUVECs (PDL 50) ( E ) and the transformed HUVEC line ECV304 ( F ) failed to respond to Matrigel. Bar, 10 m m.
FIG. 3 Morphogenetic responses of different EC types exposed to Matrigel and 3D collagen. A, early passage primary HUVECs (PDL 27) grown on Matigel formed angiogenic webs as efficiently as hTERT-HUVECs at PDL 127 ( B ). Similarly, early passage (PDL 5) primary HDMECs formed tubule-like structures after 3D collagen exposure ( C ), as did hTERT-HDMECs at PDL 50 ( D ). However, both senescent HUVECs (PDL 50) ( E ) and the transformed HUVEC line ECV304 ( F ) failed to respond to Matrigel. Bar, 10 m m.CC-BY · From the PDF
FIG. 4 Flow cytometric analysis of primary ECs and hTERT-ECs for constitutive PECAM-1 and TNFa -inducible ICAM-1 cell surface expression. A and B, both parental and hTERT-HUVECs and hTERT-HDMECs expressed . 90% PECAM ( open areas, normal IgG; shaded areas, anti-PECAM IgG). HUVECs (parental and hTERT) ( A ) and ECV304 ( C ) expressed little or no basal ICAM ( open areas ), whereas HDMECs (parental and hTERT) ( B ) and senescent HUVECs (PDL 50) ( C ) had higher basal ICAM levels (5-15%). Irrespective of basal levels, ICAM expression was strongly induced in both parental and hTERT-HUVECs and-HDMECs ( A and B ) by 20 ng/ml of TNFa ( shaded area ), whereas ICAM expression in senescent HUVECs and ECV304 ( C ) was not induced by TNFa .
FIG. 4 Flow cytometric analysis of primary ECs and hTERT-ECs for constitutive PECAM-1 and TNFa -inducible ICAM-1 cell surface expression. A and B, both parental and hTERT-HUVECs and hTERT-HDMECs expressed . 90% PECAM ( open areas, normal IgG; shaded areas, anti-PECAM IgG). HUVECs (parental and hTERT) ( A ) and ECV304 ( C ) expressed little or no basal ICAM ( open areas ), whereas HDMECs (parental and hTERT) ( B ) and senescent HUVECs (PDL 50) ( C ) had higher basal ICAM levels (5-15%). Irrespective of basal levels, ICAM expression was strongly induced in both parental and hTERT-HUVECs and-HDMECs ( A and B ) by 20 ng/ml of TNFa ( shaded area ), whereas ICAM expression in senescent HUVECs and ECV304 ( C ) was not induced by TNFa .CC-BY · From the PDF
Image 5
CC-BY · From the PDF
ECV304
ECV304CC-BY · From the PDF
FIG. 5 Growth and cell cycle control patterns of hTERT( 1 ) ECs versus primary ECs. A, growth curves of four different hTERT( 1 ) HUVEC clones and a single HAEC mass culture remained linear following continuous growth in vitro for 2-3 times the PDL of their respective parental EC controls. B, immunoblotting of pRb in primary HUVECs, HAECs, and HDMECs ( upper panel ) at subconfluency ( S ) or 72 h at confluency ( C ) showed comparable phosphorylation patterns to hTERT( 1 ) ECs ( lower panel ). C, representative photomicrographs of colony formation in soft agar (see under 'Materials and Methods'). None of our hTERT( 1 ) EC strains (HAECs at PDL 127 used as an example) ( right ) formed colonies in soft agar, whereas the ECV304 transformed cell line did ( left ).
FIG. 5 Growth and cell cycle control patterns of hTERT( 1 ) ECs versus primary ECs. A, growth curves of four different hTERT( 1 ) HUVEC clones and a single HAEC mass culture remained linear following continuous growth in vitro for 2-3 times the PDL of their respective parental EC controls. B, immunoblotting of pRb in primary HUVECs, HAECs, and HDMECs ( upper panel ) at subconfluency ( S ) or 72 h at confluency ( C ) showed comparable phosphorylation patterns to hTERT( 1 ) ECs ( lower panel ). C, representative photomicrographs of colony formation in soft agar (see under 'Materials and Methods'). None of our hTERT( 1 ) EC strains (HAECs at PDL 127 used as an example) ( right ) formed colonies in soft agar, whereas the ECV304 transformed cell line did ( left ).CC-BY · From the PDF
FIG. 7 HDMEC programmed cell death as measured by nuclear fragmentation cell death ELISA ( A and C ) and flow cytometric analysis of mitochondrial Apo2.7 positivity ( B and D ) (see under 'Materials and Methods'). A and B, basal levels of apoptosis in primary parental HDMECs showed a dynamic change as a function of PDL with higher rates at mid passage (PDL 15, double asterisks ) versus early (PDL 5) or late (PDL 25). Basal apoptotic rates of two different hTERT-HDMEC lines (hTERT1 and hTERT3) remained stable with increasing PDL, but the HDMEC3 line was significantly less apoptotic versus both primary and hTERT-HDMEC1 ( single asterisks ). C, following induction of apoptosis by treatment with either TNFa (0.1 m g/ml) 1 actinomycin D (1 m g/ml), lipopolysaccharide (0.1 m g/ml) 1 cycloheximide (50 m g/ml), UVC exposure (255 nm for 0.3 min), or serum starvation (40 h), both hTERT-HDMEC lines exhibited significantly lower nuclear fragmentation ( asterisks ) versus senescent primary HDMEC controls. D, the same trend was found for Apo2.7 flow cytometry; however, only lipopolysaccharide-induced apoptosis in hTERT-HDMEC1 reached statistical significance ( asterisk ). Statistical significance, , 0.05. Experiments were repeated three times on hTERTHDMECs. Results shown are represenative of three experiments.
FIG. 7 HDMEC programmed cell death as measured by nuclear fragmentation cell death ELISA ( A and C ) and flow cytometric analysis of mitochondrial Apo2.7 positivity ( B and D ) (see under 'Materials and Methods'). A and B, basal levels of apoptosis in primary parental HDMECs showed a dynamic change as a function of PDL with higher rates at mid passage (PDL 15, double asterisks ) versus early (PDL 5) or late (PDL 25). Basal apoptotic rates of two different hTERT-HDMEC lines (hTERT1 and hTERT3) remained stable with increasing PDL, but the HDMEC3 line was significantly less apoptotic versus both primary and hTERT-HDMEC1 ( single asterisks ). C, following induction of apoptosis by treatment with either TNFa (0.1 m g/ml) 1 actinomycin D (1 m g/ml), lipopolysaccharide (0.1 m g/ml) 1 cycloheximide (50 m g/ml), UVC exposure (255 nm for 0.3 min), or serum starvation (40 h), both hTERT-HDMEC lines exhibited significantly lower nuclear fragmentation ( asterisks ) versus senescent primary HDMEC controls. D, the same trend was found for Apo2.7 flow cytometry; however, only lipopolysaccharide-induced apoptosis in hTERT-HDMEC1 reached statistical significance ( asterisk ). Statistical significance, , 0.05. Experiments were repeated three times on hTERTHDMECs. Results shown are represenative of three experiments.CC-BY · From the PDF

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Research works printed but not linked: 66

  1. Pili, 1994, J. Natl. Cancer Inst., 86, 1303, 10.1093/jnci/86.17.1303 · DOI
  2. Rivard, 1999, Circulation, 99, 111, 10.1161/01.CIR.99.1.111 · DOI
  3. Cooper, 1994, J. Gerontol., 49, B191, 10.1093/geronj/49.5.B191 · DOI
  4. West, 1994, Arch. Dermatol., 130, 87, 10.1001/archderm.1994.01690010091014 · DOI
  5. Campisi, 1996, Cell, 84, 497, 10.1016/S0092-8674(00)81023-5 · DOI
  6. Maier, 1993, Exp. Cell Res., 208, 270, 10.1006/excr.1993.1246 · DOI
  7. Comi, 1995, Exp. Cell Res., 219, 304, 10.1006/excr.1995.1232 · DOI
  8. Maier, 1990, Science, 249, 1570, 10.1126/science.2218499 · DOI
  9. Tokunaga, 1991, Am. J. Pathol., 138, 941
  10. Carrol, 1991, J. Clin. Invest., 87, 1002, 10.1172/JCI115058 · DOI
  11. Sato, 1993, Biochem. Biophys. Res. Commun., 195, 1070, 10.1006/bbrc.1993.2153 · DOI
  12. Sholley, 1976, Am. J. Anat., 147, 243, 10.1002/aja.1001470208 · DOI
  13. Cines, 1998, Blood, 91, 3527
  14. Klagsbrun, 1991, Annu. Rev. Physiol., 53, 217, 10.1146/annurev.ph.53.030191.001245 · DOI
  15. Ades, 1992, J. Invest. Dermatol., 99, 683, 10.1111/1523-1747.ep12613748 · DOI
  16. Dubois, 1991, Exp. Cell Res., 196, 302, 10.1016/0014-4827(91)90265-V · DOI
  17. Candal, 1996, Microvasc. Res., 52, 221, 10.1006/mvre.1996.0060 · DOI
  18. Fontijn, 1995, Exp. Cell Res., 216, 199, 10.1006/excr.1995.1025 · DOI
  19. Cockerill, 1994, Lab. Invest., 71, 497
  20. Watanabe, 1997, Oncogene, 14, 2025, 10.1038/sj.onc.1201033 · DOI
  21. Watanabe, 1997, Exp. Cell Res., 233, 340, 10.1006/excr.1997.3583 · DOI
  22. Jiang, 1999, Nat. Genet., 21, 111, 10.1038/5056 · DOI
  23. Morales, 1999, Nat. Genet., 21, 115, 10.1038/5063 · DOI
  24. Karasek, 1989, J. Invest. Dermatol., 93 Suppl. 2, 33S, 10.1038/jid.1989.6 · DOI
  25. Romero, 1997, J. Cell. Physiol., 173, 84, 10.1002/(SICI)1097-4652(199710)173:1<84::AID-JCP10>3.0.CO;2-N · DOI
  26. Morgenstern, 1990, Nucleic Acids Res., 18, 3587, 10.1093/nar/18.12.3587 · DOI
  27. Kinsella, 1996, Hum. Gene Ther., 7, 1405, 10.1089/hum.1996.7.12-1405 · DOI
  28. Kim, 1997, Nucleic Acids Res., 25, 2595, 10.1093/nar/25.13.2595 · DOI
  29. Allsopp, 1992, Proc. Natl. Acad. Sci. U. S. A., 89, 10114, 10.1073/pnas.89.21.10114 · DOI · Paper page
  30. Vaziri, 1993, Am. J. Hum. Genet., 52, 661
  31. Levy, 1992, J. Mol. Biol., 225, 951, 10.1016/0022-2836(92)90096-3 · DOI · Paper page
  32. Koester, 1997, Cytometry, 29, 306, 10.1002/(SICI)1097-0320(19971201)29:4<306::AID-CYTO7>3.0.CO;2-7 · DOI
  33. Seabright, 1971, Lancet, 2, 971, 10.1016/S0140-6736(71)90287-X · DOI
  34. Dimri, 1995, Proc. Natl. Acad. Sci. U. S. A., 92, 9363, 10.1073/pnas.92.20.9363 · DOI · Paper page
  35. Hsiao, 1997, Anticancer Res., 17, 827
  36. Shay, 1991, Exp. Cell Res., 196, 33, 10.1016/0014-4827(91)90453-2 · DOI · Paper page
  37. Petzelbauer, 1999, 1, 305
  38. Lang, 1994, Development, 120, 3395, 10.1242/dev.120.12.3395 · DOI
  39. Gobé, 1997, J. Struct. Biol., 118, 63, 10.1006/jsbi.1996.3835 · DOI
  40. Sgonc, 1996, J. Clin. Invest., 98, 785, 10.1172/JCI118851 · DOI
  41. Kaplan, 1999, Nat. Med., 5, 292, 10.1038/6509 · DOI
  42. Pollman, 1999, J. Cell. Physiol., 178, 359, 10.1002/(SICI)1097-4652(199903)178:3<359::AID-JCP10>3.0.CO;2-O · DOI
  43. Karsan, 1998, 8, 19
  44. Nor, 1999, Am. J. Pathol., 154, 375, 10.1016/S0002-9440(10)65284-4 · DOI
  45. Claesson-Welsh, 1998, Proc. Natl. Acad. Sci. U. S. A., 95, 5579, 10.1073/pnas.95.10.5579 · DOI
  46. Wang, 1995, Cancer Res., 55, 2284
  47. Chang, 1997, Arch. Otolaryngol.-Head Neck Surg., 123, 507, 10.1001/archotol.1997.01900050055007 · DOI
  48. Chang, 1995, Proc. Natl. Acad. Sci. U. S. A., 92, 11190, 10.1073/pnas.92.24.11190 · DOI
  49. Counter, 1998, Proc. Natl. Acad. Sci. U. S. A., 95, 14723, 10.1073/pnas.95.25.14723 · DOI · Paper page
  50. Zhu, 1999, Proc. Natl Acad. Sci. U. S. A., 96, 3723, 10.1073/pnas.96.7.3723 · DOI
  51. Johnson, 1992, J. Cell. Physiol., 150, 17, 10.1002/jcp.1041500104 · DOI
  52. Nichols, 1987, J. Cel. Physiol., 132, 453, 10.1002/jcp.1041320307 · DOI
  53. Harley, 1992, Exp. Gerontol., 27, 375, 10.1016/0531-5565(92)90068-B · DOI
  54. Meikarnatz, 1995, J. Cell. Biochem., 58, 160, 10.1002/jcb.240580205 · DOI
  55. King, 1995, J. Cell. Biochem., 58, 175, 10.1002/jcb.240580206 · DOI
  56. Kasten, 1998, Cell Death Differ., 5, 132, 10.1038/sj.cdd.4400323 · DOI
  57. Wilkie, 1990, Nature, 346, 868, 10.1038/346868a0 · DOI
  58. Morin, 1991, Nature, 353, 454, 10.1038/353454a0 · DOI
  59. Flint, 1994, Am. J. Hum. Genet., 55, 505
  60. Hande, 1998, Mutat. Res., 404, 205, 10.1016/S0027-5107(98)00115-8 · DOI
  61. Burger, 1997, Eur. J. Cancer, 33, 638, 10.1016/S0959-8049(96)00521-7 · DOI
  62. Kondo, 1998, FASEB J., 12, 801, 10.1096/fasebj.12.10.801 · DOI
  63. Mandal, 1997, J. Biol. Chem., 272, 14183, 10.1074/jbc.272.22.14183 · DOI
  64. Gordon, 1986, Circ. Res., 59, 633, 10.1161/01.RES.59.6.633 · DOI
  65. Kaji, 1981, Exp. Cell Res., 131, 410, 10.1016/0014-4827(81)90245-7 · DOI
  66. Matsumura, 1980, Adv. Exp. Med. Biol., 129, 31, 10.1007/978-1-4684-3734-8_4 · DOI

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Metadata

Authors
Yang, J., Chang, E., Cherry, A. M., Bangs, C. D., Oei, Y., Bodnar, A., Bronstein, A., Chiu, C.-P., & Herron, G. S.
Venue
Journal of Biological Chemistry
Publisher
Elsevier BV
Published
1999-09
Volume
274
Issue
37
Pages
26141-26148
ISSN
0021-9258
DOI
10.1074/jbc.274.37.26141
Cited by
410
References
9
Language
en
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CoChat. (2026). Citation check: Human Endothelial Cell Life Extension by Telomerase Expression. https://app.cochat.ai/papers/10.1074/jbc.274.37.26141
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Yang, J., Chang, E., Cherry, A. M., Bangs, C. D., Oei, Y., Bodnar, A., Bronstein, A., Chiu, C.-P., & Herron, G. S. (1999). Human Endothelial Cell Life Extension by Telomerase Expression. Journal of Biological Chemistry. https://doi.org/10.1074/jbc.274.37.26141