GDF2 and BMP10 coordinate liver cellular crosstalk to maintain liver health
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Abstract
The liver is the largest solid organ in the body and is primarily composed of hepatocytes (HCs), endothelial cells (ECs), Kupffer cells (KCs), and hepatic stellate cells (HSCs), which spatially interact and cooperate with each other to maintain liver homeostasis. However, the complexity and molecular mechanisms underlying the crosstalk between these different cell types remain to be revealed. Here, we generated mice with conditional deletion of Gdf2 (also known as Bmp9 ) and Bmp10 in different liver cell types and demonstrated that HSCs were the major source of GDF2 and BMP10 in the liver. Using transgenic ALK1 (receptor for GDF2 and BMP10) reporter mice, we found that ALK1 is expressed on KCs and ECs other than HCs and HSCs, and GDF2 and BMP10 secreted by HSCs promote the differentiation of KCs and ECs and maintain their identity. Pdgfb expression was significantly upregulated in KCs and ECs after Gdf2 and Bmp10 deletion, ultimately leading to HSCs activation and liver fibrosis. ECs express several angiocrine factors, such as BMP2, BMP6, Wnt2, and Rspo3, to regulate HC iron metabolism and metabolic zonation. We found that these angiocrine factors were significantly decreased in ECs from Gdf2/Bmp10 HSC-KO mice, which further resulted in liver iron overload and disruption of HC zonation. In summary, we demonstrated that HSCs play a central role in mediating liver cell-cell crosstalk via the production of GDF2 and BMP10, highlighting the important role of intercellular interaction in organ development and homeostasis.
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HSCs interact with other cell populations, such as Kupffer cells and ECs, through additional mediators including GDF2 and BMP10.
“While HSCs interact with other cell populations, such as Kupffer cells and ECs, through additional mediators including GDF2 and BMP1059, our findings in HSC-depleted and Rspo3ΔHSC mice underscore the central role of HSCs interacting with and regulating hepatocytes.”
From Hepatic stellate cells control liver zonation, size and functions via R-spondin 3 (2025) · cites this paper as [59]
HSC mediators besides RSPO3, such as HGF, and possibly neurotrophin-3 or epiregulin, may be involved in additional aspects of HSC-hepatocyte cross-talk and together with ECs collaboratively control hepatocyte health and functions.
“Moreover, HSC mediators besides RSPO3, such as HGF, but possibly also neurotrophin-319 or epiregulin60 may be involved in additional aspects of HSC–hepatocyte cross-talk and—together with ECs29,59—collaboratively control hepatocyte health and functions.”
From Hepatic stellate cells control liver zonation, size and functions via R-spondin 3 (2025) · cites this paper as [59]
qHSCs are enriched in cytokines and growth factors, including hepatocyte growth factor (HGF), bone morphogenetic proteins (BMPs), and R-spondin 3, and this population has therefore also been termed cytokine- and growth factor-enriched HSCs (cyHSCs).
“Moreover, qHSCs are enriched in cytokines and growth factors, including hepatocyte growth factor (HGF), bone morphogenetic proteins (BMPs), and R-spondin 3, and this population has therefore also been termed cytokine- and growth factor-enriched HSCs (cyHSCs) [19, 224, 225].”
From Inflammation and immunity in liver homeostasis and disease: a nexus of hepatocytes, nonparenchymal cells and immune cells (2025) · cites this paper as [225]
HSCs provide signals to endothelial cells via GDF-2 and BMP10, which in turn regulate liver macrophage specialization as well as hepatocyte function and zonation.
“Similarly, HSCs provide signals to endothelial cells via GDF-2 and BMP10, which in turn regulate liver macrophage specialization as well as hepatocyte function and zonation [225].”
From Inflammation and immunity in liver homeostasis and disease: a nexus of hepatocytes, nonparenchymal cells and immune cells (2025) · cites this paper as [225]
qHSCs are considered homeostatic because they maintain liver zonation and function via R-spondin 3 and BMPs and protect hepatocytes from injury via HGF.
“qHSCs are considered homeostatic because they maintain liver zonation and function via R-spondin 3 [19] and BMPs [225] and protect hepatocytes from injury via HGF [224].”
From Inflammation and immunity in liver homeostasis and disease: a nexus of hepatocytes, nonparenchymal cells and immune cells (2025) · cites this paper as [225]
HSC-selective deletion of BMP9 and BMP10 alters Kupffer cell and endothelial cell homeostasis.
“The HSC-selective deletion of BMP9 and BMP10 alters Kupffer cell and endothelial cell homeostasis [225].”
From Inflammation and immunity in liver homeostasis and disease: a nexus of hepatocytes, nonparenchymal cells and immune cells (2025) · cites this paper as [225]
HSCs regulate Kupffer cell homeostasis via BMP9/10.
“For example, HSCs regulate Kupffer cell homeostasis via BMP9/10 [225].”
From Inflammation and immunity in liver homeostasis and disease: a nexus of hepatocytes, nonparenchymal cells and immune cells (2025) · cites this paper as [225]
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- Authors
- Zhao, D., Huang, Z., Li, X., Wang, H., Hou, Q., Wang, Y., Yan, F., Yang, W., Liu, D., Yi, S., Han, C., Hao, Y., & Tang, L.
- Affiliations
- Beijing Proteome Research Center (CN)
- Anhui Medical University (CN)
- Qingdao University (CN)
- Corresponding author
- Tang, Li
- Venue
- eLife
- Publisher
- eLife Sciences Publications, Ltd
- Published
- 2024-10-25
- Volume
- 13
- ISSN
- 2050-084X (ISSN-L)
- PMC
- PMC11509670
- OpenAlex
- W4403762433
- Cited by
- 17
- References
- 44
- Citations by year
- 2026: 8 · 2025: 9
- Type
- posted content
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- eLife (publishedVersion, cc-by)
- bioRxiv (Cold Spring Harbor Laboratory) (acceptedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
- Funders
- National Science Fund for Distinguished Young Scholars (82225009)
- National Natural Science Foundation of China (32270941)
- Topics
- Health Sciences › Medicine › Hepatology › Liver physiology and pathology
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › TGF-β signaling in diseases
- Health Sciences › Medicine › Epidemiology › Liver Disease Diagnosis and Treatment
- Keywords
- BMP9, BMP10, hepatic stellate cells, Kupffer cells, endothelial cells, hepatocytes, ALK1, PDGF-B, liver fibrosis, angiocrine factors, liver iron overload, hepatocyte zonation, liver homeostasis, conditional knockout mice
- MeSH terms
- Animals, Cell Communication, Cell Differentiation, Kupffer Cells, Liver, Mice, Knockout, Bone Morphogenetic Proteins, Hepatocytes, Endothelial Cells, Mice, Hepatic Stellate Cells, Growth Differentiation Factor 2
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