Effects of rhDecorin on TGF-β1 induced human hepatic stellate cells LX-2 activation

Shi, Yue-Feng; Zhang, Qi; Cheung, Pik-Yuen; Shi, Lin; Fong, Chi-Chun; Zhang, Yaou; Tzang, Chi-Hung; Chan, Bernard P.L.; Fong, Wang‐Fun; Chun, Jay; Kung, Hsiang‐Fu; Yang, Mengsu

doi:10.1016/j.bbagen.2006.09.012

Cited by 39 publications

(30 citation statements)

References 25 publications

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“…Administration of recombinant decorin to rats subjected to ATS-induced glomerulonephritis attenuates TGF-β-mediated fibronectin deposition (Border et al, 1992), thus inhibiting scarring during experimental renal diseases. Such antifibrotic properties have been further illustrated in a variety of organs (Al Haj Zen et al, 2006, Giri et al, 1997, Kolb et al, 2001a, Kolb et al, 2001b, Shi et al, 2006). Although reduced collagen-rich scars formed when adenovirus-derived decorin was transferred to the mice suffering from bleomycin-induced pulmonary fibrosis (Kolb et al, 2001a), this treatment also led to patchy infiltration on day 7 but later decreased compared to administering adenoviral vector alone.…”

Section: Selected Slrps In Renal Inflammatory Diseasesmentioning

confidence: 94%

Soluble biglycan as a biomarker of inflammatory renal diseases

Hsieh

Nastase

Zeng-Brouwers

et al. 2014

The International Journal of Biochemistry & Cell Biology

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Chronic renal inflammation is often associated with a progressive accumulation of various extracellular matrix constituents, including several members of the small leucine-rich proteoglycan (SLRP) gene family. It is becoming increasingly evident that the matrix-unbound SLRPs strongly regulate the progression of inflammation and fibrosis. Soluble SLRPs are generated either via partial proteolytic processing of collagenous matrices or by de novo synthesis evoked by stress or injury. Liberated SLRPs can then bind to and activate Toll-like receptors, thus modulating downstream inflammatory signaling. Preclinical animal models and human studies have recently identified soluble biglycan as a key initiator and regulator of various inflammatory renal diseases. Biglycan, generated by activated macrophages, can enter the circulation and its elevated levels in plasma and renal parenchyma correlate with unfavorable renal function and outcome. In this review, we will focus on the critical role of soluble biglycan in inflammatory signaling in various renal disorders. Moreover, we will provide new data implicating proinflammatory effects of soluble decorin in unilateral ureteral obstruction. Finally, we will critically evaluate the potential application of soluble biglycan vis-à-vis other SLRPs (decorin, lumican and fibromodulin) as a promising target and novel biomarker of inflammatory renal diseases.

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Section: Selected Slrps In Renal Inflammatory Diseasesmentioning

confidence: 94%

Soluble biglycan as a biomarker of inflammatory renal diseases

Hsieh

Nastase

Zeng-Brouwers

et al. 2014

The International Journal of Biochemistry & Cell Biology

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“…1,2,5 Decorin-Mediated Neutralization of TGF-␤ A great deal of attention has been focused on the antifibrotic properties of decorin as a neutralizing factor of TGF-␤, and decorin treatment exerts salutary effects in renal disorders involving TGF-␤ overproduction regardless of the mode of decorin administration. 9,21-24 Two decades of investigations confirmed the antifibrotic effects of decorin in several organs, such as kidney, lung, 25 heart, 26 skeletal muscle, 3 liver, 27 blood vessels, 28 skin, 29 and conjunctiva. 30 Several mechanisms of decorin-mediated inactivation of TGF-␤ are postulated, including physical interaction with TGF-␤ and interference with TGF-␤ signaling, either directly or indirectly by regulating other modulators of TGF-␤ activity, particularly fibrillin-1, myostatin, 3,8,[31][32][33] and formation of decorin/TGF-␤ complexes.…”

Section: Decorinmentioning

confidence: 99%

Small Leucine-Rich Proteoglycans in Kidney Disease

Schaefer¹

2011

Journal of the American Society of Nephrology

101

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“…TGF-β1 is a member of the transformation growth factor family which participates in the initiation and maintenance of fibrogenesis in many organs including liver. Tissue and serum levels of active TGF-β1 are elevated in fibrosis, and application of exogenous TGF-β1 can induce liver fibrosis with the molecular mechanism of TGFβ1/ALK1/ Smad1 signaling pathway [5][6][7]. Protein glycosylation is the enzymatic addition of sugars or oligosaccharides to proteins.…”

Section: Introductionmentioning

confidence: 99%