Morphological differences in the skull of ascorbic acid-deficient ODS rats

Miyajima, Kuniaki; Ito, Ritsuki; Matsuyama, Takashi; Togari, Akifumi; Matsumoto, Shosei; Iizuka, Tetsuo

doi:10.1016/0003-9969(94)00174-a

Cited by 10 publications

(9 citation statements)

References 8 publications

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“…ODS rats can not biosynthesize AsA due to their hereditary lack of L-gulonolactone oxidase (Mizushima et al, 1984), and they show remarkably reduced plasma AsA levels when fed an AsAdeficient diet (Miyajima et al, 1995;Togari et al, 1995). Rats of the experimental group were fed an AsA-deficient diet (F-2; Funabashi Farms, Chiba, Japan), with free access to water without AsA, for up to 4 weeks.…”

Section: Methodsmentioning

confidence: 99%

“…Scorbutic guinea pig results in low levels of bone formation in leg bones and collagen synthesis in articular cartilage (Kipp et al, 1996), and leads to decreased expression of mRNAs for osteocalcin, alkaline phosphatase, and type I collagen, and to increased osteopontin expression in calvarial bone (Mahmoodian et al, 1996). Scorbutic rats are characterized by low body weight, small craniofacial size, and low concentrations of plasma alkaline phosphatase (Tsunenari et al, 1991;Miyajima et al, 1995;Togari et al, 1995). The leg bones and the tail vertebra show thin cortical bone and decreased volume of trabeculae accompanied by morphological alterations in epiphyseal cartilage (Tsunenari et al, 1991;Togari et al, 1995;Ellender and Gazelakis, 1996).…”

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confidence: 99%

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Morphological influence of ascorbic acid deficiency on endochondral ossification in osteogenic disorder Shionogi rat

Sakamoto

Takano

2002

Anat. Rec.

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The influences of chronic deficiency of L-ascorbic acid (AsA) on the differentiation of osteo-chondrogenic cells and the process of endochondral ossification were examined in the mandibular condyle and the tibial epiphysis and metaphysis by using Osteogenic Disorder Shionogi (ODS) rats that bear an inborn deficiency of L-gulonolactone oxidase. Weanling male rats were kept on an AsA-free diet for up to 4 weeks, until the symptoms of scurvy became evident. The tibiae and condylar processes of scorbutic rats displayed undersized and distorted profiles with thin cortical and scanty cancellous bones. In these scorbutic bones, the osteoblasts showed characteristic expanded round profiles of rough endoplasmic reticulum, and lay on the bone surface where the osteoid layer was missing. Trabeculae formation was deadlocked, although calcification of the cartilage matrix proceeded in both types of bone. Scorbutic condylar cartilage showed severe disorganization of cell zones, such as unusual thickening of the calcification zone, whereas the tibial cartilage showed no particular alterations (except for a moderately decreased population of chondrocytes). In condylar cartilage, hypertrophic chondrocytes were encased in a thickened calcification zone, and groups of nonhypertrophic chondrocytes occasionally formed cell nests surrounded by a metachromatic matrix in the hypertrophic cell zone. These results indicate that during endochondral ossification, chronic AsA deficiency depresses osteoblast function and disturbs the differentiation pathway of chondrocytes. The influence of scurvy on mandibular condyle cartilage is different from that on articular and epiphyseal cartilage of the tibia, suggesting that AsA plays different roles in endochondral ossification in the mandibular condyle and long bones. Anat Rec 268: 93-104, 2002.

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Section: Methodsmentioning

confidence: 99%

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confidence: 99%

Morphological influence of ascorbic acid deficiency on endochondral ossification in osteogenic disorder Shionogi rat

Sakamoto

Takano

2002

Anat. Rec.

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“…The bone matrix contains over 90% of protein as collagen (Termine et al, 1990) and it is well known that ascorbic acid is an essential cofactor for collagen synthesis and maturation (Peterkofsky et al, 1991). Animal studies have demonstrated that deficiency of this vitamin leads to impaired bone mass, cartilage, and connective tissue (Poal-Manresa et al, 1970; Kipp et al, 1996; Miyajima et al 1995). In addition to its involvement in collagen synthesis, ascorbic acid has also been reported to be necessary for the proliferation and multilayering of osteoblastic cells (Bellows et al, 1986).…”

Section: Introductionmentioning

confidence: 99%

Sodium-dependent vitamin C transporter SVCT2: Expression and function in bone marrow stromal cells and in osteogenesis

et al. 2013

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Ascorbic acid (Vitamin C) has a critical role in bone formation and osteoblast differentiation, but very little is known about the molecular mechanisms of ascorbic acid entry into bone marrow stromal cells (BMSCs). To address this gap in knowledge, we investigated the identity of the transport system that is responsible for the uptake of ascorbic acid into bone marrow stromal cells (BMSCs). First, we examined the expression of the two known isoforms of the sodium-coupled ascorbic acid transporter, namely SVCT1 and SVCT2, in BMSCs (Lin-ve Sca1+ve) and bone at the mRNA level. Only SVCT2 mRNA was detected in BMSCs and bone. Uptake of ascorbic acid in BMSCs was Na+-dependent and saturable. In order to define the role of SVCT2 in BMSC differentiation into osteoblasts, BMSCs were stimulated with osteogenic media for different time intervals, and the activity of SVCT2 was monitored by ascorbic acid uptake. SVCT2 expression was up-regulated during the osteogenic differentiation of BMSCs; the expression was maximal at the earliest phase of differentiation. Subsequently, osteogenesis was inhibited in BMSCs upon knock-down of SVCT2 by lentivirus shRNA. We also found that the expression of the SVCT2 could be negatively or positively modulated by the presence of oxidant (Sin-1) or antioxidant (Ascorbic acid) compounds, respectively, in BMSCs. Furthermore, we found that this transporter is also regulated with age in mouse bone. These data show that SVCT2 plays a vital role in the osteogenic differentiation of BMSCs and that its expression is altered under conditions associated with redox reaction. Our findings could be relevant to bone tissue engineering and bone related diseases such as osteoporosis in which oxidative stress and aging plays important role.

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“…Vitamin C is not synthesized by most mammals including humans (Naidu et al 2003; Drouin et al 2011). Animal studies have demonstrated that a deficiency of this vitamin leads to impaired bone mass, cartilage, and connective tissue (Poal-Manresa, et al 1970; Kippet al 1996; Miyajima, et al 1995). These musculoskeletal tissues originate from multipotent bone marrow stromal cells (BMSCs).…”

Section: Introductionmentioning

confidence: 99%

The crucial role of vitamin C and its transporter (SVCT2) in bone marrow stromal cell autophagy and apoptosis

et al. 2015

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Vitamin C is an antioxidant that plays a vital role in various biological processes including bone formation. Previously, we reported that vitamin C is transported into bone marrow stromal cells (BMSCs) through the sodium dependent Vitamin C Transporter 2 (SVCT2) and this transporter plays an important role in osteogenic differentiation. Furthermore, this transporter is regulated by oxidative stress. To date, however, the exact role of vitamin C and its transporter (SVCT2) in ROS regulated autophagy and apoptosis in BMSCs is poorly understood. In the present study, we observed that oxidative stress decreased survival of BMSCs in a dose-dependent manner and induced growth arrest in the G1 phase of the cell cycle. These effects were accompanied by the induction of autophagy, confirmed by P62 and LC3B protein level and punctate GFP–LC3B distribution. The supplementation of vitamin C significantly rescued the BMSCs from oxidative stress by regulating autophagy. Knockdown of the SVCT2 transporter in BMSCs synergistically decreased cell survival even under low oxidative stress conditions. Also, supplementing vitamin C failed to rescue cells from stress. Our results reveal that the SVCT2 transporter plays a vital role in the mechanism of BMSC survival under stress conditions. Altogether, this study has given new insight into the role of the SVCT2 transporter in oxidative stress related autophagy and apoptosis in BMSCs.

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Morphological differences in the skull of ascorbic acid-deficient ODS rats

Cited by 10 publications

References 8 publications

Morphological influence of ascorbic acid deficiency on endochondral ossification in osteogenic disorder Shionogi rat

Morphological influence of ascorbic acid deficiency on endochondral ossification in osteogenic disorder Shionogi rat

Sodium-dependent vitamin C transporter SVCT2: Expression and function in bone marrow stromal cells and in osteogenesis

The crucial role of vitamin C and its transporter (SVCT2) in bone marrow stromal cell autophagy and apoptosis

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