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Cited by 105Chemotherapy-induced cardiotoxicity and mitigationCell death mechanisms and regulationCardiac Fibrosis and Remodeling

WNT1-inducible signaling pathway protein-1 activates diverse cell survival pathways and blocks doxorubicin-induced cardiomyocyte death

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Venkatesan, Balachandar, Prabhu, Sumanth D., Venkatachalam, Kaliyamurthi, Mummidi, Srinivas, Valente, Anthony J., Clark, Robert A., Delafontaine, Patrice, Chandrasekar, Bysani·2010·Cellular Signalling
DOI 10.1016/j.cellsig.2010.01.005PMC PMC2885703
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Abstract

The anthracycline antibiotic doxorubicin (DOX) is a potent cancer chemotherapeutic agent that exerts both acute and chronic cardiotoxicity. Here we show that in adult mouse cardiomyocytes, DOX activates (i) the pro-apoptotic p53, (ii) p38MAPK and JNK, (iii) Bax translocation, (iv) cytochrome c release, and (v) caspase 3. Further, it (vi) inhibits expression of anti-apoptotic Akt, Bcl-2 and Bcl-xL, and (vii) induces internucleosomal degradation and cell death. WNT1-inducible signaling pathway protein-1 (WISP1), a CCN family member and a matricellular protein, inhibits DOX-mediated cardiomyocyte death. WISP1 inhibits DOX-induced p53 activation, p38 MAPK and JNK phosphorylation, Bax translocation to mitochondria, and cytochrome c release into cytoplasm. Additionally, WISP1 reverses DOX-induced suppression of Bcl-2 and Bcl-xL expression and Akt inhibition. The pro-survival effects of WISP1 were recapitulated by the forced expression of mutant p53, wild-type Bcl-2, wild-type Bcl-xL, or constitutively active Akt prior to DOX treatment. WISP1 also induces the pro-survival factor Survivin via PI3K/Akt signaling. Overexpression of wild-type, but not mutant Survivin, blunts DOX cytotoxicity. Further, WISP1 stimulates PI3K-Akt-dependent GSK3beta phosphorylation and beta-catenin nuclear translocation. Importantly, WISP1 induces its own expression. Together, these results provide important insights into the cytoprotective effects of WISP1 in cardiomyocytes, and suggest a potential therapeutic role for WISP1 in DOX-induced cardiotoxicity.

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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 [8]

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Authors
Venkatesan, B., Prabhu, S. D., Venkatachalam, K., Mummidi, S., Valente, A. J., Clark, R. A., Delafontaine, P., & Chandrasekar, B.
Affiliations
  • Tulane University (US)
  • University of Louisville (US)
  • The University of Texas at San Antonio Health Science Center (US)
Corresponding author
Chandrasekar, Bysani
ORCID
Venue
Cellular Signalling
Publisher
Elsevier BV
Published
2010-05
Volume
22
Issue
5
Pages
809-820
ISSN
0898-6568 (ISSN-L)
DOI
10.1016/j.cellsig.2010.01.005
PMC
PMC2885703
OpenAlex
W2118318796
Cited by
105
References
58
Citations by year
2026: 2 · 2024: 2 · 2022: 4 · 2021: 5 · 2020: 4 · 2019: 9 · 2018: 4 · 2017: 10 · 2016: 6 · 2015: 12 · 2014: 8 · 2013: 10 · 2012: 12
FWCI
8.57
Type
journal article
Language
en
Open access
Licence
Locations
  • Cellular Signalling (publishedVersion)
  • PubMed (publishedVersion)
  • PubMed Central (acceptedVersion)
Funders
  • Office of Research and Development
  • Biomedical Laboratory Research and Development, VA Office of Research and Development
  • University of Pittsburgh
  • National Institutes of Health
  • National Heart, Lung, and Blood Institute (R01HL086787, HL-86787, HL070241, R01HL099014, R01HL080682, HL080682, R01HL070241)
Topics
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Chemotherapy-induced cardiotoxicity and mitigation
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Fibrosis and Remodeling
Keywords
WISP1, doxorubicin, cardiotoxicity, cardiomyocyte apoptosis, p53, p38 MAPK, JNK, Bax translocation, cytochrome c release, caspase-3, Bcl-2, Bcl-xL, Akt, survivin, PI3K/Akt signaling, GSK3β, β-catenin, CCN family, matricellular proteins, cell survival pathways
MeSH terms
Glycogen Synthase Kinase 3 beta, Survivin, Animals, Cell Nucleus, Cell Survival, Doxorubicin, Enzyme Activation, Male, Mice, Inbred C57BL, Microtubule-Associated Proteins, Phosphorylation, Proto-Oncogene Proteins, Repressor Proteins, Signal Transduction, Tumor Suppressor Protein p53, Cell Death, Phosphatidylinositol 3-Kinases, Mitogen-Activated Protein Kinases, Protein Transport, Myocytes, Cardiac, Glycogen Synthase Kinase 3, Intracellular Signaling Peptides and Proteins, bcl-X Protein, Inhibitor of Apoptosis Proteins, Proto-Oncogene Proteins c-akt, beta Catenin, Mice, CCN Intercellular Signaling Proteins

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