Publications

Background: Pericytes, a type of mural cells, exert important functions in the CNS. One major challenge in pericyte research is the lack of pericyte-specific and subpopulation-specific markers.

Methods: To address this knowledge gap, we first generated a novel transgenic mouse line in which vascular smooth muscle cells (vSMCs) are permanently labeled with tdTomato. Next, we isolated PDGFRβ⁺tdTomato^- pericytes and PDGFRβ⁺tdTomato⁺ vSMCs from the brains of these mice and subsequently performed RNAseq analysis to identify pericyte-enriched genes.

Results: Using this approach, we successfully identified 40 pericyte-enriched genes and 158 vSMC-enriched genes, which are involved in different biological processes and molecular functions. Using ISH/IHC analysis, we found that Pla1a and Cox4i2 were predominantly enriched in subpopulations of brain pericytes, although they also marked some non-vascular parenchymal cells.

Conclusions: These findings suggest that Pla1a and Cox4i2 preferably label subpopulations of pericytes in the brain compared to vSMCs, and thus, they may be useful in distinguishing these populations.

[Erratum to: BMB Reports 2025; 58(3): 140-145, PMID: 39757202, PMCID: PMC11955732] The BMB Reports would like to issue a correction to an article published in BMB Rep. 58(3): 140-145, titled "Celecoxib is the only nonsteroidal anti-inflammatory drug to inhibit bone progression in spondyloarthritis". The original acknowledgment contained incorrect grant information. This has now been corrected at the authors' request as follows: This research was supported by Basic Science Research Program through the National Research Foundation of Korea (NRF) grant funded by the Korea government (MSIT) (NRF-2016R1 A6A3A11930589, NRF-2016R1A6A3A11934500, NRF-2016 R1D1A3 B03931646, NRF-2019R1I1A1A01057738, NRF-2019R1l1A3A01060016, NRF-2019R1l1A1A01060116, and RS-2023-00248058). It was also supported by the Chungnam National University Hospital Research Fund 2021 (2021-CF-033). Specifically, the grant number has been updated from 2016 (2016-CF-003) to 2021 (2021-CF-033). The authors apologize for any inconvenience or confusion this error may have caused. The ACKNOWLEDGEMENTS section in the original PDF version has been updated accordingly.

[This corrects the article on p. 361 in vol. 12, PMID: 38144022.].

Micro RNAs (miRNAs) play a crucial role as regulators of various biological processes and have been implicated in the pathogenesis of mental disorders such as schizophrenia and bipolar disorders. In this study, we investigate the expression patterns of miRNAs in the PsyCourse Study (n = 1786), contrasting three broad diagnostic groups: Psychotic (Schizophrenia-spectrum disorders), Affective (Bipolar Disorder I, II and recurrent Depression), and neurotypic healthy individuals. Through comprehensive analyses, including differential miRNA expression, miRNA transcriptome-wide association study (TWAS), and predictive modelling, we identified multiple miRNAs unique to Psychotic and Affective groups as well as shared by both. Furthermore, we performed integrative analysis to identify the target genes of the dysregulated miRNAs and elucidate their potential roles in psychosis. Our findings reveal significant alterations of multiple miRNAs such as miR-584-3p and miR-99b-5p across the studied diagnostic groups, highlighting their role as molecular correlates. Additionally, the miRNA TWAS analysis discovered previously known and novel genetically dysregulated miRNAs confirming the relevance in the etiology of the diagnostic groups. Importantly, novel factors and putative molecular mechanisms underlying these groups were uncovered through the integration of miRNA-target gene interactions. This comprehensive investigation provides valuable insights into the molecular underpinnings of severe mental disorders, shedding light on the complex regulatory networks involving miRNAs.

This corrects the article on p. 653 in vol. 54, PMID: 39175341.

In December, we published an article titled "Dive Medicine Capability at Rothera Research Station (British Antarctic Survey), Adelaide Island, Antarctica" by Wood FNR, Bowen K, Hartley R, et al. The corresponding author would like to include an additional author, as their contribution was significant but was inadvertently omitted in the initial online publication. While this correction has been made in several versions circulated by the journal, not all have been updated. As a result, we are issuing an errata. The title and abstract are as follows: (Wood FNR, Bowen K, Hartley R, Stevenson J, Warner M, Watts D. Dive medicine capability at Rothera Research Station (British Antarctic Survey), Adelaide Island, Antarctica. Diving and Hyperbaric Medicine. 2024 20 December;54(4):320-327. doi: 10.28920/dhm54.4.320-327. PMID: 39675740.) Rothera is a British Antarctic Survey research station located on Adelaide Island adjacent to the Antarctic Peninsula. Diving is vital to support a long-standing marine science programme but poses challenges due to the extreme and remote environment in which it is undertaken. We summarise the diving undertaken and describe the medical measures in place to mitigate the risk to divers. These include pre-deployment training in the management of emergency presentations and assessing fitness to dive, an on-site hyperbaric chamber and communication links to contact experts in the United Kingdom for remote advice. The organisation also has experience of evacuating patients, should this be required. These measures, as well as the significant infrastructure and logistical efforts to support them, enable high standards of medical care to be maintained to divers undertaking research on this most remote continent.

[This corrects the article on p. 2064 in vol. 8, PMID: 30416856.].

Glaucomatous optic neuropathy, or glaucoma, is the world's primary cause of irreversible blindness. Glaucoma is comorbid with other neurodegenerative diseases, but how it might impact the environment of the full central nervous system to increase neurodegenerative vulnerability is unknown. Two neurodegenerative events occur early in the optic nerve, the structural link between the retina and brain: loss of anterograde transport in retinal ganglion cell (RGC) axons and early alterations in astrocyte structure and function. Here, we used whole-mount tissue clearing of full mouse brains to image RGC anterograde transport function and astrocyte responses across retinorecipient regions early in a unilateral microbead occlusion model of glaucoma. Using light sheet imaging, we found that RGC projections terminating specifically in the accessory optic tract are the first to lose transport function. Although degeneration was induced in one retina, astrocytes in both brain hemispheres responded to transport loss in a retinotopic pattern that mirrored the degenerating RGCs. A subpopulation of these astrocytes in contact with large descending blood vessels were immunopositive for LCN2, a marker associated with astrocyte reactivity. Together, these data suggest that even early stages of unilateral glaucoma have broad impacts on the health of astrocytes across both hemispheres of the brain, implying a glial mechanism behind neurodegenerative comorbidity in glaucoma.