ACIDOSIS INHIBITS OSTEOBLASTIC AND STIMULATES OSTEOCLASTIC ACTIVITY INVITRO
ACIDOSIS INHIBITS OSTEOBLASTIC AND STIMULATES OSTEOCLASTIC ACTIVITY INVITRO
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DOI：
10.1152/ajprenal.1992.262.3.f442
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发表时间：
1992-03-01
影响因子：
--
通讯作者：
BUSHINSKY, DA
中科院分区：
文献类型：
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作者：
KRIEGER, NS;SESSLER, NE;BUSHINSKY, DA
代谢性酸中毒通过物理化学和细胞介导机制诱导培养的新生小鼠颅骨净钙通量（J(Ca)）。为了确定成骨细胞在酸诱导J（Ca）中的作用，在降低pH和碳酸氢盐培养基（代谢性酸中毒（Met）模型）中培养的颅骨中评估胶原合成和碱性磷酸酶活性，并与对照组（Ctl）进行比较。胶原合成从Ctl的30.5 +/- 1.1下降到Met的25.1 +/- 0.4%，碱性磷酸酶从Ctl的403 +/- 25下降到298 +/- 21 nmol P(i).min-1。蛋白质-1。在酸中毒期间，J（Ca）与胶原合成百分比（r = -0.743, n = 11, P = 0.009）和碱性磷酸酶活性（r = -0.453, n = 22, P = 0.034）呈负相关。为了确定破骨细胞在酸诱导J（Ca）中的作用，在没有或存在破骨抑制剂降钙素（CT, 3 × 10(-9) M）的情况下，测定了Ctl和Met中破骨细胞β -葡糖醛酸酶活性。与Ctl （4.6 +/- 0.3 μ -g苯酚-1 - h-1）相比，Met增加了β -葡萄糖醛酸酶（5.9 +/- 0.2），而CT在Ctl和Met中均抑制β -葡萄糖醛酸酶（分别为3.1 +/- 0.2和3.5 +/- 0.3）。酸中毒时J（Ca）与β -葡糖醛酸酶活性直接相关（r = 0.683, n = 42, P < 0.001）。因此，体外酸中毒过程中细胞介导的J（Ca）成分似乎是由抑制成骨细胞活性和刺激破骨细胞活性共同作用的结果。
Metabolic acidosis induces net calcium flux (J(Ca)) from cultured neonatal mouse calvariae through physicochemical and cell-mediated mechanisms. To determine the role of osteoblasts in acid-induced J(Ca), collagen synthesis and alkaline phosphatase activity were assessed in calvariae incubated in reduced pH and bicarbonate medium, a model of metabolic acidosis (Met), and compared with controls (Ctl). Collagen synthesis fell from 30.5 +/- 1.1 in Ctl to 25.1 +/- 0.4% with Met, and alkaline phosphatase decreased from 403 +/- 25 in Ctl to 298 +/- 21 nmol P(i).min-1.mg protein-1 with Met. During acidosis J(Ca) was correlated inversely with percent collagen synthesis (r = -0.743, n = 11, P = 0.009) and with alkaline phosphatase activity (r = -0.453, n = 22, P = 0.034). To determine the role of osteoclasts in acid-induced J(Ca), osteoclastic beta-glucuronidase activity was determined in Ctl and Met in the absence or presence of the osteoclastic inhibitor calcitonin (CT, 3 x 10(-9) M). Met increased beta-glucuronidase (5.9 +/- 0.2) compared with Ctl (4.6 +/- 0.3-mu-g phenolphthalein released.bone-1.h-1), whereas CT inhibited beta-glucuronidase in both Ctl and Met (3.1 +/- 0.2 and 3.5 +/- 0.3, respectively). During acidosis J(Ca) was correlated directly with beta-glucuronidase activity (r = 0.683, n = 42, P < 0.001). Thus the cell-mediated component of J(Ca) during acidosis in vitro appears to result from a combination of inhibited osteoblastic and stimulated osteoclastic activity.