Evgenia V Gerasimovskaya

Summary

Affiliation: University of Colorado Health Sciences Center
Country: USA

Publications

  1. ncbi Extracellular adenosine triphosphate: a potential regulator of vasa vasorum neovascularization in hypoxia-induced pulmonary vascular remodeling
    Evgenia V Gerasimovskaya
    University of Colorado Health Sciences Center, Denver, CO 80262, USA
    Chest 128:608S-610S. 2005
  2. ncbi Extracellular ATP is an autocrine/paracrine regulator of hypoxia-induced adventitial fibroblast growth. Signaling through extracellular signal-regulated kinase-1/2 and the Egr-1 transcription factor
    Evgenia V Gerasimovskaya
    Developmental Lung Biology Research Laboratory, Department of Pediatrics, University of Colorado Health Sciences Center, Denver, Colorado 80262, USA
    J Biol Chem 277:44638-50. 2002
  3. ncbi Extracellular ATP-induced proliferation of adventitial fibroblasts requires phosphoinositide 3-kinase, Akt, mammalian target of rapamycin, and p70 S6 kinase signaling pathways
    Evgenia V Gerasimovskaya
    Developmental Lung Biology Laboratory, University of Colorado Health Sciences Center, Denver, Colorado 80262, USA
    J Biol Chem 280:1838-48. 2005
  4. ncbi Extracellular ATP is a pro-angiogenic factor for pulmonary artery vasa vasorum endothelial cells
    Evgenia V Gerasimovskaya
    Department of Pediatrics, University of Colorado at Denver and Health Sciences Center, B131, 4200 East 9th Ave, Denver, CO 80262, USA
    Angiogenesis 11:169-82. 2008
  5. ncbi PI3K, Rho, and ROCK play a key role in hypoxia-induced ATP release and ATP-stimulated angiogenic responses in pulmonary artery vasa vasorum endothelial cells
    Heather N Woodward
    Department of Pediatrics, 12700 E 19th Ave, University of Colorado Denver, Research Complex 2, Box B131, Aurora, CO 80045, USA
    Am J Physiol Lung Cell Mol Physiol 297:L954-64. 2009
  6. ncbi Activation of phosphatidylinositol 3-kinase, Akt, and mammalian target of rapamycin is necessary for hypoxia-induced pulmonary artery adventitial fibroblast proliferation
    Evgenia V Gerasimovskaya
    Developmental Lung Biology Laboratory, Univ of Colorado Health Sciences Center, 4200 E 9th Ave, Box B131, Denver, CO 80262, USA
    J Appl Physiol 98:722-31. 2005
  7. ncbi Osteopontin is an endogenous modulator of the constitutively activated phenotype of pulmonary adventitial fibroblasts in hypoxic pulmonary hypertension
    Adil Anwar
    Department of Pediatrics, University of Colorado Denver, Aurora, CO 80045, USA
    Am J Physiol Lung Cell Mol Physiol 303:L1-L11. 2012
  8. ncbi Pulmonary artery adventitial fibroblasts cooperate with vasa vasorum endothelial cells to regulate vasa vasorum neovascularization: a process mediated by hypoxia and endothelin-1
    Neil J Davie
    Department of Pediatric Cardiology, University of Colorado Health Sciences Center, 4200 East 9th Avenue, Box C218, Denver, CO 80262, USA
    Am J Pathol 168:1793-807. 2006
  9. ncbi Egr-1 antisense oligonucleotides inhibit hypoxia-induced proliferation of pulmonary artery adventitial fibroblasts
    Mark F Banks
    Developmental Lung Biology Laboratory, Univ of Colorado Health Sciences Center, 4200 E 9th Ave, Box B131, Denver, CO 80262, USA
    J Appl Physiol 98:732-8. 2005
  10. ncbi Complementary effects of extracellular nucleotides and platelet-derived extracts on angiogenesis of vasa vasorum endothelial cells in vitro and subcutaneous Matrigel plugs in vivo
    Mark Roedersheimer
    Department of Pediatrics, University of Colorado Denver, 12700 East 19th Ave, Aurora, CO 80045, USA
    Vasc Cell 3:4. 2011

Collaborators

Detail Information

Publications10

  1. ncbi Extracellular adenosine triphosphate: a potential regulator of vasa vasorum neovascularization in hypoxia-induced pulmonary vascular remodeling
    Evgenia V Gerasimovskaya
    University of Colorado Health Sciences Center, Denver, CO 80262, USA
    Chest 128:608S-610S. 2005
  2. ncbi Extracellular ATP is an autocrine/paracrine regulator of hypoxia-induced adventitial fibroblast growth. Signaling through extracellular signal-regulated kinase-1/2 and the Egr-1 transcription factor
    Evgenia V Gerasimovskaya
    Developmental Lung Biology Research Laboratory, Department of Pediatrics, University of Colorado Health Sciences Center, Denver, Colorado 80262, USA
    J Biol Chem 277:44638-50. 2002
    ..We conclude that hypoxia induces ATP release from endothelial cells and fibroblasts and that the activation of P2 purinoceptors is involved in the regulation of DNA synthesis by fibroblasts under hypoxic conditions...
  3. ncbi Extracellular ATP-induced proliferation of adventitial fibroblasts requires phosphoinositide 3-kinase, Akt, mammalian target of rapamycin, and p70 S6 kinase signaling pathways
    Evgenia V Gerasimovskaya
    Developmental Lung Biology Laboratory, University of Colorado Health Sciences Center, Denver, Colorado 80262, USA
    J Biol Chem 280:1838-48. 2005
    ....
  4. ncbi Extracellular ATP is a pro-angiogenic factor for pulmonary artery vasa vasorum endothelial cells
    Evgenia V Gerasimovskaya
    Department of Pediatrics, University of Colorado at Denver and Health Sciences Center, B131, 4200 East 9th Ave, Denver, CO 80262, USA
    Angiogenesis 11:169-82. 2008
    ..Collectively, our data support the idea that extracellular ATP participates in the expansion of the vasa vasorum that can be observed in hypoxic conditions...
  5. ncbi PI3K, Rho, and ROCK play a key role in hypoxia-induced ATP release and ATP-stimulated angiogenic responses in pulmonary artery vasa vasorum endothelial cells
    Heather N Woodward
    Department of Pediatrics, 12700 E 19th Ave, University of Colorado Denver, Research Complex 2, Box B131, Aurora, CO 80045, USA
    Am J Physiol Lung Cell Mol Physiol 297:L954-64. 2009
    ..Taken together, our findings provide novel evidence for the signaling mechanisms that link hypoxia-induced increases in extracellular ATP and vasa vasorum expansion...
  6. ncbi Activation of phosphatidylinositol 3-kinase, Akt, and mammalian target of rapamycin is necessary for hypoxia-induced pulmonary artery adventitial fibroblast proliferation
    Evgenia V Gerasimovskaya
    Developmental Lung Biology Laboratory, Univ of Colorado Health Sciences Center, 4200 E 9th Ave, Box B131, Denver, CO 80262, USA
    J Appl Physiol 98:722-31. 2005
    ....
  7. ncbi Osteopontin is an endogenous modulator of the constitutively activated phenotype of pulmonary adventitial fibroblasts in hypoxic pulmonary hypertension
    Adil Anwar
    Department of Pediatrics, University of Colorado Denver, Aurora, CO 80045, USA
    Am J Physiol Lung Cell Mol Physiol 303:L1-L11. 2012
    ..Thus our data suggest OPN as an essential contributor to the activated (highly proliferative, migratory, and proinvasive) phenotype of pulmonary adventitial fibroblasts in hypoxic PH...
  8. ncbi Pulmonary artery adventitial fibroblasts cooperate with vasa vasorum endothelial cells to regulate vasa vasorum neovascularization: a process mediated by hypoxia and endothelin-1
    Neil J Davie
    Department of Pediatric Cardiology, University of Colorado Health Sciences Center, 4200 East 9th Avenue, Box C218, Denver, CO 80262, USA
    Am J Pathol 168:1793-807. 2006
    ....
  9. ncbi Egr-1 antisense oligonucleotides inhibit hypoxia-induced proliferation of pulmonary artery adventitial fibroblasts
    Mark F Banks
    Developmental Lung Biology Laboratory, Univ of Colorado Health Sciences Center, 4200 E 9th Ave, Box B131, Denver, CO 80262, USA
    J Appl Physiol 98:732-8. 2005
    ..We conclude that Egr-1 protein expression is very sensitive to upregulation by hypoxia in pulmonary artery adventitial fibroblasts and that it plays an important role in the autonomous growth phenotype induced by hypoxia in these cells...
  10. ncbi Complementary effects of extracellular nucleotides and platelet-derived extracts on angiogenesis of vasa vasorum endothelial cells in vitro and subcutaneous Matrigel plugs in vivo
    Mark Roedersheimer
    Department of Pediatrics, University of Colorado Denver, 12700 East 19th Ave, Aurora, CO 80045, USA
    Vasc Cell 3:4. 2011
    ..abstract:..