Bartonella-induced endothelial cell proliferation is mediated by release of calcium from intracellular stores.
Bartonella-induced endothelial cell proliferation is mediated by release of calcium from intracellular stores.
复制标题
巴尔通体诱导的内皮细胞增殖是通过细胞内储存的钙的释放来介导的。
DOI：
10.1089/dna.2007.0592
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发表时间：
2007
影响因子：
3.1
通讯作者：
Anderson,BurtE
中科院分区：
文献类型：
--
作者：
McCord,AmyM;Cuevas,Javier;Anderson,BurtE
兼性胞内细菌汉赛巴尔通体在免疫功能低下的宿主中诱导独特的血管生成性病变。探讨细胞内钙池在B. henselae诱导的内皮细胞增殖，我们产生dB。henselae条件培养基（Henselae-conditioned medium，HENSE）中培养，并测试这些无细胞蛋白诱导人脐静脉内皮细胞（HUVEC）增殖、CXCL 8产生和细胞内Ca 2+信号的能力。HUVECs与LPS孵育3天后，细胞数量高于对照组。此外，当与培养基对照相比时，HUVEC产生增加量的CXCL 8以响应于E2。当HUVECs中加入Ca 2+，用钙敏感染料Fura-2/AM测量细胞内Ca 2+反应时，证实了Ca 2+升高。它被确定，这种Ca 2+的上升起源于细胞内的Ca 2+存储通过使用的Ca 2 + ATP酶抑制剂毒胡萝卜素。此外，证明了CXCL 8的产生和HUVEC增殖以Ca 2+依赖性方式增强。B. henselaecaes引起HUVECs细胞内Ca ~（2+）升高，这与B. henselae诱导的HUVEC增殖和CXCL 8产生。这些结果暗示了B细胞内Ca ~（2+）库的存在。henselae诱导的血管生成，并可能导致增加病原体诱导的血管生成的机制的理解。
The facultative intracellular bacteriumBartonella henselaeinduces unique angiogenic lesions in immunocompromised hosts. To determine the role of intracellular calcium pools inB. henselae–induced endothelial cell proliferation, we generatedB. henselae–conditioned medium (BCM) and tested the ability of these cell-free proteins to induce human umbilical vein endothelial cell (HUVEC) proliferation, CXCL8 production, and intracellular Ca2+signals. HUVECs incubated with BCM for 3 days had higher cell numbers than controls. In addition, HUVECs produced increased amounts of CXCL8 in response to BCM when compared to medium controls. When BCM was added to HUVECs and the intracellular Ca2+response measured with the calcium-sensitive dye fura-2/AM, a Ca2+rise was demonstrated. It was determined that this Ca2+rise originated from intracellular Ca2+stores through the use of the Ca2+ATPase inhibitor thapsigargin. Further, it was demonstrated that BCM enhanced CXCL8 production and HUVEC proliferation in a Ca2+-dependent manner. Conditioned medium fromB. henselaecauses an intracellular Ca2+rise in HUVECs, which is involved inB. henselae–induced HUVEC proliferation and CXCL8 production. These results implicate intracellular Ca2+pools inB. henselae–induced angiogenesis and may lead to increased understanding of the mechanisms of pathogen-induced angiogenesis.