BIVALVE MODEL FOR CALCIUM REGULATION & DEPOSITION

本研究的主要目的是证明钙（Ca） 海洋双壳软体动物（Mercenaria）的吸收、运输和沉积 是一个很好的无脊椎动物模型的钙调节， 哺乳动物系统 虽然许多相同的过程已经被知道 为了存在于无脊椎动物和脊椎动物系统中，另外的 将研究相似性以确定（1）Ca 双壳类外套膜细胞的摄取/释放类似于哺乳动物回肠 粘膜细胞（即由主动转运介导）;（2）分布 双壳贝类血液中钙的含量（游离钙%;蛋白结合钙%）与 哺乳动物血液的钙结合蛋白;（3）一种特异性钙结合蛋白存在于 双壳类外套膜细胞;（4）哺乳动物钙代谢的调节因子 （甲状旁腺素、降钙素、维生素D2、1，25二羟胆钙化醇） 影响双壳类的钙摄取/调节。 实验将利用 整个双壳类，分离的套膜细胞（内套膜和外套膜 分别为上皮细胞）和双壳类血浆。 放射性示踪剂Ca 45 将用于跟踪蛤组织中钙的吸收、储存和转移， 亚细胞组分和血浆。 蛋白质表征将是 通过聚丙烯酰胺凝胶电泳（天然和SDS）进行 PAGE）、蛋白质电印迹（PVDF膜）和放射自显影。 的 钙调节的双壳类模型有望成为一个方便和容易的 用于研究高钙血症和低钙血症的操作系统， 钙沉积和正常钙化过程的扰动。

The primary goal of this study is to demonstrate that calcium (Ca) uptake, transport and deposition in a marine bivalve mollusc (Mercenaria mercenaria) is an excellent invertebrate model for Ca regulation in the mammalian system. Although many of the same processes are already known to be present in both the invertebrate and vertebrate systems, additional similarities will be investigated to determine whether (1) Ca uptake/release by bivalve mantle cells is similar to mammalian ileal mucosal cells (i.e. mediated by active transport); (2) the distribution of Ca in bivalve blood (% free Ca2+; % protein-bound Ca) is similar to that of mammalian blood; (3) a specific Ca-binding protein is present in bivalve mantle cells; and (4) mammalian regulators of Ca metabolism (parathormone, calcitonin, vitamin D2, 1,25 dihydroxycholecalciferol) effect Ca uptake/regulation in the bivalve. Experiments will utilize whole bivalves, dissociated mantle cells (inner and outer mantle epithelia separately), and bivalve blood plasma. The radiotracer Ca45 will be used to follow Ca uptake, storage and transfer in clam tissues, subcellular fractions and plasma. Protein characterizations will be conducted by polyacrylamide gel electrophoresis (both native and SDS PAGE), protein electroblotting (PVDF membranes) and autoradiography. The bivalve model for Ca regulation promises to be a convenient and easily manipulated system for studies on hyper- and hypocalcemia, the regulation of Ca deposition, and perturbations of normal calcification processes.