Molecular, biochemical and functional characterizations of C1q/TNF family members: adipose-tissue-selective expression patterns, regulation by PPAR-γ agonist, cysteine-mediated oligomerizations, combinatorial associations and metabolic functions
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The insulin-sensitizing hormone, adiponectin, belongs to the expanding C1q/TNF (tumour necrosis factor) family of proteins. We recently identified a family of adiponectin paralogues designated as CTRP (C1q/TNF-related protein) 1-7, and in the present study describe CTRP10. In the present study, we show that CTRP1, CTRP2, CTRP3, CTRP5 and CTRP7 transcripts are expressed predominantly by adipose tissue. In contrast, placenta and eye expressed the highest levels of CTRP6 and CTRP10 transcripts respectively. Expression levels of CTRP1, CTRP2, CTRP3, CTRP6 and CTRP7 transcripts are up-regulated in 8-week-old obese (ob/ob) mice relative to lean controls. Treatment of mice with a PPAR-gamma (peroxisome-proliferator-activated receptor-gamma) agonist, rosiglitazone, increased the expression of CTRP1 and decreased CTRP6 transcript levels. All CTRPs are secreted glycoproteins when expressed in mammalian cells. CTRP1, CTRP2, CTRP3, CTRP5 and CTRP6 circulate in the blood and are potential endocrine hormones; their serum levels vary according to the sex and genetic background of mice. Importantly, serum levels of CTRP1 and CTRP6 are increased in adiponectin-null mice. Like adiponectin, all secreted CTRP proteins form trimers as their basic structural units. CTRP3, CTRP5, CTRP6 and CTRP10 trimers are further assembled into higher-order oligomeric complexes via disulfide bonding mediated by their N-terminal cysteine residues. Besides forming homo-oligomers, CTRP1/CTRP6, CTRP2/CTRP7 and adiponectin/CTRP2 are secreted as heterotrimers, thus providing a mechanism to potentially generate functionally distinct ligands. Functional characterization of one such family member, CTRP1, showed that it specifically activates Akt and p44/42-MAPK (mitogen-activated protein kinase) signalling pathways in differentiated mouse myotubes. Moreover, injection of recombinant CTRP1 into mice significantly reduced their serum glucose levels. Thus at least CTRP1 may be considered a novel adipokine. In summary, these molecular, biochemical and functional data provide an important framework to further address the physiological functions and mechanisms of the action of this family of secreted glycoproteins in normal and disease states.
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The CTRP gene family is up-regulated in ob/ob mice and highly expressed when stimulated with PPARγ agonists.
“This gene family is up-regulated in ob/ob mice and are highly expressed when stimulated with peroxisome proliferator-activated receptor gamma (PPARγ) agonists (Wong et al., 2008)”
From Physical Exercise-Induced Myokines and Muscle-Adipose Tissue Crosstalk: A Review of Current Knowledge and the Implications for Health and Metabolic Diseases (2018) · cites this paper as Wong et al., 2008
The Results section reports that several CTRP transcripts were up-regulated in adipose tissue of 8-week-old ob/ob mice, but at 12 weeks only CTRP6 was increased. It also reports that the PPARγ agonist rosiglitazone increased CTRP1 expression, decreased CTRP6 expression, and had no appreciable effect on the other CTRPs tested. The claim overgeneralizes both findings to the family as a whole. (LLM, conf=0.91)
Experimental — accuracy not yet measuredOther members of the CTRP family are expressed by adipose tissue and are described as adiponectin paralogue genes.
“Other members of the CTRP family are expressed by AT, and they are described as adiponectin paralogue genes (Wong et al., 2008).”
From Physical Exercise-Induced Myokines and Muscle-Adipose Tissue Crosstalk: A Review of Current Knowledge and the Implications for Health and Metabolic Diseases (2018) · cites this paper as Wong et al., 2008
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“…family is up-regulated in ob/ob mice and are highly expressed when stimulated with peroxisome proliferatoractivated receptor gamma (PPARγ) agonists (Wong et al., 2008), however, because it is newly discovered, there is as yet little in the literature regarding the direct crosstalk between…”
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Lack of Association Between Adiponectin Levels and Atherosclerosis in Mice
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CTRP8 and CTRP9B are novel proteins that hetero-oligomerize with C1q/TNF family members
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A Central Role for C1q/TNF-Related Protein 13 (CTRP13) in Modulating Food Intake and Body Weight
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Elevated circulating levels of CTRP1, a novel adipokine, in diabetic patients
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Globular CTRP3 promotes mitochondrial biogenesis in cardiomyocytes through AMPK/PGC-1α pathway
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CTRP2 Overexpression Improves Insulin and Lipid Tolerance in Diet-Induced Obese Mice
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CTRP3 deficiency reduces liver size and alters IL-6 and TGFβ levels in obese mice
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Pericoronary Adipose Tissue: A Novel Therapeutic Target in Obesity-Related Coronary Atherosclerosis
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Development of a novel enzyme-linked immunosorbent assay (ELISA) for measurement of serum CTRP1
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Knockdown of CTRP6 inhibits adipogenesis via lipogenic marker genes and Erk1/2 signalling pathway
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- Authors
- Wong, G. W., Krawczyk, S. A., Kitidis-Mitrokostas, C., Revett, T., Gimeno, R., & Lodish, H. F.
- Affiliations
- Whitehead Institute for Biomedical Research (US)
- Whitehead Institute for Biomedical Research, Cambridge, MA 02142, U.S.A.
- Wyeth (US)
- Corresponding author
- Wong, G. William
- Lodish, Harvey F.
- Venue
- Biochemical Journal
- Publisher
- Portland Press Ltd.
- Published
- 2008-11-12
- Volume
- 416
- Issue
- 2
- Pages
- 161-177
- ISSN
- 0264-6021 (ISSN-L)
- 1470-8728
- PMC
- PMC3936483
- OpenAlex
- W2054584654
- Cited by
- 371
- References
- 53
- Citations by year
- 2026: 7 · 2025: 13 · 2024: 20 · 2023: 21 · 2022: 29 · 2021: 30 · 2020: 35 · 2019: 32 · 2018: 26 · 2017: 24 · 2016: 35 · 2015: 27 · 2014: 18 · 2013: 13 · 2012: 18
- FWCI
- 5.71
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Biochemical Journal (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health (1f32dk067835-01)
- National Heart, Lung, and Blood Institute (K08HL077499, HL077499-01)
- National Institute of Diabetes and Digestive and Kidney Diseases (F32DK067835, R37 DK47618‐19, R37DK047618, R01DK047618)
- Topics
- Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Peroxisome Proliferator-Activated Receptors
- Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
- Keywords
- CTRP, adiponectin, adipose tissue, tissue-specific gene expression, PPARγ agonists, rosiglitazone, obesity, heterotrimers, oligomerization, disulfide bonds, Akt signaling, MAPK signaling, myotubes, insulin sensitivity, adipokines
- MeSH terms
- Adipose Tissue, Animals, Cloning, Molecular, Collagen, Humans, Insulin Resistance, Mice, Inbred Strains, Mice, Transgenic, Proteins, Transfection, Mutagenesis, Site-Directed, Stromal Cells, Plasminogen Activator Inhibitor 1, Adipocytes, Chemokine CCL2, Leptin, PPAR gamma, Mice, Adiponectin
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