教育

研究所
休斯顿大学，德克萨斯州休斯敦，2000年
博士后
德克萨斯州A＆M生物技术研究所，德克萨斯州休斯敦，2000-2003

兴趣范围

beplay苹果手机能用吗研究兴趣

我的研究的目标是定义的分子beplay苹果手机能用吗mechanisms that contribute to cartilage-related conditions in order to develop therapeutics that improve cartilage and joint health to improve the quality of life of individuals with dwarfing conditions and osteoarthritis. I study pseudoachondroplasia (PSACH), a severe dwarfing condition associated with severe and osteoarthritis early-onset. Using our pseudoachondroplasia mouse model, we defined the mechanisms underlying chondrocyte dysfunction and loss, a self-perpetuating pathological loop between ER stress, inflammation and oxidative stress, which revealed drug targets. Understanding the pathological loop between ER stress, inflammation and oxidative stress is very exciting because there is growing evidence that this pathological mechanism may be involved in many other ER stress related conditions such as neurodegenerative disorders and diabetes and has provided a foundation for the development of the first therapies for pseudoachondroplasia. We have investigated readily-available and well-tolerated antioxidants and anti-inflammatory agents to dampen the intracellular ER retention chondrocyte pathology. This approach may work on many types of secretory cells (chondrocytes, neurons, islet cells…) interrupting the ER stress-inflammation-oxidative stress loop pathology. If this type of inexpensive and well-tolerated therapy could be applied to the early stages of neurodegenerative disorders and metabolic syndrome, onset may be delayed or the pathology suppressed effecting a revolution in health care and the impact of these devastating conditions. Additionally, this pseudoachondroplasia mouse model has lead me to expand my work into the field of osteoarthritis because early-onset osteoarthritis is associated with this dwarfing condition. The inducible feature of the model allows the stimulation of ER stress in adult articular chondrocytes in order to assess the role that ER stress plays in osteoarthritis establishment and progression. Our recent findings suggest that ER stress may be a major component in idiopathic osteoarthritis.

出版物

访问PubMed个人资料页面

Posey, K.L.，Veerisetty，A.C.，Liu，P.，Wang，H.R.，Poindexter，B.J.，Bick，R.，Alcorn，J.L.，Hecht，J.T。：可诱导的Comp Mouse模型可概括人类PSACH表型。Am J Pathol 175（4）：1555-63，2009。

Posey, K.L.，Liu，P.，Wang，H.R.，Veerisetty，A.C.，Alcorn，J.L.，Hecht，J.T。：RNAi降低了突变软骨寡聚基质蛋白（Comp）的表达和细胞内保留。PLOS ONE 5（4）：E10302，2010。

Li H.，Haudenschild D.R.，Posey K.L.，Hecht J.T.，Di Cesare P.E.，Yik J.H。：与II型胶原蛋白的比较分析将软骨寡聚基质蛋白区分开为原代TGFβ反应基因。骨关节炎软骨。19（10）：1246-53，2011。

Posey K.L.，Coustry F.，Veerisetty A.C.，Liu P.，Alcorn J.L.，Hecht J.T。：CHOP（DDIT3）对于d469del-comp保留和细胞死亡至关重要，在软骨中，可诱导的伪造小鼠模型中的软骨细胞中的细胞死亡至关重要。Am J Pathol 180（2）：727-37，2012。

科特里F.，Posey K.L.，Liu P.，Alcorn J.L.，Hecht J.T。：D469DEL-COMP在软骨细胞中的保留刺激caspase非依赖性坏死性。Am J Pathol 180（2）：738-48，2012。

Posey K.L.，Coustry F.，Veerisetty A.C.，Liu P.，Alcorn J.L.，Hecht J.T。：在骨骼生长和疗法中，软骨细胞特异性病理在假骨质感的鼠模型中。J Bone Miner Res。; 29（5）：1258-68，2014。

Posey K.L., Alcorn J.L., Hecht J.T.: Pseudoachondroplasia/COMP – translating from the bench to the bedside. Matrix Biol. 37C:167-173, 2014

Posey K.L.，Coustry F.，Veerisetty A.C.，Hossain M.，Alcorn J.L.，Hecht J.T：假质体小鼠模型中的抗氧化剂和抗炎药减轻病理学。嗡嗡声摩尔遗传学。15; 24（14）：3918-28。2015。