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. 2025 Jun 27:16:268.
doi: 10.25259/SNI_20_2025. eCollection 2025.

Vascular endothelial cadherin dysfunction: A predictor of hypertensive nonlobar intracerebral hemorrhage

Tondi Maspian Tjili  1 , Julius July  2 , Eryati Darwin  3 , Yuliarni Syafrita  4 , Vanessa Angelica Suntoro  2 , Patrick Putra Lukito  5 , Jonathan Setiawan  2
Affiliations

Vascular endothelial cadherin dysfunction: A predictor of hypertensive nonlobar intracerebral hemorrhage

Tondi Maspian Tjili et al. Surg Neurol Int. .

Abstract

Background: Endothelial dysfunction plays a key role in intracerebral hemorrhage (ICH), with vascular endothelial cadherin (VE-cadherin) being essential for maintaining blood vessel integrity and the blood-brain barrier. Hypertension increases ICH risk by damaging blood vessel integrity due to inflammatory cascades. Lower VE-cadherin levels in hypertensive patients suggest its potential as an early predictor of ICH risk.

Methods: This 12-month study included 40 hypertensive control patients and 40 hypertensive patients with nonlobar ICH. Blood samples were analyzed using enzyme-linked immunosorbent assays to measure VEcadherin, interferon gamma, and interleukin-17 levels. Receiver operating characteristic analysis determined a VE-cadherin cutoff value, and a regression model assessed its association with ICH risk.

Results: A VE-cadherin cutoff value of 400.8 pg/dL was identified, with higher levels independently linked to lower odds of nonlobar ICH. VE-cadherin was the only biomarker that remained statistically significant in the regression model. These findings suggest that reduced VE-cadherin levels contribute to ICH development, and its measurement may help identify high-risk patients for early intervention.

Conclusion: VE-cadherin dysfunction in hypertension may serve as a predictor of nonlobar ICH risk. Its protective role highlights its potential as a biomarker for risk assessment and prevention strategies in hypertensive patients. These findings may pave the way for targeted interventions in hypertensive populations, warranting further research to confirm its clinical utility.

Keywords: Adherens junction; Gap junction; Hypertension; Intracerebral hemorrhage; Stroke; Vascular endothelial-cadherin.

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Conflict of interest statement

There are no conflicts of interest.

Figures

Figure 1:
Figure 1:
Receiver operating characteristic (ROC) (a) curve of age, (b) vascular endothelial cadherin, (c) interferon-gamma.
Figure 2:
Figure 2:
(a) Median error bar chart and (b) count cadherin bar chart showring the difference between hypertension only and hypertension + intracerebral hemorrhage (ICH) groups.
See this image and copyright information in PMC

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References

    1. Arif N, Zinnhardt M, Nyamay’Antu A, Teber D, Brückner R, Schaefer K, et al. PECAM-1 supports leukocyte diapedesis by tension-dependent dephosphorylation of VE-cadherin. EMBO J. 2021;40:e106113. - PMC - PubMed
    1. Caillon A, Paradis P, Schiffrin EL. Role of immune cells in hypertension. Br J Pharmacol. 2019;176:1818–28. - PMC - PubMed
    1. Cong X, Kong W. Endothelial tight junctions and their regulatory signaling pathways in vascular homeostasis and disease. Cell Signal. 2020;66:109485. - PubMed
    1. Conway D, Schwartz MA. Lessons from the endothelial junctional mechanosensory complex. F1000 Biol Rep. 2012;4:1. - PMC - PubMed
    1. Dejana E, Tournier-Lasserve E, Weinstein BM. The control of vascular integrity by endothelial cell junctions: Molecular basis and pathological implications. Dev Cell. 2009;16:209–21. - PubMed

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