The renal cortical fibroblast in renal tubulointerstitial fibrosis

Qi, Weier; Chen, Xinming; Poronnik, Philip; Pollock, Carol

doi:10.1016/j.biocel.2005.09.005

Cited by 105 publications

(92 citation statements)

References 20 publications

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“…1A) decreased with time, as demonstrated by CD31 immunostaining ( Fig. 1A-1C 2 ; ADR 42d, 296 Ϯ 34/mm 2 ). In the NS-treated group, glomeruli and tubulointerstitium showed normal histology (Fig.…”

Section: Characteristics Of Adr-induced Nephropathymentioning

confidence: 76%

“…The process of tubulointerstitial fibrosis includes the loss of renal tubules, the accumulation of interstitial myofibroblasts, and extracellular matrix (ECM) deposition [1]. Renal hypoxia and oxidative stress [2] induce the accumulation of fibroblasts and the conversion of fibroblasts to active myofibroblasts, leading to ECM deposition and the development of interstitial fibrosis [3,4]. The number of interstitial ␣-smooth muscle actinpositive [␣-SMA(ϩ)] cells, a putative maker for renal interstitial myofibroblasts, is a good prognostic indicator of progression of both human and experimental renal disease [5][6][7][8].…”

Section: Introductionmentioning

confidence: 99%

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The Contribution of Bone Marrow-Derived Cells to the Development of Renal Interstitial Fibrosis

et al. 2006

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Section: Characteristics Of Adr-induced Nephropathymentioning

confidence: 76%

Section: Introductionmentioning

confidence: 99%

The Contribution of Bone Marrow-Derived Cells to the Development of Renal Interstitial Fibrosis

et al. 2006

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“…At the cellular level, one of the main factors of fibrosis is the differentiation of a not well-defined progenitor (local mesenchymal stem cells; fibroblasts; or epithelial, smooth muscle, or stellate cells; or recruited exogenous cells such as perycites or bone marrow fibrocytes) into myofibroblasts, the cells that share a fibroblast/smooth muscle phenotype (Kisseleva & Brenner 2006, Qi et al 2006, Iredale 2007. In fact, myofibroblasts are usually absent from normal tissue.…”

Section: Introductionmentioning

confidence: 99%

Myostatin promotes a fibrotic phenotypic switch in multipotent C3H 10T1/2 cells without affecting their differentiation into myofibroblasts

Artaza¹,

Singh²,

Ferrini³

et al. 2007

Journal of Endocrinology

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Tissue fibrosis, the excessive deposition of collagen/extracellular matrix combined with the reduction of the cell compartment, defines fibroproliferative diseases, a major cause of death and a public health burden. Key cellular processes in fibrosis include the generation of myofibroblasts from progenitor cells, and the activation or switch of already differentiated cells to a fibrotic synthetic phenotype. Myostatin, a negative regulator of skeletal muscle mass, is postulated to be involved in muscle fibrosis. We have examined whether myostatin affects the differentiation of a multipotent mesenchymal mouse cell line into myofibroblasts, and/or modulates the fibrotic phenotype and Smad expression of the cell population. In addition, we investigated the role of follistatin in this process. Incubation of cells with recombinant myostatin protein did not affect the proportion of myofibroblasts in the culture, but significantly upregulated the expression of fibrotic markers such as collagen and the key profibrotic factors transforming growth factor-b1 (TGF-b1) and plasminogen activator inhibitor (PAI-1), as well as Smad3 and 4, and the pSmad2/3. An antifibrotic process evidenced by the upregulation of follistatin, Smad7, and matrix metalloproteinase 8 accompanied these changes. Follistatin inhibited TGF-b1 induction by myostatin. Transfection with a cDNA expressing myostatin upregulated PAI-1, whereas an shRNA against myostatin blocked this effect. In conclusion, myostatin induced a fibrotic phenotype without significantly affecting differentiation into myofibroblasts. The concurrent endogenous antifibrotic reaction confirms the view that phenotypic switches in multipotent and differentiated cells may affect the progress or reversion of fibrosis, and that myostatin pharmacological inactivation may be a novel therapeutic target against fibrosis.

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“…It is characterized by the trans-differentiation of myofibroblasts and excessive accumulation of ECM (8). Chronic inflammation is considered a major contributor to nephropathic changes, including renal fibrosis (15).…”

Section: Discussionmentioning

confidence: 99%

“…Renal fibrosis is characterized by the transdifferentiation of myofibroblasts and deposition of extracellular matrix (ECM) (8). During fibrosis, kidney resident cells such as fibroblasts, epithelial, endothelial or mesangial cells trans-differentiate into myofibroblasts that express and deposit excessive ECM proteins in the renal interstitial spaces, eventually leading to renal fibrosis and functional loss (9).…”

Section: Introductionmentioning

confidence: 99%

Shenqi detoxification granule combined with P311 inhibits epithelial-mesenchymal transition in renal fibrosis <i>via</i> TGF-β1-Smad-ILK pathway

Cai

Liu

et al. 2017

BST

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The renal cortical fibroblast in renal tubulointerstitial fibrosis

Cited by 105 publications

References 20 publications

The Contribution of Bone Marrow-Derived Cells to the Development of Renal Interstitial Fibrosis

The Contribution of Bone Marrow-Derived Cells to the Development of Renal Interstitial Fibrosis

Myostatin promotes a fibrotic phenotypic switch in multipotent C3H 10T1/2 cells without affecting their differentiation into myofibroblasts

Shenqi detoxification granule combined with P311 inhibits epithelial-mesenchymal transition in renal fibrosis <i>via</i> TGF-β1-Smad-ILK pathway

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