Detection of brain specific cardiolipins in plasma after experimental pediatric head injury
Anthonymuthu T. S., Kenny E. M., Hier Z. E., Clark R. S. B., Kochanek P. M., Kagan V. E., Bayır H.
Experimental Neurology
Vol.316, P. 63-73
Опубликовано: 2019
Тип ресурса: Статья
DOI:10.1016/j.expneurol.2019.04.007
Аннотация:
Cardiolipin (CL) is a mitochondria-specific phospholipid that is central to maintenance and regulation of mitochondrial bioenergetic and metabolic functions. CL molecular species display great tissue variation with brain exhibiting a distinct, highly diverse CL population. We recently showed that the appearance of unique brain-type CLs in plasma could serve as a brain-specific marker of mitochondrial/tissue injury in patients after cardiac arrest. Mitochondrial dysfunction has been increasingly implicated as a critical mechanism underlying the pathogenesis of traumatic brain injury (TBI). Therefore, we hypothesized that unique, brain-specific CL species from the injured brain are released to the peripheral circulation after TBI. To test this hypothesis, we performed a high-resolution mass spectrometry based phospholipidomics analysis of post-natal day (PND)17 rat brain and plasma after controlled cortical impact. We found a time-dependent increase in plasma CLs after TBI including the
Ключевые слова:
Brain-specific cardiolipin; Mitochondrial dysfunction; Phospholipidomics; Plasma biomarker
cardiolipin; phosphatidic acid; phosphatidylcholine; phosphatidylethanolamine; phosphatidylglycerol; phosphatidylinositol; phosphatidylserine; cardiolipin; phospholipid; animal experiment; animal model; animal tissue; Article; blood level; brain region; correlation analysis; disorders of mitochondrial functions; lipidomics; liquid chromatography-mass spectrometry; male; mass spectrometry; nonhuman; pathogenesis; perinatal period; peripheral circulation; priority journal; protein secretion; quantitative analysis; rat; systemic circulation; time; tissue specificity; traumatic brain injury; animal; blood; brain chemistry; brain cortex; head injury; injury; metabolism; mitochondrion; Sprague Dawley rat; traumatic brain injury; Animals; Brain Chemistry; Brain Injuries, Traumatic; Cardiolipins; Cerebral Cortex; Craniocerebral Trauma; Lipidomics; Male; Mass Spectrometry; Mitochondria; Phospholipids; Rats; Rats, Sprague-Dawley
Язык текста: Английский
ISSN: 1090-2430
Anthonymuthu T. S.
Kenny E. M.
Hier Z. E.
Clark R. S. B.
Kochanek P. M.
Kagan V. E. Valerian E 1946-
Bayır H.
Антхонyмутху Т. С.
Кеннy Е. М.
Хиер З. Е.
Cларк Р. С. Б.
Кочанек П. М.
Каган В. Е. Валериан Е 1946-
Байıр Х.
Detection of brain specific cardiolipins in plasma after experimental pediatric head injury
Текст визуальный непосредственный
Experimental Neurology
Academic Press
Vol.316 P. 63-73
2019
Статья
Brain-specific cardiolipin Mitochondrial dysfunction Phospholipidomics Plasma biomarker
cardiolipin phosphatidic acid phosphatidylcholine phosphatidylethanolamine phosphatidylglycerol phosphatidylinositol phosphatidylserine cardiolipin phospholipid animal experiment animal model animal tissue Article blood level brain region correlation analysis disorders of mitochondrial functions lipidomics liquid chromatography-mass spectrometry male mass spectrometry nonhuman pathogenesis perinatal period peripheral circulation priority journal protein secretion quantitative analysis rat systemic circulation time tissue specificity traumatic brain injury animal blood brain chemistry brain cortex head injury injury metabolism mitochondrion Sprague Dawley rat traumatic brain injury Animals Brain Chemistry Brain Injuries, Traumatic Cardiolipins Cerebral Cortex Craniocerebral Trauma Lipidomics Male Mass Spectrometry Mitochondria Phospholipids Rats Rats, Sprague-Dawley
Cardiolipin (CL) is a mitochondria-specific phospholipid that is central to maintenance and regulation of mitochondrial bioenergetic and metabolic functions. CL molecular species display great tissue variation with brain exhibiting a distinct, highly diverse CL population. We recently showed that the appearance of unique brain-type CLs in plasma could serve as a brain-specific marker of mitochondrial/tissue injury in patients after cardiac arrest. Mitochondrial dysfunction has been increasingly implicated as a critical mechanism underlying the pathogenesis of traumatic brain injury (TBI). Therefore, we hypothesized that unique, brain-specific CL species from the injured brain are released to the peripheral circulation after TBI. To test this hypothesis, we performed a high-resolution mass spectrometry based phospholipidomics analysis of post-natal day (PND)17 rat brain and plasma after controlled cortical impact. We found a time-dependent increase in plasma CLs after TBI including the