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SPARC regulates TGF-beta1-dependent signaling in primary glomerular mesangial cells.
J Cell Biochem. 2004 Apr 01; 91(5):915-25.JC

Abstract

Secreted protein acidic and rich in cysteine (SPARC), a member of the family of matricellular proteins, regulates the interaction of cells with pleiotropic factors and proteins of the extracellular matrix (ECM). Although it has been appreciated that transforming growth factor beta 1 (TGF-beta1) induces SPARC and collagen type I, we have recently shown that SPARC regulates the expression of TGF-beta1 and collagen type I in renal mesangial cells via a TGF-beta1-dependent pathway, and have proposed a reciprocal, autocrine regulatory feedback loop between SPARC and TGF-beta1. Herein, we sought to determine how SPARC regulates TGF-beta1-dependent signal transduction. Our data indicate that SPARC modulates the TGF-beta1-dependent phosphorylation of Smad-2 in primary mesangial cells derived from wild-type and SPARC-null mice. We also show that SPARC regulates the levels and activation of the stress-activated c-jun-N-terminal kinase (JNK) in mesangial cells by augmentation of the stimulatory effects of TGF-beta1. Furthermore, we found that SPARC increases the levels and the activity of the transcription factor c-jun. These effects of SPARC on the TGF-beta1 signaling pathway appear to be mediated through an interaction with the TGF-beta1-receptor complex, but only in the presence of TGF-beta1 bound to its cognate type II receptor. That SPARC is directly involved in the regulation of the TGF-beta1 signaling cascade is consistent with the paradigm that matricellular proteins modulate interactions among cells, growth factors, and their respective receptors.

Authors+Show Affiliations

Department of Vascular Biology, The Hope Heart Institute, Seattle, Washington 98104, USA.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, P.H.S.

Language

eng

PubMed ID

15034927

Citation

Francki, Aleksandar, et al. "SPARC Regulates TGF-beta1-dependent Signaling in Primary Glomerular Mesangial Cells." Journal of Cellular Biochemistry, vol. 91, no. 5, 2004, pp. 915-25.
Francki A, McClure TD, Brekken RA, et al. SPARC regulates TGF-beta1-dependent signaling in primary glomerular mesangial cells. J Cell Biochem. 2004;91(5):915-25.
Francki, A., McClure, T. D., Brekken, R. A., Motamed, K., Murri, C., Wang, T., & Sage, E. H. (2004). SPARC regulates TGF-beta1-dependent signaling in primary glomerular mesangial cells. Journal of Cellular Biochemistry, 91(5), 915-25.
Francki A, et al. SPARC Regulates TGF-beta1-dependent Signaling in Primary Glomerular Mesangial Cells. J Cell Biochem. 2004 Apr 1;91(5):915-25. PubMed PMID: 15034927.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - SPARC regulates TGF-beta1-dependent signaling in primary glomerular mesangial cells. AU - Francki,Aleksandar, AU - McClure,Timothy D, AU - Brekken,Rolf A, AU - Motamed,Kouros, AU - Murri,Carrie, AU - Wang,Tongwen, AU - Sage,E Helene, PY - 2004/3/23/pubmed PY - 2005/3/8/medline PY - 2004/3/23/entrez SP - 915 EP - 25 JF - Journal of cellular biochemistry JO - J Cell Biochem VL - 91 IS - 5 N2 - Secreted protein acidic and rich in cysteine (SPARC), a member of the family of matricellular proteins, regulates the interaction of cells with pleiotropic factors and proteins of the extracellular matrix (ECM). Although it has been appreciated that transforming growth factor beta 1 (TGF-beta1) induces SPARC and collagen type I, we have recently shown that SPARC regulates the expression of TGF-beta1 and collagen type I in renal mesangial cells via a TGF-beta1-dependent pathway, and have proposed a reciprocal, autocrine regulatory feedback loop between SPARC and TGF-beta1. Herein, we sought to determine how SPARC regulates TGF-beta1-dependent signal transduction. Our data indicate that SPARC modulates the TGF-beta1-dependent phosphorylation of Smad-2 in primary mesangial cells derived from wild-type and SPARC-null mice. We also show that SPARC regulates the levels and activation of the stress-activated c-jun-N-terminal kinase (JNK) in mesangial cells by augmentation of the stimulatory effects of TGF-beta1. Furthermore, we found that SPARC increases the levels and the activity of the transcription factor c-jun. These effects of SPARC on the TGF-beta1 signaling pathway appear to be mediated through an interaction with the TGF-beta1-receptor complex, but only in the presence of TGF-beta1 bound to its cognate type II receptor. That SPARC is directly involved in the regulation of the TGF-beta1 signaling cascade is consistent with the paradigm that matricellular proteins modulate interactions among cells, growth factors, and their respective receptors. SN - 0730-2312 UR - https://www.unboundmedicine.com/medline/citation/15034927/SPARC_regulates_TGF_beta1_dependent_signaling_in_primary_glomerular_mesangial_cells_ L2 - https://doi.org/10.1002/jcb.20008 DB - PRIME DP - Unbound Medicine ER -