Wnt-induced secreted protein-1 is a prohypertrophic and profibrotic growth factor
Abstract
Wnt1-induced secreted protein-1 (WISP-1) is a member of the cysteine-rich 61, connective tissue growth factor, and nephroblastoma overexpressed (CCN) family of growth factors and is expressed in the heart at low basal levels. The purpose of this study was to investigate whether WISP-1 is upregulated in postinfarct myocardium and whether WISP-1 exerts prohypertrophic and mitogenic effects stimulating myocyte hypertrophy, cardiac fibroblast (CF) proliferation, and collagen expression. Male C57Bl/6 (25 g) mice underwent permanent occlusion of the left anterior descending coronary artery. mRNA and protein levels were analyzed by Northern and Western blot analyses. Cardiomyocyte hypertrophy was quantified by protein and DNA synthesis. CF proliferation was quantified by CyQuant assay, and soluble collagen release by Sircol assay. A time-dependent increase in WISP-1 expression was detected in vivo in the noninfarct zone of the left ventricle, which peaked at 24 h (3.1-fold, P < 0.01). Similarly, biglycan expression was increased by 3.71-fold (P < 0.01). IL-1beta and TNF-alpha expression preceded WISP-1 expression in vivo and stimulated WISP-1 expression in neonatal rat ventricular myocytes in vitro. WISP-1-induced cardiomyocyte hypertrophy was evidenced by increased protein (2.78-fold), but not DNA synthesis, and enhanced Akt phosphorylation and activity. Treatment of primary CF with WISP-1 significantly stimulated proliferation at 48 h (6,966 +/- 264 vs. 5,476 +/- 307 cells/well, P…
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WISP1 promotes cytoprotection in multiple cell types through pathways that require PI 3-K and Akt and, in microglia, involve mTOR and PRAS40.
“WISP1 promotes cytoprotection in multiple cell types through pathways that not only require phosphatidylinositol-3-kinase (PI 3-K) and protein kinase B (Akt) [7, 8, 10, 11, 20, 21], but also utilize pathways in microglia that involve the mammalian target of rapamycin (mTOR) and the proline rich Akt substrate 40 kDa (PRAS40) [13].”
From Tuberous Sclerosis Protein 2 (TSC2) Modulates CCN4 Cytoprotection During Apoptotic Amyloid Toxicity in Microglia (2013) · cites this paper as [20]
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“Although multiple cellular pathways may account for the cytoprotective capacity of WISP1 [7, 8, 10, 11, 20, 21], recent work suggests that mTOR may play a significant role in providing cellular protection with WISP1 [13].”
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- Authors
- Colston, J. T., de la Rosa, S. D., Koehler, M., Gonzales, K., Mestril, R., Freeman, G. L., Bailey, S. R., & Chandrasekar, B.
- Affiliations
- The University of Texas at San Antonio Health Science Center (US)
- Loyola University Chicago (US)
- Venue
- American Journal of Physiology-Heart and Circulatory Physiology
- Publisher
- American Physiological Society
- Published
- 2007-09
- Volume
- 293
- Issue
- 3
- Pages
- H1839-H1846
- ISSN
- 0363-6135 (ISSN-L)
- 1522-1539
- OpenAlex
- W2107187767
- Cited by
- 107
- References
- 0
- Citations by year
- 2026: 2 · 2025: 2 · 2024: 4 · 2023: 2 · 2022: 2 · 2021: 7 · 2020: 5 · 2019: 7 · 2018: 5 · 2017: 10 · 2016: 3 · 2015: 16 · 2014: 3 · 2013: 7 · 2012: 13
- FWCI
- 3.52
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- American Journal of Physiology-Heart and Circulatory Physiology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Heart, Lung, and Blood Institute (HL67971, R01HL068020, HL68020, R01HL067971)
- Topics
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Fibrosis and Remodeling
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Connective Tissue Growth Factor Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Signaling Pathways in Disease
- Keywords
- WISP1, biglycan, myocardial infarction, cardiomyocyte hypertrophy, cardiac fibroblast proliferation, myocardial fibrosis, extracellular matrix, Akt signaling, IL-1β, TNF-α, post-infarction remodeling
- MeSH terms
- Animals, Cells, Cultured, Disease Models, Animal, Fibroblasts, Fibrosis, Hypertrophy, Male, Mice, Inbred C57BL, Myocardial Infarction, Myocardium, Proteoglycans, Proto-Oncogene Proteins, Tumor Necrosis Factor-alpha, Oncogene Proteins, Up-Regulation, Extracellular Matrix Proteins, Rats, Sprague-Dawley, Myocytes, Cardiac, Intercellular Signaling Peptides and Proteins, Cell Proliferation, Mice, Rats, CCN Intercellular Signaling Proteins, Biglycan
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