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Amniotic fluid stem cell-derived vesicles protect from VEGF-induced endothelial damage.
Sedrakyan, S; Villani, V; Da Sacco, S; Tripuraneni, N; Porta, S; Achena, A; Lavarreda-Pearce, M; Petrosyan, A; Soloyan, H; Filippo, R E De; Bussolati, B; Perin, L.
Afiliación
  • Sedrakyan S; GOFARR Laboratory for Organ Regenerative Research and Cell Therapeutics in Urology, Children's Hospital Los Angeles, Division of Urology, Saban Research Institute, University of Southern California, Los Angeles, California, USA.
  • Villani V; GOFARR Laboratory for Organ Regenerative Research and Cell Therapeutics in Urology, Children's Hospital Los Angeles, Division of Urology, Saban Research Institute, University of Southern California, Los Angeles, California, USA.
  • Da Sacco S; GOFARR Laboratory for Organ Regenerative Research and Cell Therapeutics in Urology, Children's Hospital Los Angeles, Division of Urology, Saban Research Institute, University of Southern California, Los Angeles, California, USA.
  • Tripuraneni N; GOFARR Laboratory for Organ Regenerative Research and Cell Therapeutics in Urology, Children's Hospital Los Angeles, Division of Urology, Saban Research Institute, University of Southern California, Los Angeles, California, USA.
  • Porta S; Department of Molecular Biotechnology and Health Sciences, University of Torino, Torino, Italy.
  • Achena A; GOFARR Laboratory for Organ Regenerative Research and Cell Therapeutics in Urology, Children's Hospital Los Angeles, Division of Urology, Saban Research Institute, University of Southern California, Los Angeles, California, USA.
  • Lavarreda-Pearce M; GOFARR Laboratory for Organ Regenerative Research and Cell Therapeutics in Urology, Children's Hospital Los Angeles, Division of Urology, Saban Research Institute, University of Southern California, Los Angeles, California, USA.
  • Petrosyan A; GOFARR Laboratory for Organ Regenerative Research and Cell Therapeutics in Urology, Children's Hospital Los Angeles, Division of Urology, Saban Research Institute, University of Southern California, Los Angeles, California, USA.
  • Soloyan H; GOFARR Laboratory for Organ Regenerative Research and Cell Therapeutics in Urology, Children's Hospital Los Angeles, Division of Urology, Saban Research Institute, University of Southern California, Los Angeles, California, USA.
  • Filippo RE; GOFARR Laboratory for Organ Regenerative Research and Cell Therapeutics in Urology, Children's Hospital Los Angeles, Division of Urology, Saban Research Institute, University of Southern California, Los Angeles, California, USA.
  • Bussolati B; Department of Molecular Biotechnology and Health Sciences, University of Torino, Torino, Italy. benedetta.bussolati@unito.it.
  • Perin L; GOFARR Laboratory for Organ Regenerative Research and Cell Therapeutics in Urology, Children's Hospital Los Angeles, Division of Urology, Saban Research Institute, University of Southern California, Los Angeles, California, USA. lperin@chla.usc.edu.
Sci Rep ; 7(1): 16875, 2017 12 04.
Article en En | MEDLINE | ID: mdl-29203902
Injection of amniotic fluid stem cells (AFSC) delays the course of progression of renal fibrosis in animals with Alport Syndrome, enhancing kidney function and improving survival. The mechanisms responsible for these protective outcomes are still largely unknown. Here, we showed that vascular endothelial growth factor (VEGF) signaling within the glomeruli of Alport mice is strongly elevated early on in the disease, causing glomerular endothelial cell damage. Intraventricular injected AFSC that homed within the glomeruli showed strong modulation of the VEGF activity, particularly in glomerular endothelial cells. To investigate this phenomenon we hypothesized that extracellular vesicles (EVs) produced by the AFSC could be responsible for the observed renoprotection. AFSC derived EVs presented exosomal and stem cell markers on their surface membrane, including VEGFR1 and VEGFR2. EVs were able to modulate VEGF in glomerular endothelial cells by effectively trapping the excess VEGF through VEGFR1-binding preventing cellular damage. In contrast, VEGFR1/sVEGFR1 knockout EVs failed to show similar protection, thus indicating that VEGF trapping is a potentially viable mechanism for AFSC-EV mediated renoprotection. Taken together, our findings establish that EVs secreted by AFSC could target a specific signaling pathway within the glomerulus, thus representing a new potential glomerulus-specific targeted intervention.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Células Madre / Células Endoteliales / Vesículas Extracelulares Tipo de estudio: Prognostic_studies Límite: Animals Idioma: En Revista: Sci Rep Año: 2017 Tipo del documento: Article País de afiliación: Estados Unidos Pais de publicación: Reino Unido
Texto completo
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Células Madre / Células Endoteliales / Vesículas Extracelulares Tipo de estudio: Prognostic_studies Límite: Animals Idioma: En Revista: Sci Rep Año: 2017 Tipo del documento: Article País de afiliación: Estados Unidos Pais de publicación: Reino Unido