BRIGHT ASARE-BEDIAKO

All Publications

• Resilient Calvarial Bone Marrow Supports Retinal Repair in Type 2 Diabetes. Advanced science (Weinheim, Baden-Wurttemberg, Germany) Asare-Bediako, B., Calzi, S. L., Behnsen, J. G., Prasad, R., Blaszkiewicz, M., Adu-Rutledge, Y., Rosencrans, R. F., Floyd, J. L., Rennhack, A., Stanford, D., Lin, A., Lydic, T. A., Sheridan, C. M., Boulton, M. E., Townsend, K. L., Busik, J. V., Grant, M. B. 2026: e19680

  Abstract

  Using micro-computed tomography, we identified a network of skull channels in the calvarium of type 2 diabetic (T2D) mice that remained structurally intact and numerically stable despite long-standing disease. The retention of calvaria bone marrow structural integrity was associated with preserved hematopoietic capacity under chronic diabetic conditions, which was not observed in the bone marrow of long bones. A distinctive feature of the calvarial bone marrow compartment was its direct exposure to cerebrospinal fluid (CSF), a property not shared by tibial bone marrow. To characterize the biochemical environment of the murine calvarium, we profiled oxysterols in CSF using mass spectrometry. The CSF exhibited elevated levels of neurotrophic and anti-inflammatory oxysterols, including 22-hydroxycholesterol (22-OHC) and 27-hydroxycholesterol (27-OHC). To assess whether this protective oxysterol signature was conserved in humans, we analyzed CSF samples from diabetic and non-diabetic individuals with obesity-associated idiopathic intracranial hypertension (IIH). Human CSF contained 7α-hydroxy-3-oxo-4-cholestenoic acid (7-HOCA), a metabolite of 27-OHC, supporting the conservation of this neuroprotective profile across species. Given the anatomical proximity of the calvarium to the eye, we hypothesized that calvaria bone marrow may serve as a reservoir for immune cells recruited to the injured or infected retina. The calvaria bone marrow was the predominant source of myeloid angiogenic cells (MACs) and neutrophils, mobilizing these cells at levels approximately 20-fold higher than long bones. These findings demonstrate that calvarial bone marrow plays a critical role in retinal immune defense, while maintaining both structural integrity and functional capacity despite chronic T2D.

  View details for DOI 10.1002/advs.202519680

  View details for PubMedID 41486419

• Endothelial MEMO1 Regulates Angiogenic Signaling in a Model of Retinopathy of Prematurity. FASEB bioAdvances Ramshekar, A., Asare-Bediako, B., Nguyen, J., Suresh, A., Simmons, A., Bretz, C. A., Wang, H., Kunz, E., Zaugg, C. J., Wallace-Carrete, C., Hartnett, M. E. 2025; 7 (9): e70051

  Abstract

  Vascular endothelial growth factor (VEGF) is important in both developmental and pathologic angiogenesis in retinopathy of prematurity (ROP). Using a rat model representative of ROP, we found that regulation of VEGF signaling through VEGF receptor 2 (VEGFR2) in retinal microvascular endothelial cells (RMVECs) extended developmental angiogenesis but reduced pathologic angiogenesis, that is, intravitreal neovascularization (IVNV). We identified an adaptor protein, MEMO1, in IVNV in the rat model and tested the hypothesis that MEMO1 in RMVECs was important in IVNV by regulating signaling through VEGFR2. Instead, we found MEMO1 knockdown enhanced phosphorylation of VEGF-induced VEGFR2 and STAT3 and increased wound closure in vitro using cultured human RMVECs. Furthermore, MEMO1 overexpression suppressed VEGF-induced VEGFR2 and STAT3 phosphorylation and dampened VEGF-induced RMVEC wound closure. In contrast, in the absence of VEGF, MEMO1 overexpression promoted RMVEC proliferation in the wound closure assay and AKT phosphorylation, supporting a role for MEMO1 in VEGF-independent angiogenic processes. In vivo, retinal endothelial cell-specific knockdown of MEMO1 in the rat ROP model significantly increased IVNV but did not affect developmental angiogenesis. Our findings support a novel regulatory role for MEMO1 where MEMO1 limits VEGF-driven IVNV and promotes VEGF-independent angiogenic signaling. These results suggest MEMO1 may serve as a protective modulator of pathological angiogenesis in ROP and represent a potential therapeutic target to limit IVNV while preserving physiologic angiogenesis.

  View details for DOI 10.1096/fba.2025-00146

  View details for PubMedID 40936746

  View details for PubMedCentralID PMC12422028

• Phosphorylation of Y1212 (p-Y1212) on VEGFR2 affects developmental angiogenesis and neurogenesis in the retina Asare-Bediako, B., Satheesh, S., Ramshekar, A., Tankersley, M., Beri, S., Bright, M. ASSOC RESEARCH VISION OPHTHALMOLOGY INC. 2025

  View details for Web of Science ID 001560014200012

• Elucidating the role of MEMO1 in EPO-triggered signaling in retinal microvascular endothelial cells Ramshekar, A., Asare-Bediako, B., Jasmine Nguyen, Suresh, A., Hartnett, M. ASSOC RESEARCH VISION OPHTHALMOLOGY INC. 2024

  View details for Web of Science ID 001312227700347

• Short-term selective activation of phospho-Y1175 (p-Y1175) on VEGFR2 suppresses retinal endothelial cell migration Asare-Bediako, B., Ramshekar, A., Nguyen, J., Suresh, A., Hartnett, M. ASSOC RESEARCH VISION OPHTHALMOLOGY INC. 2024

  View details for Web of Science ID 001312227706162

• The calvarium bone marrow responds to acute retinal injury and is resilient to chronic diabetes compared to long bone marrow Calzi, S., Asare-Bediako, B., Prasad, R., Adu-Agyeiwaah, Y., Rosencrans, R. F., Floyd, J., Stanford, D., Lin, A., Lydic, T. A., Boulton, M., Busik, J., Grant, M. B. ASSOC RESEARCH VISION OPHTHALMOLOGY INC. 2024

  View details for Web of Science ID 001312227701023