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《Science》11月26日内容提要（中英文对照）
一项新的研究发现，由螺杆菌感染造成的癌症，起源于骨髓细胞，而不是胃内表面膜中的上皮干细胞。这一发现与流行的假设相违，假设认为上皮癌症，比如幽门螺杆菌引起的胃癌，是由组织干细胞变异造成的。如果骨髓细胞也与人类的上皮癌症有关，那么科学家应该修正他们对这类癌症的起源和发展的了解，考虑新的治疗方法。JeanMarie Houghton 和同事将来自骨髓的细胞注入小鼠，然后用螺杆菌感染造成小鼠的慢性炎症，并跟踪了注入细胞的活动。他们发现，来自骨髓的细胞能够在胃粘膜恢复生长，并导致了粘膜上异常细胞的增殖，最终导致上皮癌症。
报告：Gastric Cancer Originating from Bone Marrow-Derived Cells, JeanMarie Houghton, et al.
Gastric Cancer Originating from Bone Marrow-Derived Cells
JeanMarie Houghton,1* Calin Stoicov,1 Sachiyo Nomura,2,3 Arlin B. Rogers,4 Jane Carlson,1 Hanchen Li,1 Xun Cai,1 James G. Fox,4 James R. Goldenring,2,5 Timothy C. Wang1*
Epithelial cancers are believed to originate from transformation of tissue stem cells. However, bone marrow–derived cells (BMDCs), which are frequently recruited to sites of tissue injury and inflammation, might also represent a potential source of malignancy. We show that although acute injury, acute inflammation, or transient parietal cell loss within the stomach do not lead to BMDC recruitment, chronic infection of C57BL/6 mice with Helicobacter, a known carcinogen, induces repopulation of the stomach with BMDCs. Subsequently, these cells progress through metaplasia and dysplasia to intraepithelial cancer. These findings suggest that epithelial cancers can originate from marrow-derived sources and thus have broad implications for the multistep model of cancer progression.
1 Department of Medicine and Cancer Biology, University of Massachusetts Medical School, Worcester, MA 01605, USA.
2 Epithelial Biology Program, Department of Surgery and Vanderbilt-Ingram Cancer Center, Vanderbilt University School of Medicine, Nashville, TN 37232, USA.
3 Department of Gastrointestinal Surgery, Graduate School of Medicine, University of Tokyo, Bunkyo-ku, Tokyo, 113-8655, Japan.
4 Division of Comparative Medicine, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.
5 The Veterans Administration Medical Center, Nashville, TN 37232, USA.
一个小鼠蛋白在动脉斑块形成中的作用
一项对小鼠的研究揭示了一个重要的蛋白质在动脉硬化中起的作用。动脉硬化是指脂肪沉积和纤维组织造成的动脉阻塞，是一个可能威胁生命的症状。一个国际小组研究了Jnk2蛋白质信号在由于缺少ApoE蛋白质而易患动脉硬化的小鼠身上的作用。ApoE和Jnk2两个蛋白质都缺少的小鼠表现出动脉硬化症状的减少，它们形成了较少的泡沫细胞，这些细胞充满了脂肪，与阻塞动脉的斑块形成有关。在有Jnk2蛋白的小鼠身上，一个抑制这个蛋白质的药物也减少了斑块的形成。同样，用骨髓移植的方法从巨噬细胞上剔除Jnk2蛋白质，也减少了小鼠的动脉硬化。Romeo Ricci和和作者说，巨噬细胞上的Jnk2可能给新的动脉硬化药物提供一个有用的靶标。Jnk2似乎加强了一个清除脂肪的蛋白质的活性，这个蛋白质促进泡沫细胞的形成，这也许能解释为什么缺少Jnk2的小鼠有更健康的动脉。
报告：Requirement of JNK2 for Scavenger Receptor A-Mediated Foam Cell Formation in Atherogenesis, Romeo Ricci, et al.
Requirement of JNK2 for Scavenger Receptor A-Mediated Foam Cell Formation in Atherogenesis
Romeo Ricci,1,2* Grzegorz Sumara,1,2 Izabela Sumara,3 Izabela Rozenberg,1 Michael Kurrer,4 Alexander Akhmedov,1 Martin Hersberger,5 Urs Eriksson,7 Franz R. Eberli,1 Burkhard Becher,6 Jan Borén,8 Mian Chen,9 Myron I. Cybulsky,9 Kathryn J. Moore,10 Mason W. Freeman,10 Erwin F. Wagner,11 Christian M. Matter,1 Thomas F. Lüscher1
In vitro studies suggest a role for c-Jun N-terminal kinases (JNKs) in proatherogenic cellular processes. We show that atherosclerosis-prone ApoE–/– mice simultaneously lacking JNK2 (ApoE–/– JNK2–/– mice), but not ApoE–/– JNK1–/– mice, developed less atherosclerosis than do ApoE–/– mice. Pharmacological inhibition of JNK activity efficiently reduced plaque formation. Macrophages lacking JNK2 displayed suppressed foam cell formation caused by defective uptake and degradation of modified lipoproteins and showed increased amounts of the modified lipoprotein-binding and -internalizing scavenger receptor A (SR-A), whose phosphorylation was markedly decreased. Macrophage-restricted deletion of JNK2 was sufficient to decrease atherogenesis. Thus, JNK2-dependent phosphorylation of SR-A promotes uptake of lipids in macrophages, thereby regulating foam cell formation, a critical step in atherogenesis.
对成生胰岛素细胞的进一步了解
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作者:admin@医学,生命科学 2010-10-10 17:11
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