Type I collagen induces mesenchymal cell differentiation into myofibroblasts through YAP-induced TGF-β1 activation

Liu, Xiaoling; Long, Xinyu; Liu, Weiwei; Zhao, Yanrong; Hayashi, Toshihiko; Yamato, Masayuki; Mizuno, Kazunori; Fujisaki, Hitomi; Tashiro, Shin‐ichi; Ogura, Toshiyuki; Atsuzawa, Yuji; Ikejima, Takashi

doi:10.1016/j.biochi.2018.05.005

Cited by 43 publications

(38 citation statements)

References 89 publications

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“…It has been reported that TGF-β family members TGF-β1 and BMP stimulate the expression of cardiac-specific proteins. The physiological functions of TGF-β1 include regulation of cell adhesion, proliferation and differentiation [ 32–34 ]. Studies have shown that TGF-β1 plays an important role in cell differentiation and vascular remodeling, and induces differentiation of stem cells [ 33 ].…”

Section: Discussionmentioning

confidence: 99%

Cell-derived extracellular matrix-coated silk fibroin scaffold for cardiogenesis of brown adipose stem cells through modulation of TGF-β pathway

Liu

Sun

Dong

et al. 2020

Regenerative Biomaterials

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The cell-derived extracellular matrix (ECM)-modified scaffolds have advantages of mimic tissue specificity and been thought to better mimic the native cellular microenvironment in vitro. ECM derived from cardiac fibroblasts (CFs) are considered as key elements that provide a natural cell growth microenvironment and change the fate of cardiomyocytes (CMs). Here, a new hybrid scaffold is designed based on silk fibroin (SF) scaffold and CFs-derived ECM. CFs were seeded on the SF scaffold for 10 days culturing and decellularized to produce CFs-derived ECM-coated SF scaffold. The results showed that the cell-derived ECM-modified silk fibroin scaffold material contained collagen, laminin, fibronectin and other ECM components with myocardial-like properties. Further to explore its effects on brown adipose stem cells (BASCs) differentiation into CMs. We found that the CF-derived ECM-coated scaffold also increased the expression of CM-specific proteins (e.g. cardiac troponin T and α-actinin) of BASCs. Notably, the β1-integrin-dependent transforming growth factor-β1 signaling pathway was also involved in the regulation of CF-derived ECM by promoting the differentiation of BASCs into CMs. Overall, these findings provide insights into the bionic manufacturing of engineered cardiac tissues (ECTs) and establish a theoretical basis for the construction of ECTs.

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Section: Discussionmentioning

confidence: 99%

Cell-derived extracellular matrix-coated silk fibroin scaffold for cardiogenesis of brown adipose stem cells through modulation of TGF-β pathway

Liu

Sun

Dong

et al. 2020

Regenerative Biomaterials

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“…The staining of YAP was performed as described previously (Liu, Long, Liu, Zhao et al, ). Briefly, cells were fixed using PFA for 20 min, and then permeabilized by 0.15% Triton X‐100 for 12 min.…”

Section: Methodsmentioning

confidence: 99%

“…In fibrosis, the deposition of collagen fibrils induces the nuclear translocation of YAP to aggravate the progression of fibrosis (Herrera, Henke, & Bitterman, ). Our previous studies indicated that col I played a positive role in the activation of YAP that promoted the migration and differentiation of 3T3‐L1 cells into myofibroblasts (Liu, Long, Liu, Zhao et al, ; Xu et al, ). It was reported that ****LATS (inhibitory kinase of YAP) could modulate adipocyte proliferation and differentiation via hippo signaling.…”

Section: Introductionmentioning

confidence: 99%

Type I collagen inhibits adipogenic differentiation via YAP activation in vitro

Liu

Long

Gao

et al. 2019

Journal Cellular Physiology

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Extracellular matrix (ECM) has a marked influence on adipose tissue development.Adipose tissue formation is initiated with proliferation of preadipocytes and migration before undergoing further differentiation into mature adipocytes. Previous studies showed that collagen I (col I) provides a good substratum for 3T3-L1 preadipocytes to grow and migrate. However, it remains unclear whether and how col I regulates adipogenic differentiation of preadipocytes. This study reports that lipid accumulation, representing in vitro adipogenesis of the 3T3-L1 preadipocytes or the mouse primary adipocyte precursor cells derived from subcutaneous adipose tissue in the inguinal region is inhibited by the culture on col I, owing to downregulation of adipogenic factors. Previous study shows that col I enhances 3T3-L1 cell migration via stimulating the nuclear translocation of yes-associated protein (YAP). In this study, we report that downregulation of YAP is associated with in vitro adipogenesis of preadipocytes as well as with in vivo adipose tissue of high-fat diet fed mice. Increased expression of YAP in the cells cultured on col I-coated dishes is correlated with repression of adipogenic differentiation processes. The inactivation of YAP using YAP inhibitor, verteporfin, or YAP small-interfering RNA enhanced adipogenic differentiation and reversed the inhibitory effect of col I. Activation of YAP either by the transfection of YAP plasmid or the silence of large tumor suppressor 1 (LATS1), an inhibitory kinase of YAP, inhibited adipogenic differentiation. The results indicate that col I inhibits adipogenic differentiation via YAP activation in vitro. K E Y W O R D S adipogenic differentiation, collage I, preadipocyte, YAP

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“…Specifically, in the ACM context, the altered PG distribution induces the retention of YAP into the cytoplasm with activation of Hippo pathway and suppression of canonical Wnt-related gene expression (Wada et al, 2011;Zhou and Zhao, 2018). Furthermore, during myofibroblasts differentiation, the YAP/TAZ nuclear localization is associated with Wnt activation and TGFβ1 increase level with consequent SMAD phosphorylation in fibrotic tissues (Liu et al, , 2018Piersma et al, 2015).…”

Section: Molecular Mechanismsmentioning

confidence: 99%

Fibrosis in Arrhythmogenic Cardiomyopathy: The Phantom Thread in the Fibro-Adipose Tissue

et al. 2020

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Arrhythmogenic cardiomyopathy (ACM) is an inherited heart disorder, predisposing to malignant ventricular arrhythmias leading to sudden cardiac death, particularly in young and athletic patients. Pathological features include a progressive loss of myocardium with fibrous or fibro-fatty substitution. During the last few decades, different clinical aspects of ACM have been well investigated but still little is known about the molecular mechanisms that underlie ACM pathogenesis, leading to these phenotypes. In about 50% of ACM patients, a genetic mutation, predominantly in genes that encode for desmosomal proteins, has been identified. However, the mutation-associated mechanisms, causing the observed cardiac phenotype are not always clear. Until now, the attention has been principally focused on the study of molecular mechanisms that lead to a prominent myocardium adipose substitution, an uncommon marker for a cardiac disease, thus often recognized as hallmark of ACM. Nonetheless, based on Task Force Criteria for the diagnosis of ACM, cardiomyocytes death associated with fibrous replacement of the ventricular free wall must be considered the main tissue feature in ACM patients. For this reason, it urges to investigate ACM cardiac fibrosis. In this review, we give an overview on the cellular effectors, possible triggers, and molecular mechanisms that could be responsible for the ventricular fibrotic remodeling in ACM patients.

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Type I collagen induces mesenchymal cell differentiation into myofibroblasts through YAP-induced TGF-β1 activation

Cited by 43 publications

References 89 publications

Cell-derived extracellular matrix-coated silk fibroin scaffold for cardiogenesis of brown adipose stem cells through modulation of TGF-β pathway

Cell-derived extracellular matrix-coated silk fibroin scaffold for cardiogenesis of brown adipose stem cells through modulation of TGF-β pathway

Type I collagen inhibits adipogenic differentiation via YAP activation in vitro

Fibrosis in Arrhythmogenic Cardiomyopathy: The Phantom Thread in the Fibro-Adipose Tissue

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