Jun Chen
National Institutes of Health
6 Papers
84 Citations
Jun Chen is an academic researcher from National Institutes of Health. The author has contributed to research in topics: Kinase & Hypothalamic–pituitary–adrenal axis. The author has an hindex of 6, co-authored 6 publications.
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Papers
Maternal Deprivation in Rats is Associated with Corticotrophin‐Releasing Hormone (CRH) Promoter Hypomethylation and Enhances CRH Transcriptional Responses to Stress in Adulthood
TL;DR: It is demonstrated that HPA axis hypersensitivity caused by neonatal stress causes long‐lasting enhanced CRH transcriptional activity in the PVN of both sexes.
Vasopressin Does Not Mediate Hypersensitivity Of The Hypothalamic Pituitary Adrenal Axis During Chronic Stress
Jun Chen,Sharla Young,Sivan Subburaju,Jack Sheppard,Alexander Kiss,Helen C. Atkinson,SA Wood,Stafford L. Lightman,Claudine Serradeil-Le Gal,Greti Aguilera +9 more
TL;DR: In spite of the increased vasopressinergic activity, repeatedly restrained rats showed lower ACTH and corticosterone responses to 10 min white noise compared with handled controls, suggesting that the increased VasopressInergic activity characteristic of chronic stress plays roles other than mediating the hypersensitivity of the HPA axis to a novel stress.
Anti-apoptotic actions of vasopressin in h32 neurons involve map kinase transactivation and bad phosphorylation
TL;DR: The data suggest that VP has anti-apoptotic activity in neurons and that VP may act as a neuroprotective agent in the brain.
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Antiapoptotic effects of vasopressin in the neuronal cell line H32 involve protein kinase Calpha and beta.
TL;DR: The data demonstrate that VP exerts antiapoptosis through multiple pathways; while PKCα and β together with extracellular signal‐regulated kinases/MAPK activation mediates Bad phosphorylation (inactivation), the full protective action of VP requires additional activation of PKB (PI3K/protein kinase B) pathway.
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The parvocellular vasopressinergic system and responsiveness of the hypothalamic pituitary adrenal axis during chronic stress.
TL;DR: The overall evidence supports a limited role of VP regulating acute ACTH responses to some acute stressors and points to cell proliferation and pituitary remodelling as alternative roles for the marked increases in parvocellular vasopressinergic activity during prolonged activation of the HPA axis.