SPARC oppositely regulates inflammation and fibrosis in bleomycin-induced lung damage.

Claudio Tripodo, Alessandra Santangelo, Ivano Arioli, Sabina Sangaletti, Claudio Tripodo, Barbara Cappetti, Silvia Piconese, Claudia Chiodoni, Mariella Parenza, Silvia Miotti, Mario P. Colombo

Risultato della ricerca: Article

34 Citazioni (Scopus)

Abstract

Fibrosis results from inflammatory tissue damage and impaired regeneration. In the context of bleomycin-induced pulmonary fibrosis, we demonstrated that the matricellular protein termed secreted protein acidic and rich in cysteine (SPARC) distinctly regulates inflammation and collagen deposition, depending on its cellular origin. Reciprocal Sparc(-/-) and wild-type (WT) bone marrow chimeras revealed that SPARC expression in host fibroblasts is required and sufficient to induce collagen fibrosis in a proper inflammatory environment. Accordingly, Sparc(-/-) >WT chimeras showed exacerbated inflammation and fibrosis due to the inability of Sparc(-/-) macrophages to down-regulate tumor necrosis factor production because of impaired responses to tumor growth factor-β. Hence, the use of bone marrow cells expressing a dominant-negative form of tumor growth factor-β receptor type II under the monocyte-specific CD68 promoter, as a decoy, phenocopied Sparc(-/-) donor chimeras. Our results point to an unexpected dual role of SPARC in oppositely influencing the outcome of fibrosis.
Lingua originaleEnglish
pagine (da-a)3000-3010
Numero di pagine11
RivistaTHE AMERICAN JOURNAL OF PATHOLOGY
Volume179
Stato di pubblicazionePublished - 2011

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Cysteine
Fibrosis
Inflammation
Lung
Proteins
Collagen
Growth Factor Receptors
Pulmonary Fibrosis
Bone Marrow Cells
Regeneration
Monocytes
Neoplasms
Intercellular Signaling Peptides and Proteins
Down-Regulation
Tumor Necrosis Factor-alpha
Fibroblasts
Bone Marrow
Macrophages
indium-bleomycin

All Science Journal Classification (ASJC) codes

  • Pathology and Forensic Medicine

Cita questo

Tripodo, C., Santangelo, A., Arioli, I., Sangaletti, S., Tripodo, C., Cappetti, B., ... Colombo, M. P. (2011). SPARC oppositely regulates inflammation and fibrosis in bleomycin-induced lung damage. THE AMERICAN JOURNAL OF PATHOLOGY, 179, 3000-3010.

SPARC oppositely regulates inflammation and fibrosis in bleomycin-induced lung damage. / Tripodo, Claudio; Santangelo, Alessandra; Arioli, Ivano; Sangaletti, Sabina; Tripodo, Claudio; Cappetti, Barbara; Piconese, Silvia; Chiodoni, Claudia; Parenza, Mariella; Miotti, Silvia; Colombo, Mario P.

In: THE AMERICAN JOURNAL OF PATHOLOGY, Vol. 179, 2011, pag. 3000-3010.

Risultato della ricerca: Article

Tripodo, C, Santangelo, A, Arioli, I, Sangaletti, S, Tripodo, C, Cappetti, B, Piconese, S, Chiodoni, C, Parenza, M, Miotti, S & Colombo, MP 2011, 'SPARC oppositely regulates inflammation and fibrosis in bleomycin-induced lung damage.', THE AMERICAN JOURNAL OF PATHOLOGY, vol. 179, pagg. 3000-3010.
Tripodo C, Santangelo A, Arioli I, Sangaletti S, Tripodo C, Cappetti B e altri. SPARC oppositely regulates inflammation and fibrosis in bleomycin-induced lung damage. THE AMERICAN JOURNAL OF PATHOLOGY. 2011;179:3000-3010.
Tripodo, Claudio ; Santangelo, Alessandra ; Arioli, Ivano ; Sangaletti, Sabina ; Tripodo, Claudio ; Cappetti, Barbara ; Piconese, Silvia ; Chiodoni, Claudia ; Parenza, Mariella ; Miotti, Silvia ; Colombo, Mario P. / SPARC oppositely regulates inflammation and fibrosis in bleomycin-induced lung damage. In: THE AMERICAN JOURNAL OF PATHOLOGY. 2011 ; Vol. 179. pagg. 3000-3010.
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AU - Santangelo, Alessandra

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AU - Sangaletti, Sabina

AU - Tripodo, Claudio

AU - Cappetti, Barbara

AU - Piconese, Silvia

AU - Chiodoni, Claudia

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AU - Miotti, Silvia

AU - Colombo, Mario P.

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AB - Fibrosis results from inflammatory tissue damage and impaired regeneration. In the context of bleomycin-induced pulmonary fibrosis, we demonstrated that the matricellular protein termed secreted protein acidic and rich in cysteine (SPARC) distinctly regulates inflammation and collagen deposition, depending on its cellular origin. Reciprocal Sparc(-/-) and wild-type (WT) bone marrow chimeras revealed that SPARC expression in host fibroblasts is required and sufficient to induce collagen fibrosis in a proper inflammatory environment. Accordingly, Sparc(-/-) >WT chimeras showed exacerbated inflammation and fibrosis due to the inability of Sparc(-/-) macrophages to down-regulate tumor necrosis factor production because of impaired responses to tumor growth factor-β. Hence, the use of bone marrow cells expressing a dominant-negative form of tumor growth factor-β receptor type II under the monocyte-specific CD68 promoter, as a decoy, phenocopied Sparc(-/-) donor chimeras. Our results point to an unexpected dual role of SPARC in oppositely influencing the outcome of fibrosis.

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