ArticleScientific reports2017
Overexpressing the novel autocrine/endocrine adipokine WISP2 induces hyperplasia of the heart, white and brown adipose tissues and prevents insulin resistance.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed.
- Dual Roles of CCN5/WISP2 in Cytosol and Secretome for Maintaining Muscle Homeostasis and Preventing Sarcopenia.Journal of cachexia, sarcopenia and muscle · 2026Article
- The role of epicardial adipose tissue remodelling in heart failure with preserved ejection fraction.Cardiovascular research · 2025Review
- CCN5/WISP2 serum levels in patients with coronary artery disease and type 2 diabetes and its correlation with inflammation and insulin resistance; a machine learning approach.Biochemistry and biophysics reports · 2024Article
- A positive association of serum CCN5/WISP2 levels with the risk of developing gestational diabetes mellitus: a case-control study.The journal of physiological sciences : JPS · 2023Article
- Recent progress on the role of cellular communication network factors (CCN) 3, 4 and 6 in regulating adiposity, liver fibrosis and pancreatic islets.Journal of cell communication and signaling · 2023Review
- New insights into the inter-organ crosstalk mediated by ChREBP.Frontiers in endocrinology · 2023Review
- A STAT5-Smad3 dyad regulates adipogenic plasticity of visceral adipose mesenchymal stromal cells during chronic inflammation.NPJ Regenerative medicine · 2022Article
- Metabolic Effects of CCN5/WISP2 Gene Deficiency and Transgenic Overexpression in Mice.International journal of molecular sciences · 2021Review
- Altered pattern of circulating miRNAs in HIV lipodystrophy perturbs key adipose differentiation and inflammation pathways.JCI insight · 2021Article
- Article
- BMP7 overexpression in adipose tissue induces white adipogenesis and improves insulin sensitivity in ob/ob mice.International journal of obesity (2005) · 2021Article
- Wntless regulates lipogenic gene expression in adipocytes and protects against diet-induced metabolic dysfunction.Molecular metabolism · 2020Article
- Article
- Adipose Tissue Dysfunction as Determinant of Obesity-Associated Metabolic Complications.International journal of molecular sciences · 2019Review
- The role of adipose tissue in cardiovascular health and disease.Nature reviews. Cardiology · 2019 · on this mapReview
- The Diabetes Gene and Wnt Pathway Effector TCF7L2 Regulates Adipocyte Development and Function.Diabetes · 2018Article
- CCN5/WISP2 and metabolic diseases.Journal of cell communication and signaling · 2018Review
- Article
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18 authors.
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Abstract
WISP2 is a novel adipokine, most highly expressed in the adipose tissue and primarily in undifferentiated mesenchymal cells. As a secreted protein, it is an autocrine/paracrine activator of canonical WNT signaling and, as an intracellular protein, it helps to maintain precursor cells undifferentiated. To examine effects of increased WISP2 in vivo, we generated an aP2-WISP2 transgenic (Tg) mouse. These mice had increased serum levels of WISP2, increased lean body mass and whole body energy expenditure, hyperplastic brown/white adipose tissues and larger hyperplastic hearts. Obese Tg mice remained insulin sensitive, had increased glucose uptake by adipose cells and skeletal muscle in vivo and ex vivo, increased GLUT4, increased ChREBP and markers of adipose tissue lipogenesis. Serum levels of the novel fatty acid esters of hydroxy fatty acids (FAHFAs) were increased and transplantation of Tg adipose tissue improved glucose tolerance in recipient mice supporting a role of secreted FAHFAs. The growth-promoting effect of WISP2 was shown by increased BrdU incorporation in vivo and Tg serum increased mesenchymal precursor cell proliferation in vitro. In contrast to conventional canonical WNT ligands, WISP2 expression was inhibited by BMP4 thereby allowing normal induction of adipogenesis. WISP2 is a novel secreted regulator of mesenchymal tissue cellularity.
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