Mitogenic Properties of Endogenous and Pharmacological Doses of Macrophage Inflammatory Protein-2 after 70% Hepatectomy in the Mouse
Open accessAbstract
Recent studies show CXC chemokine elevations after hepatic resection; blockade of epithelial neutrophil-activating protein (ENA-78), a CXC chemokine, retards hepatic regeneration after resection. Additional studies demonstrate that exogenous macrophage inflammatory protein (MIP)-2, another CXC chemokine, is therapeutic in a murine acetaminophen toxicity model when other therapies fail. The current investigations study MIP-2's effects on the cellular mechanisms involved in liver regeneration in mice after 70% hepatectomy. Administration of exogenous MIP-2 after 70% hepatectomy dramatically increased hepatocyte proliferation as measured by 5-bromo-2'-deoxyuridine staining. Signal transducer and activator of transcription-3 (stat-3) was also detected in greater abundance and persisted in hepatic nuclear extracts from MIP-2-treated mice compared with control mice after hepatic resection. Further, inhibition of the MIP-2 receptor, CXCR2, decreased baseline hepatocyte proliferation and stat-3 expression in the setting of partial hepatectomy. These data show that MIP-2 is important for hepatocyte proliferation after partial hepatectomy and that pharmacological MIP-2 doses after hepatic injury accelerate hepatic regeneration.
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CXC chemokines have proliferative effects on hepatocytes, and CXCR2-knockout mice experience delayed liver regeneration after PHx.
“CXC chemokines have proliferative effects on hepatocytes, and CXCR2-knockout mice experience delayed liver regeneration after PHx (40, 41).”
From Senescent hepatic stellate cells promote liver regeneration through IL-6 and ligands of CXCR2 (2022) · cites this paper as [40]
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Tan, C. Y., Lai, R. C., Wong, W., Dan, Y. Y., Lim, S.-K., & Ho, H. K. (2014) · Stem Cell Research & Therapy · doi:10.1186/scrt465 · Cited by 548 · see citing works
Senescent hepatic stellate cells promote liver regeneration through IL-6 and ligands of CXCR2
Cheng, N., Kim, K.-H., & Lau, L. F. (2022) · JCI Insight · doi:10.1172/jci.insight.158207 · Cited by 87 · see citing works
“CXC chemokines have proliferative effects on hepatocytes, and CXCR2-knockout mice experience delayed liver regeneration after PHx (40, 41).”
- Authors
- Ren, X., Carpenter, A., Hogaboam, C., & Colletti, L.
- Affiliations
- University of Michigan (US)
- Corresponding author
- Colletti, Lisa
- ORCID
- Hogaboam, Cory
- Venue
- The American Journal of Pathology
- Publisher
- Elsevier BV
- Published
- 2003-08
- Volume
- 163
- Issue
- 2
- Pages
- 563-570
- ISSN
- 0002-9440 (ISSN-L)
- PMC
- PMC1868215
- OpenAlex
- W2002452156
- Cited by
- 64
- References
- 4
- Citations by year
- 2024: 2 · 2023: 3 · 2022: 4 · 2021: 1 · 2020: 1 · 2019: 2 · 2018: 1 · 2017: 2 · 2016: 1 · 2015: 4 · 2014: 3 · 2013: 4 · 2012: 2
- FWCI
- 3.06
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- American Journal Of Pathology (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- American Heart Association
- National Institutes of Health
- National Institute of Diabetes and Digestive and Kidney Diseases (R01DK53224, R01DK053224)
- Topics
- Health Sciences › Medicine › Hepatology › Liver physiology and pathology
- Health Sciences › Medicine › Rehabilitation › Wound Healing and Treatments
- Health Sciences › Medicine › Oncology › Chemokine receptors and signaling
- Keywords
- CXCL2, CXC chemokines, partial hepatectomy, liver regeneration, hepatocyte proliferation, STAT3 signaling, CXCL5, chemokine receptor blockade, acetaminophen toxicity
- MeSH terms
- Animals, Antimetabolites, Body Weight, Bromodeoxyuridine, Cell Nucleus, DNA-Binding Proteins, Female, Hepatectomy, Liver Regeneration, Mice, Inbred CBA, Mitogens, Organ Size, Trans-Activators, Chemokines, Hepatocytes, Receptors, Interleukin-8B, STAT3 Transcription Factor, Mice, Chemokine CXCL2
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