Mesenchymal stromal cells improve renal injury in anti-Thy 1 nephritis by modulating inflammatory cytokines and scatter factors

Teresa Rampino, Marilena Gregorini, Giulia Bedino, Giovanni Piotti, Elisa Gabanti, Adalberto Ibatici, Nadia Sessarego, Cristina Piacenza, Chiara Teresa Balenzano, Pasquale Esposito, Francesca Bosio, Grazia Soccio, Francesco Frassoni, Antonio Dal Canton

Research output: Contribution to journalArticle

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Abstract

MSC (mesenchymal stromal cells) can differentiate into renal adult cells, and have anti-inflammatory and immune-modulating activity. In the present study, we investigated whether MSC have protective/reparative effects in anti-Thy1 disease, an Ab (antibody)-induced mesangiolysis resulting in mesangioproliferative nephritis.We studied five groups of rats: (i) rats injected with anti-Thy1.1 Ab on day 0 (group A); (ii) rats injected with anti-Thy1.1 Ab on day 0+MSC on day 3 (group B); (iii) rats injected with anti-Thy1.1 Ab on day 0+mesangial cells on day 3 (group C); (iv) rats injected with saline on day 0+MSC on day 3 (group D); and (v) rats injected with saline on day 0 (group E). Rats were killed on days 1, 3, 7 and 14. MSC prevented the increase in serum creatinine, proteinuria, glomerular monocyte influx and glomerular histopathological injury. Furthermore, MSC suppressed the release of IL-6 (interleukin-6) and TGF-β (transforming growth factor-β), modulated glomerular PDGF-β (platelet-derived growth factor-β), and reset the scatter factors and their receptors, potentiating HGF (hepatocyte growth factor)/Met and inactivating MSP (macrophage-stimulating protein)/Ron (receptor origin nantaise). Few MSC were found in the kidney. These results indicate that MSC improve anti-Thy 1 disease not by replacing injured cells, but by preventing cytokine-driven inflammation and modulating PDGF-β and the scatter factors, i.e. systems that regulate movement and proliferation of monocytes and mesangial cells.

Original languageEnglish
Pages (from-to)25-36
Number of pages12
JournalClinical Science
Volume120
Issue number1
DOIs
Publication statusPublished - Jan 2011

Fingerprint

Hepatocyte Growth Factor
Nephritis
Mesenchymal Stromal Cells
Cytokines
Kidney
Wounds and Injuries
Anti-Idiotypic Antibodies
Mesangial Cells
Platelet-Derived Growth Factor
Monocytes
Proto-Oncogene Proteins c-met
anti-Thy antibody
Transforming Growth Factors
Proteinuria
Interleukin-6
Creatinine
Anti-Inflammatory Agents
Inflammation
Antibodies
Serum

Keywords

  • Anti-Thy 1 nephritis
  • Hepatocyte growth factor
  • Interleukin
  • Mesangioproliferative nephritis
  • Mesenchymal stromal cell
  • Scatter factor

ASJC Scopus subject areas

  • Medicine(all)

Cite this

Mesenchymal stromal cells improve renal injury in anti-Thy 1 nephritis by modulating inflammatory cytokines and scatter factors. / Rampino, Teresa; Gregorini, Marilena; Bedino, Giulia; Piotti, Giovanni; Gabanti, Elisa; Ibatici, Adalberto; Sessarego, Nadia; Piacenza, Cristina; Balenzano, Chiara Teresa; Esposito, Pasquale; Bosio, Francesca; Soccio, Grazia; Frassoni, Francesco; Dal Canton, Antonio.

In: Clinical Science, Vol. 120, No. 1, 01.2011, p. 25-36.

Research output: Contribution to journalArticle

Rampino, Teresa ; Gregorini, Marilena ; Bedino, Giulia ; Piotti, Giovanni ; Gabanti, Elisa ; Ibatici, Adalberto ; Sessarego, Nadia ; Piacenza, Cristina ; Balenzano, Chiara Teresa ; Esposito, Pasquale ; Bosio, Francesca ; Soccio, Grazia ; Frassoni, Francesco ; Dal Canton, Antonio. / Mesenchymal stromal cells improve renal injury in anti-Thy 1 nephritis by modulating inflammatory cytokines and scatter factors. In: Clinical Science. 2011 ; Vol. 120, No. 1. pp. 25-36.
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AB - MSC (mesenchymal stromal cells) can differentiate into renal adult cells, and have anti-inflammatory and immune-modulating activity. In the present study, we investigated whether MSC have protective/reparative effects in anti-Thy1 disease, an Ab (antibody)-induced mesangiolysis resulting in mesangioproliferative nephritis.We studied five groups of rats: (i) rats injected with anti-Thy1.1 Ab on day 0 (group A); (ii) rats injected with anti-Thy1.1 Ab on day 0+MSC on day 3 (group B); (iii) rats injected with anti-Thy1.1 Ab on day 0+mesangial cells on day 3 (group C); (iv) rats injected with saline on day 0+MSC on day 3 (group D); and (v) rats injected with saline on day 0 (group E). Rats were killed on days 1, 3, 7 and 14. MSC prevented the increase in serum creatinine, proteinuria, glomerular monocyte influx and glomerular histopathological injury. Furthermore, MSC suppressed the release of IL-6 (interleukin-6) and TGF-β (transforming growth factor-β), modulated glomerular PDGF-β (platelet-derived growth factor-β), and reset the scatter factors and their receptors, potentiating HGF (hepatocyte growth factor)/Met and inactivating MSP (macrophage-stimulating protein)/Ron (receptor origin nantaise). Few MSC were found in the kidney. These results indicate that MSC improve anti-Thy 1 disease not by replacing injured cells, but by preventing cytokine-driven inflammation and modulating PDGF-β and the scatter factors, i.e. systems that regulate movement and proliferation of monocytes and mesangial cells.

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