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Autophagy in Neurogenic Hypertension induced by Systemic Inflammation
Author(s) -
Wu Kay LH,
Chan Julie,
Chan Samuel
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.905.2
Subject(s) - rostral ventrolateral medulla , autophagy , inflammation , systemic inflammation , medicine , atg5 , sympathetic nervous system , endocrinology , reactive oxygen species , chemistry , medulla oblongata , microbiology and biotechnology , central nervous system , biology , blood pressure , apoptosis , biochemistry
The reactive oxygen species (ROS) in the central nervous system increase sympathetic outflow contributing to neurogenic hypertension. We reported preciously that ROS in the rostral ventrolateral medulla (RVLM), where sympathetic premotor neurons located, increases sympathetic outflow and mediates neurogenic hypertension following sustained systemic inflammation. Autophagy serves to balance organelle biogenesis, protein synthesis and their clearance. Cross‐talk with ROS engages autophagy to mediate stress signaling including synaptic plasticity under pathological status. In this study, we examined whether ROS activates the autophagic pathway to increase the sympathetic outflow and arterial pressure. Autophagy markers, including beclin‐1, Atg5, Atg12 and LC3 II, in RVLM were significantly increases under sustained systemic inflammation. Intracisternal infusion of ROS scavenger, tempol or mitoTEMPO, suppressed autophagy marker protein increase and the induced pressor response. Inhibition of autophagy in RVLM by 3‐MA reversed the pressor response. At cellular level, LC3 II immunoreactivity was colocalized with synaptophysin in RVLM and was inhibited by tempol. Together, these data suggest that autophagy in RVLM mediates ROS‐induced neurogenic hypertension under sustained systemic hypertension. This study is supported by CMRPG8A0801 to KLHW from Kaohsiung Chang Gung Memorial Hospital.