Human intrinsic factor secretion: immunocytochemical demonstration of membrane-associated vesicular transport in parietal cells
Human intrinsic factor secretion: immunocytochemical demonstration of membrane-associated vesicular transport in parietal cells
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人内因子分泌：壁细胞膜相关囊泡运输的免疫细胞化学证明
作者：
J. Levine;P. Nakane;R. Allen
人胃壁细胞合成并分泌内因子和胃酸。与酸分泌的细胞机制相反，对IF分泌的机制知之甚少。为了阐明这些机制，我们在五肽胃泌素刺激（6微克/千克皮下注射）之前和之后从三名受试者获得胃分泌物和连续胃底活检。使用超微结构免疫过氧化物酶技术，使用一个良好的特点，单特异性抗体，以人类IF的活组织检查，IF被定位。IF输出定量使用特定的放射免疫测定同时获得的胃分泌物。在刺激前，IF与分散在整个细胞质中的小管囊泡和粗面内质网（RER）中的小管囊泡相关。与IF相关的小管囊泡在刺激后8分钟内迁移到分泌小管的外周。在胃液中IF分泌量最大的8 ~ 30 min之间，IF出现在分泌微绒毛上。IF分泌的停止正好与与tubulovesicles相关的IF耗尽。IF出现在核周间隙，RER作为IF与小管囊泡结合分泌。这些观察结果表明，IF分泌依赖于膜相关的囊泡运输，并提供支持膜易位融合假说来解释分泌过程中壁细胞中发生的形态学变化。
The human gastric parietal cell synthesizes and secretes intrinsic factor (IF) and acid. In contrast to the cellular mechanisms of acid secretion, little is known about the mechanisms of IF secretion. To elucidate these mechanisms we obtained gastric secretions and sequential fundic biopsies from three subjects before and after pentagastrin stimulation (6 microgram/Kg s.c.). IF was localized in the biopsies using an ultrastructural immunoperoxidase technique using a well-characterized, monospecific antibody to human IF. IF output was quantified using a specific radioimmunoassay in concurrently obtained gastric secretions. Before stimulation, IF was associated with tubulovesicles scattered throughout the cytoplasm and with some in rough endoplasmic reticulum (RER). The tubulovesicles associated with IF migrated to the periphery of the secretory canaliculi within 8 min of stimulation. IF was present on secretory microvilli between 8 and 30 min when IF output in gastric juice was at its maximum. The cessation of IF secretion coincided with the depletion of IF associated with tubulovesicles. IF appeared in the perinuclear space and RER as the IF associated with tubulovesicles was secreted. These observations indicate that IF secretion depends upon membrane-associated vesicular transport and provides support for a membrane translocation-fusion hypothesis to explain the morphologic changes that occur in the parietal cell during secretion.