Abstract
BackgroundIn bone metabolism, Ca2+ disturbance and oxidative damage are the main biochemical factors related to pathology. Osteoblasts are bone-forming cells that also control bone endocrinology. Endocrine hormones and proteins are matured, folded, and secreted in the endoplasmic reticulum (ER). ER stress has emerged as a new pathological mechanism to explain bone disturbance. Here we studied the role of porcine placenta hydrolysates (PPHs) in the regulation of ER stress.MethodsCell viability was determined in vitro using trypan blue dye exclusion. ER stress and apoptosis were evaluated using immunoblotting and a caspase kit. The fluorescent Ca2+-binding dye Fura-2/AM was used to measure changes in intracellular Ca2+ ([Ca2+]i). ROS levels, NADPH oxidase activity, and superoxide dismutase (SOD) activity were also measured.ResultsPPHs protected MC3T3-E1 osteoblastic cells against thapsigargin (Tg)-induced ER stress. Moreover, PPHs regulated caspase-12 and −3 activities, thereby protecting against cell death, and also regulated Tg-induced Ca2+ release. The Ca2+ chelator BAPT/AM also regulated caspase-12 and −3 activities and prevented Ca2 stress-induced cell death. In the presence of PPHs or BAPTA/AM, Ca2+-related ROS were also regulated, as demonstrated by alterations in NADPH oxidase and SOD activity.ConclusionsPPHs appear to regulate bone metabolism disturbance by controlling Ca2+ concentrations, and thus ER stress and ROS, in osteoblasts cultured in vitro.Electronic supplementary materialThe online version of this article (doi:10.1186/s12906-016-1202-1) contains supplementary material, which is available to authorized users.
Highlights
In bone metabolism, Ca2+ disturbance and oxidative damage are the main biochemical factors related to pathology
We found that caspase-12 activity increased significantly after Tg treatment, whereas treatment with porcine placenta hydrolysates (PPHs) markedly reduced Tginduced caspase-12 activity in MC3T3-E1 cells (Fig. 1b)
MC3T3-E1 cells were treated with Tg in the presence or absence of PPHs and the levels of various apoptosis-related proteins were analyzed by immunoblotting
Summary
Ca2+ disturbance and oxidative damage are the main biochemical factors related to pathology. Osteoblasts are bone-forming cells that control bone endocrinology. Endocrine hormones and proteins are matured, folded, and secreted in the endoplasmic reticulum (ER). ER stress has emerged as a new pathological mechanism to explain bone disturbance. An imbalance between bone resorption and bone formation is the dominant mechanism causing osteoporosis [1, 2]. Since new bone formation primarily depends on osteoblasts, factors that disturb their bone-forming characteristics can lead to bone formation defects or related pathological conditions. Osteoblasts are secretory cells with well-developed endoplasmic reticulum (ER) cristae. The balance of osteoblasts and osteoclastic cells is carefully controlled [1, 3, 4].
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