Expression of SV40 virus large T antigen by recombinant adenoviruses activates proliferation of corneal endothelium in vitro.

Feldman, Sandy T.; Gjerset, Ruth A.; Gately, Dennis; Chien, Kenneth R.; Feramisco, James R.

doi:10.1172/jci116381

Cited by 22 publications

(16 citation statements)

References 24 publications

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“…Medium was collected 3 days after infection, and the amount of chemokines was assessed by commercially available ELISAs. Values are amount of chemokine secreted (pg/mLϮSEM) over 24 hours by 10 products strongly suggests that specific E1 Ϫ -driven cellular signaling pathways, not the nonspecific activation observed with endotoxin, regulate E1 Ϫ E4 ϩ Advector-mediated adhesion molecule expression.…”

Section: E4mentioning

confidence: 99%

“…Advectors that could infect quiescent ECs provide ideal vectors to introduce genes into vascular endothelium as well as neointimal cells with high efficiency and low toxicity. [1][2][3][4][5][6] Advectors expressing the genes for anti-␣ 1 -antitrypsin, 7 catalase 8 and NO synthetase, 9 simian virus-40 T antigen, 10 and many other genes have successfully been delivered to ECs in vitro or in vivo. However, expression of genes by Advectors has been hampered by infiltration of inflammatory cells and intravascular activation of neointimal cells.…”

mentioning

confidence: 99%

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Infection of Endothelium With E1 ⁻ E4 ⁺ , but Not E1 ⁻ E4 ⁻ , Adenovirus Gene Transfer Vectors Enhances Leukocyte Adhesion and Migration by Modulation of ICAM-1, VCAM-1, CD34, and Chemokine Expression

Rafii

Dias

Meeus

et al. 2001

Circulation Research

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Abstract-Intravascular introduction of replication-deficient adenoviral vectors (Advectors) provides an ideal model of delivery of transgenes for the treatment of various vascular abnormalities. On the basis of the knowledge that Advectors can induce inflammatory responses after intravascular administration, we speculated that cellular activation by Advector infection could directly modulate the endothelial cell (EC) adhesion molecule/chemokine expression repertoire. Infection of human umbilical vein ECs or bone marrow microvascular ECs with an E1 Ϫ E4 ϩ Advector resulted in the upregulation of intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), and CD34, but not E-selectin, P-selectin, CD36, CD13, CD44, HLA-DR or PECAM. Upregulation of ICAM-1, VCAM-1, and CD34 was apparent 12 hours after infection and persisted for weeks after infection. Selective induction of adhesion molecules was mediated by the presence of the E4 gene in the Advector, because infection of ECs with an E1 Ϫ E4Ϫ Advector had no effect on adhesion molecule expression.

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Section: E4mentioning

confidence: 99%

mentioning

confidence: 99%

Infection of Endothelium With E1 ⁻ E4 ⁺ , but Not E1 ⁻ E4 ⁻ , Adenovirus Gene Transfer Vectors Enhances Leukocyte Adhesion and Migration by Modulation of ICAM-1, VCAM-1, CD34, and Chemokine Expression

Rafii

Dias

Meeus

et al. 2001

Circulation Research

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“…17 Several methods have been used to enhance HCE cell proliferation, such as addition of growth factors to the cultured media, EDTA, to destroy the tight junctions and viral oncogene transformation. [18][19][20][21][22] All of these (C) One pair of corneas from a 59-year-old donor incubated as in (B) was fixed with 4% paraformaldehyde, embedded with optimal cutting temperature (OCT), cut into 6 mm serial sections, and immunostained with Ki-67 antibody. Ki-67 positive cells are shown in the endothelium.…”

Section: Discussionmentioning

confidence: 99%

Aspirin-Triggered Lipoxin A4 (15-epi-LXA4) Increases the Endothelial Viability of Human Corneas Storage in Optisol-GS

Kakazu²,

Bazán³

et al. 2011

Journal of Ocular Pharmacology and Therapeutics

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Purpose: The human corneal endothelium has a very low mitotic rate, and with aging there is a decrease in the number of cells. 15-epi-LXA4 is an anti-inflammatory, bioactive lipid formed when aspirin acetylates cyclooxygenease-2 and redirects cyclooxygenease-2 catalytic activity away from prostaglandins. The purpose of the current study was to evaluate the action of 15-epi-LXA4 in the endothelium viability of human corneas stored in Optisol-GS. Methods: Human corneal endothelial (HCE) cells along with the Descemet's membrane were isolated from fresh human eyes obtained from National Disease Research Interchange. Cell phenotype was identified by using the tight junctions cell marker ZO-1. LXA4 receptor (FPR2/ALX) was detected by immunostaining of HCE cells and human corneal tissue using a polyclonal antibody. Cell proliferation was evaluated with Ki-67 antibody. To measure cell migration, confluent HCE cells were wounded by a linear scraping with a sterile pipette tip in the center of the well and incubated for 24 h with or without 15-epi-LXA4. To evaluate the reparative capacity of 15-epi-LXA4, 7 pairs of human corneas were incubated in Dulbecco's modified Eagle's medium/F12 media at 37°C with or without 100 nM 15-epi-LXA4 for 24 h and then stored at 4°C in Optisol-GS for 12 days. Endothelial viability was assessed by 2 staining techniques: a viability/cytotoxicity kit and trypan blue combined with alizarin red S. Results: HCE cells and the endothelium of human corneal sections strongly expressed the LXA4 receptor. There was a 3-fold increase in cell proliferation when HCE cells were incubated with 100 nM 15-epi-LXA4 for 24 h. No significant migration was observed after 24 h incubation with 15-epi-LXA4. Corneas incubated for 24 h in Dulbecco's modified Eagle's medium/F12 media in the presence of 15-epi-LXA4 and then stored for 12 days in Optisol-GS had a 36% to 56% increase in viability compared with controls without 15-epi-LXA4. Conclusions: 15-epi-LXA4 is an important mediator that protects the integrity of the human endothelium during corneal preservation in Optisol-GS.

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“…Therefore, promoting HCECs from the G 1 phase into the S phase is the most critical step in enhancing HCEC proliferation. Methods to enhance HCEC proliferation include: viral oncogene transformation of HCECs [12,18-21], addition of positive growth factors such as epidermal growth factor (EGF), basic fibroblast growth factor (bFGF), or nerve growth factor (NGF) to the culture medium [22], addition of an animal-derived extracellular matrix (ECM) [23-25], and addition of ethylenediaminetetraacetate acid (EDTA) to destroy the tight junctions between HCECs [25-29]. All these methods have limitations, including the long-term safety of transfected HCECs, the low efficiency and limited cell number of untransfected cultures, and the inability to subculture HCECs for more than a few passages [8].…”

Section: Introductionmentioning

confidence: 99%

The M100: Face categorization begins within 100 ms of stimulus presentation

Dong²,

Liu³

et al. 2010

Journal of Vision

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PurposeTo determine whether mouse embryonic stem cell conditioned medium (ESC-CM) increases the proliferative capacity of human corneal endothelial cells (HCECs) in vitro.MethodsPrimary cultures of HCECs were established from explants of the endothelial cell layer, including the Descemet’s membrane. Cells were cultured in human corneal endothelium medium (CEM) containing 25% ESC-CM for the experimental group and CEM alone for the control group. Phase-contrast microscopy and reverse-transcription polymerase chain reaction (RT–PCR) were used to identify HCECs. The eruption time and HCEC morphology were observed under phase-contrast microscopy. We detected the protein expression of zona occludens protein-1 (ZO-1; a tight junction protein) and the Na+-K+-ATPase by western blot analysis and immunocytochemistry. The mRNA expression of the Na+-K+-ATPase, voltage-dependent anion channel 3 (VDAC3), solute carrier family 4, sodium bicarbonate cotransporter member 4 (SLC4A4), and chloride channel protein 3 (CLCN3) were detected by RT–PCR. To explore the proliferation capacity of HCECs, the colony forming efficiency (CFE) was determined by Giemsa staining and the cellular proliferation marker of Ki-67 protein (Ki-67) positive cells were detected by immunocytochemistry and flow cytometry. Progression of the cell cycle and apoptosis were analyzed by flow cytometry. Negative regulation of the cell cycle, as measured by cyclin-dependent kinase inhibitor p21 (p21) levels, was detected by western blot analysis and immunocytochemistry.ResultsIn primary culture, HCECs in the 25%ESC-CM group erupted with polygonal appearance on day 2, while those in the CEM group erupted with slightly larger cells on day 3–4. HCECs in the 25%ESC-CM group could be subcultured until passage 6 without enlargement of cell volume, while those in the CEM group were enlarged and lost their polygonal appearance by passage 2. HCECs in both the 25%ESC-CM and CEM groups expressed ZO-1, Na+-K+-ATPase, VDAC3, SLC4A4, and CLCN3. The number of Ki67 positive cells, CFE, and percentage of cells entering the S and G2 phases were higher in the 25%ESC-CM group than in the CEM group. The number of apoptotic cells and p21 protein expression both decreased in the 25%ESC-CM group.ConclusionsUse of 25%ESC-CM significantly increased the number of proliferating cells. These effects may be achieved through inhibition of p21 expression and apoptosis. These results suggested that 25%ESC-CM may be a new tool for cultivating HCECs for transplantation.

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Expression of SV40 virus large T antigen by recombinant adenoviruses activates proliferation of corneal endothelium in vitro.

Cited by 22 publications

References 24 publications

Infection of Endothelium With E1 ⁻ E4 ⁺ , but Not E1 ⁻ E4 ⁻ , Adenovirus Gene Transfer Vectors Enhances Leukocyte Adhesion and Migration by Modulation of ICAM-1, VCAM-1, CD34, and Chemokine Expression

Infection of Endothelium With E1 ⁻ E4 ⁺ , but Not E1 ⁻ E4 ⁻ , Adenovirus Gene Transfer Vectors Enhances Leukocyte Adhesion and Migration by Modulation of ICAM-1, VCAM-1, CD34, and Chemokine Expression

Aspirin-Triggered Lipoxin A4 (15-epi-LXA4) Increases the Endothelial Viability of Human Corneas Storage in Optisol-GS

The M100: Face categorization begins within 100 ms of stimulus presentation

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Expression of SV40 virus large T antigen by recombinant adenoviruses activates proliferation of corneal endothelium in vitro.

Cited by 22 publications

References 24 publications

Infection of Endothelium With E1 − E4 + , but Not E1 − E4 − , Adenovirus Gene Transfer Vectors Enhances Leukocyte Adhesion and Migration by Modulation of ICAM-1, VCAM-1, CD34, and Chemokine Expression

Infection of Endothelium With E1 − E4 + , but Not E1 − E4 − , Adenovirus Gene Transfer Vectors Enhances Leukocyte Adhesion and Migration by Modulation of ICAM-1, VCAM-1, CD34, and Chemokine Expression

Aspirin-Triggered Lipoxin A4 (15-epi-LXA4) Increases the Endothelial Viability of Human Corneas Storage in Optisol-GS

The M100: Face categorization begins within 100 ms of stimulus presentation

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Product

Resources

About

Infection of Endothelium With E1 ⁻ E4 ⁺ , but Not E1 ⁻ E4 ⁻ , Adenovirus Gene Transfer Vectors Enhances Leukocyte Adhesion and Migration by Modulation of ICAM-1, VCAM-1, CD34, and Chemokine Expression

Infection of Endothelium With E1 ⁻ E4 ⁺ , but Not E1 ⁻ E4 ⁻ , Adenovirus Gene Transfer Vectors Enhances Leukocyte Adhesion and Migration by Modulation of ICAM-1, VCAM-1, CD34, and Chemokine Expression