Valéry L. E. van Bruggen
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Valéry L. E. van Bruggen has a total of 7 co-authors. Here are the top co-authors by number of shared publications:
- Bart P. F. Rutten
Department of Psychiatry and Neuropsychology, Mental Health and Neuroscience Research Institute, Maastricht University Medical Centre, Maastricht, The Netherlands
1 shared publication - Carine J. Peutz-Kootstra
Department of Pathology, Maastricht University Medical Center+, Cardiovascular Research Institute Maastricht (CARIM), Maastricht, The Netherlands
1 shared publication - Chris P. M. Reutelingsperger
Department of Biochemistry, CARIM School for Cardiovascular Disease, Maastricht University, Maastricht, The Netherlands
1 shared publication - Daan R. M. G. Ophelders
Department of Pediatrics, Maastricht University Medical Center, 6202 AZ Maastricht, The Netherlands
1 shared publication - Hyun Young Park
Department of Psychiatry and Neuropsychology, School for Mental Health and Neuroscience (MHeNS), Maastricht University, Maastricht, The Netherlands
1 shared publication - Reint K. Jellema
Department of Pediatrics, School of Oncology and Reproduction (GROW), Maastricht University, 6229 ER Maastricht, The Netherlands
1 shared publication
Latest Publications
- Open Access
- 21 March 2023
- Published by MDPI AG in International Journal of Molecular Sciences
- Vol. 24 (6) , 5929
Time Dependent Changes in the Ovine Neurovascular Unit; A Potential Neuroprotective Role of Annexin A1 in Neonatal Hypoxic-Ischemic Encephalopathy
Perinatal brain injury following hypoxia-ischemia (HI) is characterized by high mortality rates and long-term disabilities. Previously, we demonstrated that depletion of Annexin A1, an essential mediator in BBB integrity, was associated with a temporal loss of blood-brain barrier (BBB) integrity after HI. Since the molecular and cellular mechanisms mediating the impact of HI are not fully scrutinized, we aimed to gain mechanistic insight into the dynamics of essential BBB structures following global HI in relation to ANXA1 expression. Global HI was induced in instrumented preterm ovine fetuses by transient umbilical cord occlusion (UCO) or sham occlusion (control). BBB structures were assessed at 1, 3, or 7 days post-UCO by immunohistochemical analyses of ANXA1, laminin, collagen type IV, and PDGFRβ for pericytes. Our study revealed that within 24 h after HI, cerebrovascular ANXA1 was depleted, which was followed by depletion of laminin and collagen type IV 3 days after HI. Seven days post-HI, increased pericyte coverage, laminin and collagen type IV expression were detected, indicating vascular remodeling. Our data demonstrate novel mechanistic insights into the loss of BBB integrity after HI, and effective strategies to restore BBB integrity should potentially be applied within 48 h after HI. ANXA1 has great therapeutic potential to target HI-driven brain injury.
- 21 March 2023
- Published by MDPI AG in International Journal of Molecular Sciences
- Vol. 24 (6) , 5929
Open AccessTime Dependent Changes in the Ovine Neurovascular Unit; A Potential Neuroprotective Role of Annexin A1 in Neonatal Hypoxic-Ischemic Encephalopathy
Perinatal brain injury following hypoxia-ischemia (HI) is characterized by high mortality rates and long-term disabilities. Previously, we demonstrated that depletion of Annexin A1, an essential mediator in BBB integrity, was associated with a temporal loss of blood-brain barrier (BBB) integrity after HI. Since the molecular and cellular mechanisms mediating the impact of HI are not fully scrutinized, we aimed to gain mechanistic insight into the dynamics of essential BBB structures following global HI in relation to ANXA1 expression. Global HI was induced in instrumented preterm ovine fetuses by transient umbilical cord occlusion (UCO) or sham occlusion (control). BBB structures were assessed at 1, 3, or 7 days post-UCO by immunohistochemical analyses of ANXA1, laminin, collagen type IV, and PDGFRβ for pericytes. Our study revealed that within 24 h after HI, cerebrovascular ANXA1 was depleted, which was followed by depletion of laminin and collagen type IV 3 days after HI. Seven days post-HI, increased pericyte coverage, laminin and collagen type IV expression were detected, indicating vascular remodeling. Our data demonstrate novel mechanistic insights into the loss of BBB integrity after HI, and effective strategies to restore BBB integrity should potentially be applied within 48 h after HI. ANXA1 has great therapeutic potential to target HI-driven brain injury.