# CTRP13-Mediated Effects on Endothelial Cell Function and Their Potential Role in Obesity

**Authors:** Muhammad Aslam, Ling Li, Sina Nürnberger, Bernd Niemann, Susanne Rohrbach

PMC · DOI: 10.3390/cells13151291 · Cells · 2024-07-31

## TL;DR

This study shows that CTRP13, a protein linked to obesity, affects endothelial cell function and may contribute to vascular disease.

## Contribution

The study reveals that CTRP13 is upregulated in endothelial cells during obesity and has vaso-modulatory effects.

## Key findings

- CTRP13 is expressed in endothelial cells and is elevated in obese individuals.
- CTRP13 reduces endothelial cell proliferation and alters cell cycle progression via AMPK.
- High glucose and TNF-alpha increase CTRP13 expression in endothelial cells.

## Abstract

Background: Obesity, a major component of cardiometabolic syndrome, contributes to the imbalance between pro- and anti-atherosclerotic factors via dysregulation of adipocytokine secretion. Among these adipocytokines, the C1q/TNF-related proteins (CTRPs) play a role in the modulation of atherosclerosis development and progression. Here, we investigated the vascular effects of CTRP13. Results: CTRP13 is not only expressed in adipose tissue but also in vessels/endothelial cells (ECs) of mice, rats, and humans. Obese individuals (mice, rats, and humans) showed higher vascular CTRP13 expression. Human Umbilical Vein Endothelial Cells (HUVECs), cultured in the presence of serum from obese mice, mimicked this obesity-associated effect on CTRP13 protein expression. Similarly, high glucose conditions and TNF-alpha, but not insulin, resulted in a strong increase in CTRP13 in these cells. Recombinant CTRP13 induced a reduction in EC proliferation via AMPK. In addition, CTRP13 reduced cell cycle progression and increased p53 phosphorylation and p21 protein expression, but reduced Rb phosphorylation, with the effects largely depending on alpha-2 AMPK as suggested by adenoviral overexpression of dominant-negative (DN) or wild-type (WT) alpha 1/alpha 2 AMPK. Conclusion: The present study demonstrates that CTRP13 expression is induced in ECs under diabetic conditions and that CTRP13 possesses significant vaso-modulatory properties which may have an impact on vascular disease progression in patients.

## Linked entities

- **Genes:** C1QL3 (complement C1q like 3) [NCBI Gene 389941], PRKAA1 (protein kinase AMP-activated catalytic subunit alpha 1) [NCBI Gene 5562], TP53 (tumor protein p53) [NCBI Gene 7157], CDKN1A (cyclin dependent kinase inhibitor 1A) [NCBI Gene 1026], RB1 (RB transcriptional corepressor 1) [NCBI Gene 5925]
- **Proteins:** C1QL3 (complement C1q like 3), PRKAA1 (protein kinase AMP-activated catalytic subunit alpha 1), TP53 (tumor protein p53), CDKN1A (cyclin dependent kinase inhibitor 1A), RB1 (RB transcriptional corepressor 1), TNF (tumor necrosis factor)
- **Chemicals:** glucose (PubChem CID 5793), insulin (PubChem CID 70678557)
- **Diseases:** obesity (MONDO:0011122), atherosclerosis (MONDO:0005311)
- **Species:** Mus musculus (taxon 10090), Rattus norvegicus (taxon 10116), Homo sapiens (taxon 9606)

## Full-text entities

- **Genes:** TP53 (tumor protein p53) [NCBI Gene 7157] {aka BCC7, BMFS5, LFS1, P53, TRP53}, C1QL3 (complement C1q like 3) [NCBI Gene 389941] {aka C1QTNF13, C1ql, CTRP13, K100}, TNF (tumor necrosis factor) [NCBI Gene 7124] {aka DIF, IMD127, TNF-alpha, TNFA, TNFSF2, TNLG1F}, PRKAA1 (protein kinase AMP-activated catalytic subunit alpha 1) [NCBI Gene 5562] {aka AMPK, AMPK alpha 1, AMPKa1}, INS (insulin) [NCBI Gene 3630] {aka IDDM, IDDM1, IDDM2, ILPR, IRDN, MODY10}, H3P16 (H3 histone pseudogene 16) [NCBI Gene 644914] {aka H3.6, H3F3AP6, p21}
- **Diseases:** diabetic (MESH:D003920), cardiometabolic syndrome (MESH:D024821), atherosclerosis (MESH:D050197), vascular disease (MESH:D014652), Obese (MESH:D009765)
- **Chemicals:** glucose (MESH:D005947)
- **Species:** Rattus norvegicus (brown rat, species) [taxon 10116], Homo sapiens (human, species) [taxon 9606], Mus musculus (house mouse, species) [taxon 10090]

## Full text

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## Figures

8 figures with captions in the complete paper: https://tomesphere.com/paper/PMC11311976/full.md

## References

67 references — full list in the complete paper: https://tomesphere.com/paper/PMC11311976/full.md

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Source: https://tomesphere.com/paper/PMC11311976