Temperature induces brain-intake shift of recombinant high-density lipoprotein after traumatic brain injury.

Publisher: BioMed Central Country of Publication: England NLM ID: 101152208 Publication Model: Electronic Cited Medium: Internet ISSN: 1477-3155 (Electronic) Linking ISSN: 14773155 NLM ISO Abbreviation: J Nanobiotechnology Subsets: MEDLINE

Original Publication: London : BioMed Central, 2003-

Brain Injuries, Traumatic*/metabolism ; Brain Injuries, Traumatic*/therapy ; Recombinant Proteins* ; Brain*/metabolism ; Blood-Brain Barrier*/metabolism ; Lipoproteins, HDL*/metabolism ; Receptors, LDL*/metabolism; Animals ; Mice ; Male ; Mice, Inbred C57BL ; Low Density Lipoprotein Receptor-Related Protein-1/metabolism ; Hypothermia, Induced ; Neurons/metabolism ; Humans ; Endothelial Cells/metabolism ; Neuroprotective Agents/pharmacology ; Microglia/metabolism ; Astrocytes/metabolism ; Temperature ; Hyperthermia/metabolism

Competing Interests: Declarations. Ethics approval and consent to participate: This study received approval from the Institutional Animal Care and Use Committee of Renji Hospital, School of Medicine, Shanghai Jiao Tong University (Approval number: 2023–106). Consent for publication: All authors have approved the manuscript and agree for the submission. Competing interests: The authors declare no competing interests.
Traumatic brain injury (TBI) is one of the leading public health concerns in the world. Therapeutic hypothermia is routinely used in severe TBI, and pathophysiological hyperthermia, frequently observed in TBI patients, has an unclear impact on drug transport in the injured brain due to a lack of study on its effects. We investigated the effect of post-traumatic therapeutic hypothermia at 33°C and pathophysiological hyperthermia at 39°C on brain transport and cell uptake of neuroprotectants after TBI. Recombinant high-density lipoprotein (rHDL), which possesses anti-inflammatory, antioxidant activity, and blood-brain barrier (BBB) permeability, was chosen as the model drug. First, we found that mild hypothermia and hyperthermia impaired rHDL transport to the brain and lesion targeting in controlled cortical impact mice. Second, we investigated the temperature-induced rHDL uptake shift by various brain cell types. Mild hypothermia impeded the uptake of rHDL by endothelial cells, neurons, microglia, and astrocytes. Hyperthermia impeded the uptake of rHDL by endothelial cells and neurons while promoting its uptake by microglia and astrocytes. In an attempt to understand the mechanisms behind the above phenomena, it was found that temperature induced brain-intake shift of rHDL through the regulation of low-density lipoprotein receptor (LDLR) and LDLR-related protein 1 (LRP1) stability in brain cells. We therefore reported the full view of the temperature-induced brain-intake shift of rHDL after TBI for the first time. It would be of help in coordinating pharmacotherapy with temperature management in individualization and precision medicine.
(© 2024. The Author(s).)

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82071358 the National Natural Science Foundation of China; 20224Z0012 the Shanghai Talent Development Fund; 18YF1413400 the Shanghai Sailing Program; 21XD1422400 Program of Shanghai Academic/Technology Research Leader

Keywords: Brain transport; Cellular uptake; Hyperthermia; Mild hypothermia; Pharmacotherapy

0 (Recombinant Proteins)
0 (Lipoproteins, HDL)
0 (Receptors, LDL)
0 (Low Density Lipoprotein Receptor-Related Protein-1)
0 (Lrp1 protein, mouse)
0 (Neuroprotective Agents)

Date Created: 20241219 Date Completed: 20241219 Latest Revision: 20250104

20250114

PMC11656847

10.1186/s12951-024-03016-z

39695696