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Article ; Online: The extracellular matrix glycoprotein fibrillin-1 in health and disease

Li Li / Junxin Huang / Youhua Liu

Frontiers in Cell and Developmental Biology, Vol

2024 Volume 11

Abstract: Fibrillin-1 (FBN1) is a large, cysteine-rich, calcium binding extracellular matrix glycoprotein encoded by FBN1 gene. It serves as a structural component of microfibrils and provides force-bearing mechanical support in elastic and nonelastic connective ... ...

Abstract	Fibrillin-1 (FBN1) is a large, cysteine-rich, calcium binding extracellular matrix glycoprotein encoded by FBN1 gene. It serves as a structural component of microfibrils and provides force-bearing mechanical support in elastic and nonelastic connective tissue. As such, mutations in the FBN1 gene can cause a wide variety of genetic diseases such as Marfan syndrome, an autosomal dominant disorder characterized by ocular, skeletal and cardiovascular abnormalities. FBN1 also interacts with numerous microfibril-associated proteins, growth factors and cell membrane receptors, thereby mediating a wide range of biological processes such as cell survival, proliferation, migration and differentiation. Dysregulation of FBN1 is involved in the pathogenesis of many human diseases, such as cancers, cardiovascular disorders and kidney diseases. Paradoxically, both depletion and overexpression of FBN1 upregulate the bioavailability and signal transduction of TGF-β via distinct mechanisms in different settings. In this review, we summarize the structure and expression of FBN1 and present our current understanding of the functional role of FBN1 in various human diseases. This knowledge will allow to develop better strategies for therapeutic intervention of FBN1 related diseases.
Keywords	FBN1 ; extracellular matrix ; marfan syndrome ; TGF-β ; chronic kidney diseases ; Biology (General) ; QH301-705.5
Subject code	610
Language	English
Publishing date	2024-01-01T00:00:00Z
Publisher	Frontiers Media S.A.
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Matrix Metalloproteinase-10 in Kidney Injury Repair and Disease

Xiaoli Sun / Youhua Liu

International Journal of Molecular Sciences, Vol 23, Iss 2131, p

2022 Volume 2131

Abstract: Matrix metalloproteinase-10 (MMP-10) is a zinc-dependent endopeptidase with the ability to degrade a broad spectrum of extracellular matrices and other protein substrates. The expression of MMP-10 is induced in acute kidney injury (AKI) and chronic ... ...

Abstract	Matrix metalloproteinase-10 (MMP-10) is a zinc-dependent endopeptidase with the ability to degrade a broad spectrum of extracellular matrices and other protein substrates. The expression of MMP-10 is induced in acute kidney injury (AKI) and chronic kidney disease (CKD), as well as in renal cell carcinoma (RCC). During the different stages of kidney injury, MMP-10 may exert distinct functions by cleaving various bioactive substrates including heparin-binding epidermal growth factor (HB-EGF), zonula occludens-1 (ZO-1), and pro-MMP-1, -7, -8, -9, -10, -13. Functionally, MMP-10 is reno-protective in AKI by promoting HB-EGF-mediated tubular repair and regeneration, whereas it aggravates podocyte dysfunction and proteinuria by disrupting glomerular filtration integrity via degrading ZO-1. MMP-10 is also involved in cancerous invasion and emerges as a promising therapeutic target in patients with RCC. As a secreted protein, MMP-10 could be detected in the circulation and presents an inverse correlation with renal function. Due to the structural similarities between MMP-10 and the other MMPs, development of specific inhibitors targeting MMP-10 is challenging. In this review, we summarize our current understanding of the role of MMP-10 in kidney diseases and discuss the potential mechanisms of its actions.
Keywords	MMP-10 ; acute kidney injury ; chronic kidney disease ; renal fibrosis ; proteinuria ; HB-EGF ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
Subject code	616
Language	English
Publishing date	2022-02-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Profiling of N6-methyladenosine methylation in porcine longissimus dorsi muscle and unravelling the hub gene ADIPOQ promotes adipogenesis in an m6A-YTHDF1–dependent manner

Huanfa Gong / Tao Gong / Youhua Liu / Yizhen Wang / Xinxia Wang

Journal of Animal Science and Biotechnology, Vol 14, Iss 1, Pp 1-

2023 Volume 16

Abstract: Abstract Background Intramuscular fat (IMF) content is a critical indicator of pork quality, and abnormal IMF is also relevant to human disease as well as aging. Although N6-methyladenosine (m6A) RNA modification was recently found to regulate ... ...

Abstract	Abstract Background Intramuscular fat (IMF) content is a critical indicator of pork quality, and abnormal IMF is also relevant to human disease as well as aging. Although N6-methyladenosine (m6A) RNA modification was recently found to regulate adipogenesis in porcine intramuscular fat, however, the underlying molecular mechanisms was still unclear. Results In this work, we collected 20 longissimus dorsi muscle samples with high (average 3.95%) or low IMF content (average 1.22%) from a unique heterogenous swine population for m6A sequencing (m6A-seq). We discovered 70 genes show both differential RNA expression and m6A modification from high and low IMF group, including ADIPOQ and SFRP1, two hub genes inferred through gene co-expression analysis. Particularly, we observed ADIPOQ, which contains three m6A modification sites within 3′ untranslated and protein coding region, could promote porcine intramuscular preadipocyte differentiation in an m6A-dependent manner. Furthermore, we found the YT521‑B homology domain family protein 1 (YTHDF1) could target and promote ADIPOQ mRNA translation. Conclusions Our study provided a comprehensive profiling of m6A methylation in porcine longissimus dorsi muscle and characterized the involvement of m6A epigenetic modification in the regulation of ADIPOQ mRNA on IMF deposition through an m6A-YTHDF1-dependent manner.
Keywords	ADIPOQ ; Intramuscular fat ; N6-methyladenosine ; Pig ; YTHDF1 ; Animal culture ; SF1-1100 ; Veterinary medicine ; SF600-1100
Subject code	570
Language	English
Publishing date	2023-04-01T00:00:00Z
Publisher	BMC
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: LRP5 and LRP6 in Wnt Signaling

Qian Ren / Jiongcheng Chen / Youhua Liu

Frontiers in Cell and Developmental Biology, Vol

Similarity and Divergence

2021 Volume 9

Abstract: The canonical Wnt/β-catenin signaling plays a fundamental role in regulating embryonic development, injury repair and the pathogenesis of human diseases. In vertebrates, low density lipoprotein receptor-related proteins 5 and 6 (LRP5 and LRP6), the ... ...

Abstract	The canonical Wnt/β-catenin signaling plays a fundamental role in regulating embryonic development, injury repair and the pathogenesis of human diseases. In vertebrates, low density lipoprotein receptor-related proteins 5 and 6 (LRP5 and LRP6), the single-pass transmembrane proteins, act as coreceptors of Wnt ligands and are indispensable for Wnt signal transduction. LRP5 and LRP6 are highly homologous and widely co-expressed in embryonic and adult tissues, and they share similar function in mediating Wnt signaling. However, they also exhibit distinct characteristics by interacting with different protein partners. As such, each of them possesses its own unique functions. In this review, we systematically discuss the similarity and divergence of LRP5 and LRP6 in mediating Wnt and other signaling in the context of kidney diseases. A better understanding of the precise role of LRP5 and LRP6 may afford us to identify and refine therapeutic targets for the treatment of a variety of human diseases.
Keywords	LRP5 ; LRP6 ; Wnt ; β-catenin ; YAP ; kidney fibrosis ; Biology (General) ; QH301-705.5
Subject code	570
Language	English
Publishing date	2021-05-01T00:00:00Z
Publisher	Frontiers Media S.A.
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: High Fat Diet Induces Kidney Injury via Stimulating Wnt/β-Catenin Signaling

Ying Yu / Hongyan Mo / Hui Zhuo / Chen Yu / Youhua Liu

Frontiers in Medicine, Vol

2022 Volume 9

Abstract: High fat diet could cause kidney injury, and the underlying mechanism remains incompletely understood. In this study, we investigated the role of Wnt signaling in this process. Mice were fed with high-fat diet in vivo, and podocytes were stimulated with ... ...

Abstract	High fat diet could cause kidney injury, and the underlying mechanism remains incompletely understood. In this study, we investigated the role of Wnt signaling in this process. Mice were fed with high-fat diet in vivo, and podocytes were stimulated with palmitate in vitro. In mice fed with high-fat diet, renal function was impaired, accompanied by induction of various proinflammatory cytokines and proteinuria. Renal expression of Wnt ligands was also significantly induced, with Wnt1 and Wnt3a being the most pronounced, in high-fat diet mice, compared with normal diet controls. Intervention with ICG-001, a small molecule Wnt/β-catenin inhibitor, improved renal function, inhibited proinflammatory cytokines expression, reduced proteinuria and alleviated podocyte injury. In palmitate-treated podocytes, intracellular lipid deposition was increased, Wnt1 and Wnt3a expression was up-regulated, which was accompanied by an increased proinflammatory cytokines expression and podocyte injury. These lesions caused by palmitate were largely alleviated by ICG-001. Furthermore, ICG-001 also restored the expression of phosphorylated AMPK repressed by palmitate in podocytes or a high-fat diet in mice. These studies suggest that Wnt/β-catenin signaling is involved in the pathogenesis of high-fat diet-induced kidney injury. Targeting this signaling may be a potential therapeutic strategy for alleviating obesity-related nephropathy.
Keywords	high fat ; obesity ; Wnt/β-catenin ; kidney injury ; podocyte ; ICG-001 ; Medicine (General) ; R5-920
Language	English
Publishing date	2022-04-01T00:00:00Z
Publisher	Frontiers Media S.A.
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Design, Synthesis and Bioactivity of Novel Pyrimidine Sulfonate Esters Containing Thioether Moiety

Changkun Li / Youhua Liu / Xiaoli Ren / Yanni Tan / Linhong Jin / Xia Zhou

International Journal of Molecular Sciences, Vol 24, Iss 4691, p

2023 Volume 4691

Abstract: Pesticides play an important role in crop disease and pest control. However, their irrational use leads to the emergence of drug resistance. Therefore, it is necessary to search for new pesticide-lead compounds with new structures. We designed and ... ...

Abstract	Pesticides play an important role in crop disease and pest control. However, their irrational use leads to the emergence of drug resistance. Therefore, it is necessary to search for new pesticide-lead compounds with new structures. We designed and synthesized 33 novel pyrimidine derivatives containing sulfonate groups and evaluated their antibacterial and insecticidal activities. Results: Most of the synthesized compounds showed good antibacterial activity against Xanthomonas oryzae pv. Oryzae ( Xoo ), Xanthomonas axonopodis pv. Citri ( Xac ), Pseudomonas syringae pv. actinidiae ( Psa ) and Ralstonia solanacearum (Rs), and certain insecticidal activity. A 5 , A 31 and A 33 showed strong antibacterial activity against Xoo , with EC 50 values of 4.24, 6.77 and 9.35 μg/mL, respectively. Compounds A 1 , A 3 , A 5 and A 33 showed remarkable activity against Xac (EC 50 was 79.02, 82.28, 70.80 and 44.11 μg/mL, respectively). In addition, A 5 could significantly improve the defense enzyme (superoxide dismutase, peroxidase, phenylalanine ammonia-lyase and catalase) activity of plants against pathogens and thus improve the disease resistance of plants. Moreover, a few compounds also showed good insecticidal activity against Plutella xylostella and Myzus persicae . The results of this study provide insight into the development of new broad-spectrum pesticides.
Keywords	pyrimidine ; sulfonate ; synthesis ; antibacterial activity ; defense enzyme ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
Subject code	540
Language	English
Publishing date	2023-02-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: DHA alleviates diet-induced skeletal muscle fiber remodeling via FTO/m6A/DDIT4/PGC1α signaling

Wei Chen / Yushi Chen / Ruifan Wu / Guanqun Guo / Youhua Liu / Botao Zeng / Xing Liao / Yizhen Wang / Xinxia Wang

BMC Biology, Vol 20, Iss 1, Pp 1-

2022 Volume 19

Abstract: Abstract Background Obesity leads to a decline in the exercise capacity of skeletal muscle, thereby reducing mobility and promoting obesity-associated health risks. Dietary intervention has been shown to be an important measure to regulate skeletal ... ...

Abstract	Abstract Background Obesity leads to a decline in the exercise capacity of skeletal muscle, thereby reducing mobility and promoting obesity-associated health risks. Dietary intervention has been shown to be an important measure to regulate skeletal muscle function, and previous studies have demonstrated the beneficial effects of docosahexaenoic acid (DHA; 22:6 ω-3) on skeletal muscle function. At the molecular level, DHA and its metabolites were shown to be extensively involved in regulating epigenetic modifications, including DNA methylation, histone modifications, and small non-coding microRNAs. However, whether and how epigenetic modification of mRNA such as N6-methyladenosine (m6A) mediates DHA regulation of skeletal muscle function remains unknown. Here, we analyze the regulatory effect of DHA on skeletal muscle function and explore the involvement of m6A mRNA modifications in mediating such regulation. Results DHA supplement prevented HFD-induced decline in exercise capacity and conversion of muscle fiber types from slow to fast in mice. DHA-treated myoblasts display increased mitochondrial biogenesis, while slow muscle fiber formation was promoted through DHA-induced expression of PGC1α. Further analysis of the associated molecular mechanism revealed that DHA enhanced expression of the fat mass and obesity-associated gene (FTO), leading to reduced m6A levels of DNA damage-induced transcript 4 (Ddit4). Ddit4 mRNA with lower m6A marks could not be recognized and bound by the cytoplasmic m6A reader YTH domain family 2 (YTHDF2), thereby blocking the decay of Ddit4 mRNA. Accumulated Ddit4 mRNA levels accelerated its protein translation, and the consequential increased DDIT4 protein abundance promoted the expression of PGC1α, which finally elevated mitochondria biogenesis and slow muscle fiber formation. Conclusions DHA promotes mitochondrial biogenesis and skeletal muscle fiber remodeling via FTO/m6A/DDIT4/PGC1α signaling, protecting against obesity-induced decline in skeletal muscle function.
Keywords	DHA ; FTO ; Muscle fiber ; Obesity ; PGC1α ; Biology (General) ; QH301-705.5
Subject code	610
Language	English
Publishing date	2022-02-01T00:00:00Z
Publisher	BMC
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Insulin-like growth factor 2 mRNA-binding protein 3 promotes kidney injury by regulating β-catenin signaling

Dongyan Song / Jingyue Shang / Yinyi Long / Menghua Zhong / Li Li / Jiongcheng Chen / Yadie Xiang / Huishi Tan / Haili Zhu / Xue Hong / Fan Fan Hou / Haiyan Fu / Youhua Liu

JCI Insight, Vol 8, Iss

2023 Volume 2

Abstract: Wnt/β-catenin is a developmental signaling pathway that plays a crucial role in driving kidney fibrosis after injury. Activation of β-catenin is presumed to be regulated through the posttranslational protein modification. Little is known about whether β- ... ...

Abstract	Wnt/β-catenin is a developmental signaling pathway that plays a crucial role in driving kidney fibrosis after injury. Activation of β-catenin is presumed to be regulated through the posttranslational protein modification. Little is known about whether β-catenin is also subjected to regulation at the posttranscriptional mRNA level. Here, we report that insulin-like growth factor 2 mRNA-binding protein 3 (IGF2BP3) plays a pivotal role in regulating β-catenin. IGF2BP3 was upregulated in renal tubular epithelium of various animal models and patients with chronic kidney disease. IGF2BP3 not only was a direct downstream target of Wnt/β-catenin but also was obligatory for transducing Wnt signal. In vitro, overexpression of IGF2BP3 in kidney tubular cells induced fibrotic responses, whereas knockdown of endogenous IGF2BP3 prevented the expression of injury and fibrosis markers in tubular cells after Wnt3a stimulation. In vivo, exogenous IGF2BP3 promoted β-catenin activation and aggravated kidney fibrosis, while knockdown of IGF2BP3 ameliorated renal fibrotic lesions after obstructive injury. RNA immunoprecipitation and mRNA stability assays revealed that IGF2BP3 directly bound to β-catenin mRNA and stabilized it against degradation. Furthermore, knockdown of IGF2BP3 in tubular cells accelerated β-catenin mRNA degradation in vitro. These studies demonstrate that IGF2BP3 promotes β-catenin signaling and drives kidney fibrosis, which may be mediated through stabilizing β-catenin mRNA. Our findings uncover a previously underappreciated dimension of the complex regulation of Wnt/β-catenin signaling and suggest a potential target for therapeutic intervention of fibrotic kidney diseases.
Keywords	Nephrology ; Medicine ; R
Subject code	570
Language	English
Publishing date	2023-01-01T00:00:00Z
Publisher	American Society for Clinical investigation
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Circular RNA circBNC2 inhibits epithelial cell G2-M arrest to prevent fibrotic maladaptive repair

Peng Wang / Zhitao Huang / Yili Peng / Hongwei Li / Tong Lin / Yingyu Zhao / Zheng Hu / Zhanmei Zhou / Weijie Zhou / Youhua Liu / Fan Fan Hou

Nature Communications, Vol 13, Iss 1, Pp 1-

2022 Volume 19

Abstract: G2/M arrest of epithelial cells leads to fibrosis with unclear mechanisms. This study identifies a protein-encoding circRNA, circBNC2, which inhibits epithelial cells G2/M arrest to prevent fibrotic maladaptive repair in damaged kidney and liver, ... ...

Abstract	G2/M arrest of epithelial cells leads to fibrosis with unclear mechanisms. This study identifies a protein-encoding circRNA, circBNC2, which inhibits epithelial cells G2/M arrest to prevent fibrotic maladaptive repair in damaged kidney and liver, revealing a potential intervention target for fibrosis.
Keywords	Science ; Q
Language	English
Publishing date	2022-10-01T00:00:00Z
Publisher	Nature Portfolio
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Author Correction

Qian Yuan / Qian Ren / Li Li / Huishi Tan / Meizhi Lu / Yuan Tian / Lu Huang / Boxin Zhao / Haiyan Fu / Fan Fan Hou / Lili Zhou / Youhua Liu

Nature Communications, Vol 13, Iss 1, Pp 1-

A Klotho-derived peptide protects against kidney fibrosis by targeting TGF-β signaling

2022 Volume 1

Keywords	Science ; Q
Language	English
Publishing date	2022-11-01T00:00:00Z
Publisher	Nature Portfolio
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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