A-kinase anchor protein 12 promotes oligodendrogenesis and cognitive recovery in carbon monoxide therapy for traumatic brain injury DOI
Yoon Kyung Choi,

Takakuni Maki,

Anna C. Liang

et al.

Journal of Cerebral Blood Flow & Metabolism, Journal Year: 2025, Volume and Issue: unknown

Published: Jan. 25, 2025

Therapeutic drug development for central nervous system injuries, such as traumatic brain injury (TBI), presents significant challenges. TBI results in primary mechanical damage followed by secondary injury, leading to cognitive dysfunction and memory loss. Our recent study demonstrated the potential of carbon monoxide-releasing molecules (CORMs) improve recovery enhancing neurogenesis. However, a comprehensive strategy requires not only neurogenesis but also oligodendrogenesis. In this study, we elucidate critical role A-kinase anchor protein 12 (AKAP12), scaffolding predominantly expressed intact pericytes, oligodendrocyte regeneration during CO therapy TBI. CORM treatment increased AKAP12 expression, which enhanced myelin intensity mitigated TBI-induced addition, promotes generation new oligodendrocytes, process that is impaired deficiency. Notably, even after TBI, function was restored wild-type mice following treatment, effect absent Akap12 knockout mice. These findings highlight importance CO-induced upregulation, particularly supporting oligodendrogenesis Understanding these mechanisms holds promise targeted therapies address TBI-associated impairments.

Language: Английский

A-kinase anchor protein 12 promotes oligodendrogenesis and cognitive recovery in carbon monoxide therapy for traumatic brain injury DOI
Yoon Kyung Choi,

Takakuni Maki,

Anna C. Liang

et al.

Journal of Cerebral Blood Flow & Metabolism, Journal Year: 2025, Volume and Issue: unknown

Published: Jan. 25, 2025

Therapeutic drug development for central nervous system injuries, such as traumatic brain injury (TBI), presents significant challenges. TBI results in primary mechanical damage followed by secondary injury, leading to cognitive dysfunction and memory loss. Our recent study demonstrated the potential of carbon monoxide-releasing molecules (CORMs) improve recovery enhancing neurogenesis. However, a comprehensive strategy requires not only neurogenesis but also oligodendrogenesis. In this study, we elucidate critical role A-kinase anchor protein 12 (AKAP12), scaffolding predominantly expressed intact pericytes, oligodendrocyte regeneration during CO therapy TBI. CORM treatment increased AKAP12 expression, which enhanced myelin intensity mitigated TBI-induced addition, promotes generation new oligodendrocytes, process that is impaired deficiency. Notably, even after TBI, function was restored wild-type mice following treatment, effect absent Akap12 knockout mice. These findings highlight importance CO-induced upregulation, particularly supporting oligodendrogenesis Understanding these mechanisms holds promise targeted therapies address TBI-associated impairments.

Language: Английский

Citations

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