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约翰 • 霍普金斯大学曹旭教授：骨骼内感受系统调节骨稳态 及关节疼痛
- 来源：
- 学校官网
- 收录时间：
- 2024-12-04 11:15:07
- 时间：
- 2024-12-09 09:00:00
- 地点：
- 广州国际校区C3-c204
- 报告人：
- 曹旭（约翰•霍普金斯大学教授）
- 学校：
- -/-
- 关键词：
- bone, PGE2, skeletal interoception, mechanical loading, osteogenesis, osteoarthritis, low back pain, ankle osteoarthritis
- 简介：
- Skeleton provides mechanical support and metabolic mineral reserve for the animals. PGE2 is secreted osteoblastic cells regulated by mechanical stress to activate its receptor EP4 in sensory nerves, which inhibits sympathetic activity through the central nervous system to induce osteoblast differentiation for the bone formation as PGE2 skeletal interoception circuit. Interoception is a type of brain circuit that monitors the internal state to regulate the complex interactions between the brain and peripheral organs. Life started on earth about 4 billion years ago, only 500 million years after the birth of earth. It took 3 billion years of molecular and cellular evolution to develop nerve circuits of the brain under earth gravity, suggesting skeletal interoception as an ancient circuit with fundamental functions in life. Our recent study reveals that skeletal interoception regulates weight bearing bones in response to mechanical loading. PGE2 skeleton interception also regulates expression of hypothalamic neuropeptide Y (NPY) and induces lipolysis of adipose tissue for osteoblastic bone formation. The hypothalamus of the brain regulates bone remodeling and structure by perceiving bone prostaglandin E2 (PGE2) concentration in response to mechanical loading. Bone PGE2 levels are in proportion to their weight bearing. Deletion of cyclooxygenase-2 (COX2) or PGE2 in the osteoblast lineage cells or knockout of receptor 4 (EP4) in sensory nerve blunts bone formation in response to mechanical loading. Moreover, mechanical loading induces cAMP-response element binding protein (CREB) phosphorylation in the hypothalamic arcuate nucleus (ARC) to inhibit sympathetic tyrosine hydroxylase (TH) expression in the paraventricular nucleus (PVN) for osteogenesis. Elevated PGE2 interoception erodes the skeletal integrity and causes major skeletal disorders including osteoarthritis, low back pain and particularly ankle osteoarthritis (AOA) and its pain.
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报告介绍：
Skeleton provides mechanical support and metabolic mineral reserve for the animals. PGE2 is secreted osteoblastic cells regulated by mechanical stress to activate its receptor EP4 in sensory nerves, which inhibits sympathetic activity through the central nervous system to induce osteoblast differentiation for the bone formation as PGE2 skeletal interoception circuit. Interoception is a type of brain circuit that monitors the internal state to regulate the complex interactions between the brain and peripheral organs. Life started on earth about 4 billion years ago, only 500 million years after the birth of earth. It took 3 billion years of molecular and cellular evolution to develop nerve circuits of the brain under earth gravity, suggesting skeletal interoception as an ancient circuit with fundamental functions in life. Our recent study reveals that skeletal interoception regulates weight bearing bones in response to mechanical loading. PGE2 skeleton interception also regulates expression of hypothalamic neuropeptide Y (NPY) and induces lipolysis of adipose tissue for osteoblastic bone formation. The hypothalamus of the brain regulates bone remodeling and structure by perceiving bone prostaglandin E2 (PGE2) concentration in response to mechanical loading. Bone PGE2 levels are in proportion to their weight bearing. Deletion of cyclooxygenase-2 (COX2) or PGE2 in the osteoblast lineage cells or knockout of receptor 4 (EP4) in sensory nerve blunts bone formation in response to mechanical loading. Moreover, mechanical loading induces cAMP-response element binding protein (CREB) phosphorylation in the hypothalamic arcuate nucleus (ARC) to inhibit sympathetic tyrosine hydroxylase (TH) expression in the paraventricular nucleus (PVN) for osteogenesis. Elevated PGE2 interoception erodes the skeletal integrity and causes major skeletal disorders including osteoarthritis, low back pain and particularly ankle osteoarthritis (AOA) and its pain.
报告人介绍：
曹旭教授于1991年获得南卡罗来纳大学生物化学博士学位，随后在华盛顿大学从事博士后研究工作。1996年加入了阿拉巴马大学病理系，并先后担任助理教授、副教授和教授。2009年被美国约翰·霍普金斯大学聘为Lee Rilley讲席教授，并担任骨骼与肌肉研究中心主任。曹旭教授主要从事骨重建机理，骨性关节炎及其他骨骼疾病的研究，在《Nature Medicine》等顶级学术期刊上发表了学术论文150余篇。曹旭教授还担任《Bone Research》和《Biomaterials Translational》学术期刊的创刊主编，是《Nature》《Science》《Cell》及《Nature Medicine》等世界知名学术期刊的审稿人。
