Role of activator protein-1 on the effect of arginine-glycine-aspartic acid containing peptides on transforming growth factor-β1 promoter activity

Ruiz-Torres, María Piedad; Pérez-Rivero, Gema; Díez-Marqués, María L.; González-Moya, Mercedes; Ortega, R.; Rodrı́guez-Puyol, Manuel; Rodríguez‐Puyol, Diego

doi:10.1016/j.biocel.2006.07.012

Cited by 11 publications

(5 citation statements)

References 41 publications

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“…[8] In addition to its contribution to the initial chondrogenesis, RGD peptide has also been reported to interact with a v and b 1 integrin subunits (i.e., avb3 and a5b1), which activates integrin-linked kinase (ILK) via the phosphoinositol-3 kinase pathway. [25,26] This leads to enhanced TGF-b promoter activity, where TGF-b is a key mediator in chondrogenesis. Moreover, ILK has been identified as an effector of growth factor signaling and may converge with TGF-b1 signaling pathways to regulate cellular activities.…”

Section: Immunohistological Analysismentioning

confidence: 98%

Injectable Biodegradable Poly(ethylene glycol)/RGD Peptide Hybrid Hydrogels for in vitro Chondrogenesis of Human Mesenchymal Stem Cells

Liu

Tian

Wang

et al. 2010

Macromol. Rapid Commun.

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In this study, an injectable and biodegradable poly(ethylene glycol) (PEG)/arginine-glycine-aspartic (RGD) peptide hybrid hydrogel has been synthesized and used as a biomimetic scaffold for encapsulation of human mesenchymal stem cells (hMSCs). Tetrahydroxyl PEG was functionalized with acrylate, and then reacted with thiol-containing peptide (RGD). Gelation occurred within 30 min with the addition of cells and PEG-dithiol via Michael addition. The hydrogels synthesized with a peptide concentration of 1.0-5.0 mM achieved significantly greater cell viability when compared to the hydrogels without the RGD peptide. However, the effect of RGD on chondrogenesis was found to be dose-dependent. Immunohistology studies demonstrated that hMSCs encapsulated in the hydrogel matrix with 1.0 mM RGD and TGF-β3 showed enhanced positive staining for aggrecan and type II collagen as compared to that with 5.0 mM RGD and unmodified PEG hydrogels. RT-PCR results further revealed that the cells in hydrogels with 1 mM RGD expressed significantly higher levels of type II collagen than those in PEG hydogels without RGD peptide. These findings have demonstrated that the PEG-RGD hydrogels can be a promising scaffold to deliver hMSCs for cartilage repair.

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Section: Immunohistological Analysismentioning

confidence: 98%

Injectable Biodegradable Poly(ethylene glycol)/RGD Peptide Hybrid Hydrogels for in vitro Chondrogenesis of Human Mesenchymal Stem Cells

Liu

Tian

Wang

et al. 2010

Macromol. Rapid Commun.

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“…TGF-␤ 1 overexpression causes renal fibrosis (18). TGF-␤ 1 is regulated by molecules such as ROS, collagens, heat shock protein 70, angiotensin, or glucose (12,13,16,33,34,39,53,60). In turn, TGF-␤ 1 directly stimulates the synthesis of extracellular matrix proteins such as fibronectin (16), collagen (17), or connective tissue growth factor (58).…”

mentioning

confidence: 99%

Relevant role of PKG in the progression of fibrosis induced by TNF-like weak inducer of apoptosis

Martín

Mora

Cortés

et al. 2014

American Journal of Physiology-Renal Physiology

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TNF-like weak inducer of apoptosis (TWEAK) is an inflammatory cytokine that activates the FGF-inducible 14 receptor. Both TWEAK and the FGF-inducible 14 receptor are constitutively expressed in the kidney. TWEAK has been shown to modulate several biological responses, such as inflammation, proliferation, differentiation, and apoptosis, that contribute to kidney injury. However, the role of TWEAK in fibrosis and TWEAK-activated intracellular signaling pathways remain poorly understood. We tested the hypothesis that TWEAK can be a potent inducer of renal fibrosis by increasing transforming growth factor (TGF)-β1 expression (a well-known switch in the fibrosis process) through PKG-I downregulation. We showed that in human mesangial cells, TWEAK increased TGF-β1 expression and activity, leading to higher levels of the extracellular matrix protein fibronectin and decreased PKG-I expression and activity via the Ras pathway. PKG-I activation with 8-bromo-cGMP, Ras inactivation with dominant negative Ras, or Ras pathway inhibition with the ERK1/2 inhibitor PD-98059 resulted in the prevention of TWEAK-induced TGF-β1 upregulation. In vivo, exogenous administration of TWEAK to wild-type mice downregulated kidney PKG-I and increased kidney TGF-β1 expression. These effects were blunted in H-Ras knockout mice. Together, these data demonstrate, for the first time, the key role of PKG-I in TGF-β1 induction by TWEAK in kidney cells.

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“…To determine whether the different ECM proteins expressed in tubular fibrosis can modulate ILK‐dependent water reabsorption, we cultured mIMCD3 cells on a layer of Col I or the control ECM protein Gel (27, 28). Both ILK and AQP2 expression significantly decreased in the mIMCD3 cells grown on Col I compared with those grown on Gel ( Fig.…”

Section: Resultsmentioning

confidence: 99%

“…As part of the multiprotein transmembrane complex, integrin-linked kinase (ILK) is a widely expressed scaffold protein that is crucial in several processes and diseases, from fibrosis to cancer (23,24). ILK modulates the activity of different transcription factors by affecting some of the above-mentioned kinases that may regulate AQP2 (25)(26)(27)(28)(29)(30). It also promotes changes in cytoskeletal functions, facilitating the caveolar trafficking of the vesicles to the cell surface (31).…”

mentioning

confidence: 99%

Integrin‐linked kinase regulates tubular aquaporin‐2 content and intracellular location: a link between the extracellular matrix and water reabsorption

Cano-Peñalver

Griera

Serrano³

et al. 2014

FASEB j.

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One of the clinical alterations observed in chronic renal disease (CRD) is the impaired urine concentration, known as diabetes insipidus (DI). Tubulointerstitial fibrosis of the kidney is also a pathological finding observed in CRD and involves composition of extracellular matrix (ECM). However, an association between these two events has not been elucidated. In this study, we showed that the extracellular-to-intracellular scaffold protein integrin-linked kinase (ILK) regulates expression of tubular water channel aquaporin-2 (AQP2) and its apical membrane presence in the renal tubule. Basally, polyuria and decreased urine osmolality were present in ILK conditional-knockdown (cKD-ILK) adult mice compared with nondepleted ILK littermates. No changes were observed in arginine-vasopressin (AVP) blood levels, renal receptor (V2R), or AQP3 expression. However, tubular AQP2 was decreased in expression and apical membrane presence in cKD-ILK mice, where the canonical V2R/cAMP axis activation is still functional, but independent of the absence of ILK. Thus, cKD-ILK constitutes a nephrogenic diabetes insipidus (NDI) model. AQP2 and ILK colocalize in cultured inner medullary collecting duct (mIMCD3) cells. Specific ILK siRNAs and collagen I (Col) decrease ILK and AQP2 levels and AQP2 presence on the membrane of tubular mIMCD3 cells, which impairs the capacity of the cells to transport water under hypotonic stress. The present work points to ILK as a therapeutic target in NDI.

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Role of activator protein-1 on the effect of arginine-glycine-aspartic acid containing peptides on transforming growth factor-β1 promoter activity

Cited by 11 publications

References 41 publications

Injectable Biodegradable Poly(ethylene glycol)/RGD Peptide Hybrid Hydrogels for in vitro Chondrogenesis of Human Mesenchymal Stem Cells

Injectable Biodegradable Poly(ethylene glycol)/RGD Peptide Hybrid Hydrogels for in vitro Chondrogenesis of Human Mesenchymal Stem Cells

Relevant role of PKG in the progression of fibrosis induced by TNF-like weak inducer of apoptosis

Integrin‐linked kinase regulates tubular aquaporin‐2 content and intracellular location: a link between the extracellular matrix and water reabsorption

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