Search tips
Search criteria

Results 1-5 (5)

Clipboard (0)
more »
Year of Publication
Document Types
1.  Ascorbic acid insufficiency induces the severe defect on bone formation via the down-regulation of osteocalcin production 
Anatomy & Cell Biology  2013;46(4):254-261.
The L-gulono-γ-lactone oxidase gene (Gulo) encodes an essential enzyme in the synthesis of ascorbic acid from glucose. On the basis of previous findings of bone abnormalities in Gulo-/- mice under conditions of ascorbic acid insufficiency, we investigated the effect of ascorbic acid insufficiency on factors related to bone metabolism in Gulo-/- mice. Four groups of mice were raised for 4 weeks under differing conditions of ascorbic acid insufficiency, namely, wild type; ascorbic acid-sufficient Gulo-/- mice, 3-week ascorbic acid-insufficient Gulo-/- mice, and 4-week ascorbic acid-insufficient Gulo-/- mice. Four weeks of ascorbic acid insufficiency resulted in significant weight loss in Gulo-/- mice. Interestingly, average plasma osteocalcin levels were significantly decreased in Gulo-/- mice after 3 weeks of ascorbic acid insufficiency. In addition, the tibia weight in ascorbic acid-sufficient Gulo-/- mice was significantly higher than that in the other three groups. Moreover, significant decreases in trabecular bone volume near to the growth plate, as well as in trabecular bone attachment to the growth plate, were evident in 3- or 4-week ascorbic acid-insufficient Gulo-/-. In summary, ascorbic acid insufficiency in Gulo-/- mice results in severe defects in normal bone formation, which are closely related to a decrease in plasma osteocalcin levels.
PMCID: PMC3875843  PMID: 24386598
L-Gulonolactone oxidase; Ascorbic acid; Osteogenesis; Osteocalcin
2.  Suppression of in vitro murine T cell proliferation by human adipose tissue-derived mesenchymal stem cells is dependent mainly on cyclooxygenase-2 expression 
Anatomy & Cell Biology  2013;46(4):262-271.
Mesenchymal stem cells (MSCs) of human origin have been frequently applied to experimental animal models to evaluate their immunomodulatory functions. MSCs are known to be activated by cytokines from T cells, predominantly by interferon-γ (IFN-γ), in conjunction with other cytokines such as tumor necrosis factor-α (TNF-α) and interlukin-1β. Because IFN-γ is not cross-reactive between human and mouse species, the manner in which human MSCs administered in experimental animals are activated and stimulated to function has been questioned. In the present study, we established MSCs from human adipose tissue. They successfully suppressed the proliferation of not only human peripheral blood mononuclear cells but also mouse splenic T cells. When these human MSCs were stimulated with a culture supernatant of mouse T cells or recombinant murine TNF-α, they expressed cyclooxygenase-2 (COX-2), but not indoleamine 2,3-dioxygenase. The dominant role of COX-2 in suppressing mouse T cell proliferation was validated by the addition of COX-2 inhibitor in the co-culture, wherein the suppressed proliferation was almost completely recovered. In conclusion, human MSCs in a murine environment were activated, at least in part, by TNF-α and mainly used COX-2 as a tool for the suppression of in vitro T cell proliferation. These results should be considered when interpreting results for human MSCs in experimental animals.
PMCID: PMC3875844  PMID: 24386599
Mesenchymal stem cells; Humans; Cyclooxygenase-2; Immunomodulation
3.  Students' perception of anatomy education at a Korean medical college with respect to time and contents 
Anatomy & Cell Biology  2013;46(2):157-162.
Among medical education institutions worldwide, the time allotted for anatomy instruction has decreased without any reasonable time optimization suggestions. In addition, the utility of cadaver dissection has long been debated. Herein, we surveyed students' perceptions of anatomy education with respect to time and hands-on cadaver dissection, at Seoul National University College of Medicine. With the help of a questionnaire, we surveyed third- and fourth-year students at our institute who had completed the anatomy module as freshmen as well as their clinical clerkship. At our institute, students complete 50 hours of anatomy lectures and 120 hours of dissection laboratory during their first year. According to the survey responses, they generally considered these durations to be adequate for achieving their anatomy education goals. Almost all the students regarded the dissection laboratory as an essential and most helpful modality. Thus, we suggest that these ranges of time along with cadaver dissection could be useful guidelines for optimized anatomy education. The survey data also indicated that a more clinically oriented anatomy education could improve students' results.
PMCID: PMC3713280  PMID: 23869263
Anatomy education; Cadaver dissection; Korean medical college
4.  Vitamin C acts indirectly to modulate isotype switching in mouse B cells 
Anatomy & Cell Biology  2010;43(1):25-35.
Vitamin C, one of essential micronutrients, has been reported to modulate the humoral immune responses in some mammals. We investigated whether vitamin C might modulate this response in mice by directly affecting B cells. Splenic B cells were isolated and activated by CD40- and B cell receptor-ligation in vitro. The cells were cultured with a pretreatment of vitamin C from 0 to 1 mM of concentrations. Vitamin C slightly increased apoptosis of B cells dose-dependently and behaved as an antioxidant. We found that in vivo administration of vitamin C by intraperitoneal injection affected isotype switching as previously reported: the titer of antigen-specific IgG1 antibody was decreased, while that of IgG2a was unaffected. Somewhat different from those observed in vivo, in vitro exposure to vitamin C slightly decreased isotype switching to IgG1 and increased isotype switching to IgG2a. Pretreatment with vitamin C in the safe range did not affect either proliferation of cultured B cells or the expression of CD80 and CD86 in those cells. Taken together, in vivo results suggest that vitamin C acts to modulate isotype switching in the mouse. However, because of our in vitro results, we suggest that the modulation exerted by vitamin C in vivo is by indirectly affecting B cells, perhaps by directly influencing other immune cells such as dendritic cells.
PMCID: PMC2998772  PMID: 21190002
Vitamin C; antioxidant; reactive oxygen species; mouse B cell; isotype switching
5.  Mega-dose vitamin C attenuated lung inflammation in mouse asthma model 
Anatomy & Cell Biology  2010;43(4):294-302.
Asthma is a Th2-dependent disease mediated by IgE and Th2 cytokines, and asthmatic patients suffer from oxidative stresses from abnormal airway inflammation. Vitamin C is a micro-nutrient functioning as an antioxidant. When administered at a mega-dose, vitamin C has been reported to shift immune responses toward Th1. Thus, we tried to determine whether vitamin C exerted beneficial effects in asthma animal model. Asthma was induced in mice by sensitizing and challenging with ovalbumin. At the time of challenge, 3~5 mg of vitamin C was administered and the effects were evaluated. Vitamin C did not modulate Th1/Th2 balance in asthma model. However, it decreased airway hyperreactivity to methacholine, decreased inflammatory cell numbers in brochoalveolar lavage fluid, and moderate reduction of perivascular and peribronchiolar inflammatory cell infiltration. These results suggest that vitamin C administered at the time of antigen challenge exerted anti-inflammatory effects. Further studies based on chronic asthma model are needed to evaluate a long-term effect of vitamin C in asthma. In conclusion, even though vitamin C did not show any Th1/Th2 shifting effects in this experiment, it still exerted moderate anti-inflammatory effects. Considering other beneficial effects and inexpensiveness of vitamin C, mega-dose usage of vitamin C could be a potential supplementary modality for the management of asthma.
PMCID: PMC3026181  PMID: 21267403
Asthma; Vitamin C; Lung inflammation; Th1/Th2 balance

Results 1-5 (5)